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Alzheimer’s may have once spread from person to person, but the risk of that happening today is incredibly low

<p><em><a href="https://theconversation.com/profiles/steve-macfarlane-4722">Steve Macfarlane</a>, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a></em></p> <p>An article published this week in the prestigious journal <a href="https://www.nature.com/articles/s41591-023-02729-2">Nature Medicine</a> documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.</p> <p>The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.</p> <p>Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.</p> <p>The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop <a href="https://www.vdh.virginia.gov/epidemiology/epidemiology-fact-sheets/creutzfeldt-jakob-disease-cjd/">Creuztfeldt-Jakob disease</a> (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.</p> <h2>What’s CJD got to do with Alzehimer’s?</h2> <p>CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.</p> <p>Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised <a href="https://en.wikipedia.org/wiki/United_Kingdom_BSE_outbreak">public health concerns</a> over the eating of beef products in the United Kingdom in the 1980s.</p> <h2>Human growth hormone used to come from donated organs</h2> <p>Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.</p> <p>But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around <a href="https://www.cdc.gov/mmwr/preview/mmwrhtml/00000563.htm">16,000 donated glands</a>.</p> <p>An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.</p> <p>hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.</p> <h2>What are the latest findings about Alzheimer’s disease?</h2> <p>The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.</p> <p>The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.</p> <p>They considered other explanations for the findings but concluded donated hGH was the likely cause.</p> <p>Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.</p> <p>Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is <a href="https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-017-0488-7">increasing evidence</a> these proteins spread in the brain in a <a href="https://pubmed.ncbi.nlm.nih.gov/8086126/">similar way to prion diseases</a>. So the mode of transmission the authors propose is certainly plausible.</p> <p>However, given the amyloid protein deposits in the brain <a href="https://www.nia.nih.gov/news/estimates-amyloid-onset-may-predict-alzheimers-progression">at least 20 years</a> before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.</p> <h2>When was this process used in Australia?</h2> <p>In Australia, donated pituitary material <a href="https://www.health.gov.au/sites/default/files/documents/2022/07/the-cjd-review-final-report.pdf">was used</a> from 1967 to 1985 to treat people with short stature and infertility.</p> <p><a href="https://www.health.gov.au/sites/default/files/documents/2022/07/the-cjd-review-final-report.pdf">More than 2,000 people</a> received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.</p> <p>The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are <a href="https://www.mja.com.au/journal/2010/193/6/iatrogenic-creutzfeldt-jakob-disease-australia-time-amend-infection-control">considered to be</a> incredibly small.</p> <p>Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4356853/">around 5%</a> of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.</p> <h2>The risk is very low – and you can’t ‘catch’ it like a virus</h2> <p>The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.</p> <p>Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.</p> <p>The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/222374/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p> <p><a href="https://theconversation.com/profiles/steve-macfarlane-4722"><em>Steve Macfarlane</em></a><em>, Head of Clinical Services, Dementia Support Australia, &amp; Associate Professor of Psychiatry, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a></em></p> <p><em>Image credits: Getty Images </em></p> <p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/alzheimers-may-have-once-spread-from-person-to-person-but-the-risk-of-that-happening-today-is-incredibly-low-222374">original article</a>.</em></p>

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Do stress and depression increase the risk of Alzheimer’s disease? Here’s why there might be a link

<p><em><a href="https://theconversation.com/profiles/yen-ying-lim-355185">Yen Ying Lim</a>, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a> and <a href="https://theconversation.com/profiles/ivana-chan-1477100">Ivana Chan</a>, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a></em></p> <p>Dementia affects more than <a href="https://www.who.int/news-room/fact-sheets/detail/dementia">55 million people</a> around the world. A number of factors can increase a person’s risk of developing dementia, <a href="https://link.springer.com/article/10.14283/jpad.2023.119">including</a> high blood pressure, poor sleep, and physical inactivity. Meanwhile, keeping cognitively, physically, and socially active, and limiting alcohol consumption, can <a href="https://www.thelancet.com/article/S0140-6736(20)30367-6/fulltext">reduce the risk</a>.</p> <p>Recently, a <a href="https://alzres.biomedcentral.com/articles/10.1186/s13195-023-01308-4">large Swedish study</a> observed that chronic stress and depression were linked to a higher risk of developing <a href="https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12638">Alzheimer’s disease</a>, the most common form of dementia. The researchers found people with a history of both chronic stress and depression had an even greater risk of the disease.</p> <p>Globally, around <a href="https://www.who.int/news-room/fact-sheets/detail/depression">280 million people</a> have depression, while roughly <a href="https://www.who.int/news-room/fact-sheets/detail/anxiety-disorders">300 million people</a> experience anxiety. With so many people facing mental health challenges at some stage in their lives, what can we make of this apparent link?</p> <h2>What the study did and found</h2> <p>This study examined the health-care records of more than 1.3 million people in Sweden aged between 18 and 65. Researchers looked at people diagnosed with chronic stress (technically chronic stress-induced exhaustion disorder), depression, or both, between 2012 and 2013. They compared them with people not diagnosed with chronic stress or depression in the same period.</p> <p>Participants were then followed between 2014 and 2022 to determine whether they received a diagnosis of mild cognitive impairment or dementia, in particular Alzheimer’s disease. <a href="https://alz-journals.onlinelibrary.wiley.com/doi/10.1016/j.jalz.2016.07.151">Mild cognitive impairment</a> is often seen as the precursor to dementia, although not everyone who has mild cognitive impairment will progress to dementia.</p> <p>During the study period, people with a history of either chronic stress or depression were around twice as likely to be diagnosed with mild cognitive impairment or Alzheimer’s disease. Notably, people with both chronic stress and depression were up to four times more likely to be diagnosed with mild cognitive impairment or Alzheimer’s disease.</p> <h2>Important considerations</h2> <p>In interpreting the results of this study, there are some key things to consider. First, the diagnosis of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9438479/">chronic stress-induced exhaustion disorder</a> is unique to the Swedish medical system. It is characterised by at least six months of intensive stress without adequate recovery. Symptoms include exhaustion, sleep disturbance and concentration difficulties, with a considerable reduction in ability to function. Mild stress may not have the same effect on dementia risk.</p> <p>Second, the number of people diagnosed with dementia in this study (the absolute risk) was very low. Of the 1.3 million people studied, 4,346 were diagnosed with chronic stress, 40,101 with depression, and 1,898 with both. Of these, the number who went on to develop Alzheimer’s disease was 14 (0.32%), 148 (0.37%) and 9 (0.47%) respectively.</p> <p>These small numbers may be due to a relatively young age profile. When the study began in 2012–2013, the average age of participants was around 40. This means the average age in 2022 was around 50. Dementia is typically diagnosed in <a href="https://www.health.gov.au/topics/dementia/about-dementia">people aged over 65</a> and diagnosis <a href="https://karger.com/dem/article-abstract/34/5-6/292/99009/Overdiagnosis-of-Dementia-in-Young-Patients-A?redirectedFrom=fulltext">in younger ages</a> may be less reliable.</p> <p>Finally, it’s possible that in some cases stress and depressive symptoms may reflect an awareness of an already declining memory ability, rather than these symptoms constituting a risk factor in themselves.</p> <p>This last consideration speaks to a broader point: the study is observational. This means it can’t tell us one thing caused the other – only that there is an association.</p> <h2>What does other evidence say?</h2> <p><a href="https://link.springer.com/article/10.14283/jpad.2023.119">Many studies</a> indicate that significant symptoms of depression, anxiety and stress are related to higher dementia risk. However, the nature of this relationship is unclear. For example, are depressive and anxiety symptoms a risk factor for dementia, or are they consequences of a declining cognition? It’s likely to be a bit of both.</p> <p>High <a href="https://pubmed.ncbi.nlm.nih.gov/32082139/">depressive and anxiety symptoms</a> are commonly reported in people with mild cognitive impairment. However, studies in middle-aged or younger adults suggest they’re important dementia risk factors too.</p> <p>For example, similar to the Swedish study, other <a href="https://www.sciencedirect.com/science/article/pii/S0165032719323031">studies</a> have suggested people with a history of depression are twice as likely to develop dementia than those without this history. In addition, in middle-aged adults, high anxiety symptoms are associated with <a href="https://pubmed.ncbi.nlm.nih.gov/34648818/">poorer cognitive function</a> and <a href="https://bmjopen.bmj.com/content/8/4/e019399">greater dementia risk</a> in later life.</p> <h2>Why the link?</h2> <p>There are several potential pathways through which stress, anxiety and depression could increase the risk of dementia.</p> <p>Animal studies suggest cortisol (a hormone produced when we’re stressed) can increase risk of Alzheimer’s disease by causing the accumulation of key proteins, <a href="https://pubmed.ncbi.nlm.nih.gov/34159699/">amyloid and tau</a>, in the brain. The accumulation of these proteins can result in increased <a href="https://www.mdpi.com/1422-0067/23/18/10572">brain inflammation</a>, which affects the brain’s nerves and supporting cells, and can ultimately lead to brain volume loss and memory decline.</p> <p>Another potential pathway is through <a href="https://www.sciencedirect.com/science/article/pii/S1087079217300114?via%3Dihub">impaired sleep</a>. Sleep disturbances are common in people with chronic stress and depression. Similarly, people with Alzheimer’s disease commonly report sleep disturbances. Even in people with <a href="https://pubmed.ncbi.nlm.nih.gov/34668959/">early Alzheimer’s disease</a>, disturbed sleep is related to poorer memory performance. Animal studies suggest poor sleep can also enhance accumulation of <a href="https://pubmed.ncbi.nlm.nih.gov/31408876/">amyloid and tau</a>.</p> <p>We still have a lot to learn about why this link might exist. But evidence-based strategies which target chronic stress, anxiety and depression may also play a role in reducing the risk of dementia.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/215065/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p> <p><a href="https://theconversation.com/profiles/yen-ying-lim-355185"><em>Yen Ying Lim</em></a><em>, Associate Professor, Turner Institute for Brain and Mental Health, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a> and <a href="https://theconversation.com/profiles/ivana-chan-1477100">Ivana Chan</a>, PhD candidate, clinical psychology, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a></em></p> <p><em>Image credits: Getty Images</em></p> <p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/do-stress-and-depression-increase-the-risk-of-alzheimers-disease-heres-why-there-might-be-a-link-215065">original article</a>.</em></p>

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Promising Alzheimer’s drug offers hope for a bright future in treatment

<p>A remarkable and significant breakthrough in the fight against Alzheimer’s disease is ushering in a new era of hope and possibilities for patients grappling with early onset dementia.</p> <p>Scientists and researchers are celebrating this groundbreaking development, viewing it as a tremendous opportunity to transform the landscape of Alzheimer's treatment.</p> <p>The drug in question, donanemab, developed by Eli Lilly, has shown remarkable success in clinical trials and is anticipated to receive approval from the Food and Drug Administration later this year, according to a report in the <a href="https://nypost.com/2023/07/17/alzheimers-drug-donanemab-lowers-risk-of-dementia/" target="_blank" rel="noopener"><em>New York Post</em></a>.</p> <p>Individuals who participated in the donanemab trials experienced a remarkable 40% reduction in the risk of transitioning from mild cognitive impairment to mild or moderate dementia. This is an extraordinary advancement that brings renewed optimism to those affected by this devastating condition.</p> <p>Donanemab would be the third Alzheimer’s drug to emerge in recent months, following the introduction of Leqembi and Aduhelm. This is just the beginning of an exciting new chapter in the realm of molecular therapies for Alzheimer's, as expressed by Dr. Gil Rabinovici, director of the University of California San Francisco’s Memory and Ageing Centre, in an editorial for <em>JAMA</em>.</p> <p>Dr. Daniel Skovronsky, the chief scientific and medical officer at Lilly, has emphasised the significance of this breakthrough. He states, "This will be a very important and meaningful drug," as quoted in <em>Fierce Biotech</em>. Skovronsky further adds, "[T]here’s a huge opportunity here for patients." Such resolute optimism is inspiring, reflecting the tremendous potential this drug holds for transforming lives.</p> <p>Similar to Leqembi and Aduhelm, donanemab is a monoclonal antibody designed to target plaque in the brain, specifically the amyloid protein. These amyloid plaques are responsible for the propagation of another protein called tau, which contributes to the development of Alzheimer's disease.</p> <p>Notably, the donanemab trial also revealed that the drug slowed cognitive decline by an impressive 35% compared to a placebo in individuals with low to intermediate levels of tau protein in the brain. In fact, donanemab demonstrated superior efficacy in clearing amyloid plaques when compared to Aduhelm and Leqembi.</p> <p>Moreover, unlike Leqembi, which necessitates long-term usage, patients taking donanemab may follow a fixed-duration dosing schedule, potentially allowing some individuals to discontinue the treatment after a certain period. "I expect that many patients will be able to stop dosing even as soon as 12 months," Skovronsky affirmed. This stands as a significant departure from being prescribed a lifelong medication, providing an exciting and meaningful prospect for patients.</p> <p>While it is important to note that these new Alzheimer’s drugs do carry limitations and risks, medical experts remain cautiously optimistic. Donanemab, along with the other emerging drugs, has been associated with brain swelling and bleeding. Tragically, three individuals in the donanemab clinical trial lost their lives due to these side effects.</p> <p>The risk of brain swelling and bleeding is heightened among those carrying the APOE4 gene, which is associated with an increased susceptibility to Alzheimer’s. Furthermore, individuals with more advanced stages of the disease showed minimal to no benefit compared to those who received a placebo.</p> <p>As a result, it is possible that donanemab will be recommended primarily for individuals with low to intermediate levels of tau proteins, indicating milder forms of the disease.</p> <p>Nevertheless, Skovronsky and other medical experts maintain their optimism regarding the FDA's approval, expressing the urgent need for it to come to fruition. Skovronsky highlights, "Every day that goes by, there are some patients who pass through this early stage of Alzheimer’s disease and become more advanced, and they won’t benefit from treatment. That’s a very pressing sense of urgency."</p> <p>While challenges and risks remain, the emergence of donanemab and its potential approval by the FDA represents a beacon of hope for the millions of individuals and families affected by Alzheimer's disease. It symbolises the start of a new chapter in the fight against this debilitating condition, offering renewed prospects for a brighter future filled with effective treatments and improved quality of life.</p> <p><em>Image: Shutterstock</em></p> <p> </p>

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Why understanding how spiders spin silk may hold clues for treating Alzheimer’s disease

<p><a href="https://theconversation.com/profiles/michael-landreh-1328287">Michael Landreh</a>, <em><a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a></em> and <a href="https://theconversation.com/profiles/anna-rising-1440132">Anna Rising</a>, <em><a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a></em></p> <p>Really, we should envy spiders. Imagine being able to make silk like they do, flinging it around to get from place to place, always having a <a href="https://pubs.acs.org/doi/10.1021/acsmacrolett.8b00678">strong-as-steel safety line</a> or spinning a comfy hammock whenever they need a rest.</p> <p>The fascinating properties of spider silk make it no wonder that scientists have been trying to unravel its secrets for decades.</p> <p>If we could understand and recreate the spinning process, we could produce artificial spider silk for a <a href="https://www.sciencedirect.com/science/article/abs/pii/S0141813021021292">range of medical applications</a>. For example, artificial silk can help <a href="https://doi.org/10.1016/j.biomaterials.2021.120692">regenerate the nerves that connect our brain and limbs</a>, and can shuttle <a href="https://doi.org/10.1021/acs.biomac.0c01138">drug molecules directly into the cells where they are needed</a>.</p> <figure><iframe src="https://www.youtube.com/embed/zNtSAQHNONo?wmode=transparent&amp;start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> <p>Spider silk is made of <a href="https://www.sciencedirect.com/topics/engineering/spidroins">proteins called spidroins</a>, which the spider stores in a silk gland in its abdomen. There are several types of spidroin for spinning different sorts of silk. Spiders <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673682/">store them as a liquid</a> that resembles oil droplets.</p> <p>But one of the questions that has eluded scientists so far is how spiders turn these liquid droplets into silk. We decided to investigate why the spidroins form droplets, to get us closer to replicating a spider’s spinning process.</p> <h2>Weaving a web</h2> <p>The trick that spiders use to speed up their spinning process can be used to spin better artificial silk, or even develop new spinning processes.</p> <p>In 2017, we learned to <a href="https://www.nature.com/articles/ncomms15504">make synthetic silk fibres</a> by emulating the silk gland, but we did not know how things work inside the spider. Now we know that forming droplets first <a href="https://pubmed.ncbi.nlm.nih.gov/37084706/">speeds up the conversion to these fibres</a>.</p> <p>An important clue to how the droplets and fibres are related came from an unexpected area of our research – on <a href="https://pubmed.ncbi.nlm.nih.gov/23013511/">Alzheimer’s and Parkinson’s diseases</a>. Proteins that are involved in these diseases, called <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/alpha-synuclein#:%7E:text=%CE%B1%2DSynuclein%20is%20a%20highly,linked%20to%20familial%20Parkinson%20disease.">alpha-synuclein</a> and <a href="https://www.alz.org/media/Documents/alzheimers-dementia-tau-ts.pdf">tau</a>, can assemble into tiny, oil-like droplets in human cells.</p> <p>Tau is a protein that helps stabilise the internal skeleton of nerve cells (neurons) in the brain. This internal skeleton has a tube-like shape through which nutrients and other essential substances travel to reach different parts of the neuron.</p> <p>In Alzheimer’s disease, an abnormal form of tau builds up and clings to the normal tau proteins, creating “tau tangles”.</p> <p>Alpha-synuclein is found in large quantities in <a href="https://www.webmd.com/mental-health/what-is-dopamine">dopamine-producing nerve cells</a>. Abnormal forms of this protein are linked to Parkinson’s disease.</p> <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip"><img src="https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=600&amp;h=400&amp;fit=crop&amp;dpr=1 600w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=600&amp;h=400&amp;fit=crop&amp;dpr=2 1200w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=600&amp;h=400&amp;fit=crop&amp;dpr=3 1800w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;h=503&amp;fit=crop&amp;dpr=1 754w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=754&amp;h=503&amp;fit=crop&amp;dpr=2 1508w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=754&amp;h=503&amp;fit=crop&amp;dpr=3 2262w" alt="Beautiful spider web with water drops close-up" /></a><figcaption><span class="caption">The trick spiders use to speed up their spinning process can be used to spin better artificial silk.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/beautiful-spider-web-water-drops-close-155560781">Aastels/Shutterstock</a></span></figcaption></figure> <p>Oil droplets of either one of these proteins form in humans when they become entangled, like boiled spaghetti on a plate. At first, the proteins are flexible and elastic, much like spidroin oil droplets.</p> <p>But if the proteins remain entangled, they get stuck together which alters their shape, changing them into rigid fibres. These can be toxic to human cells – for example, in neurodegenerative conditions such as Alzheimer’s.</p> <p>However, <a href="https://pubmed.ncbi.nlm.nih.gov/33148640/">spidroins can form droplets</a> too. This left us wondering if the same mechanism that causes neurodegeneration in humans could help the spider to convert liquid spidroins into rigid silk fibres.</p> <p>To find out, we used a <a href="https://www.nature.com/articles/nchembio.2269">synthetic spidroin called NT2RepCT</a>, which can be produced by bacteria. Under the microscope, we could see that this synthetic spidroin formed liquid droplets when it was dissolved in phosphate buffer, a type of salt found in the spider’s silk gland. This allowed us to replicate spider silk spinning conditions in the lab.</p> <h2>Silky science</h2> <p>Next, we studied how the spidroin proteins act when they form droplets. To answer this question, we turned to an analysis technique <a href="https://www.britannica.com/science/mass-spectrometry">called mass spectrometry</a>, to measure how the weight of the proteins changed when they formed droplets. To our surprise, we saw that the spidroin proteins, which normally form pairs, instead split into single molecules.</p> <p>We needed to do more work to find out how these protein droplets help spiders spin silk. Previous research has shown spidroins have different parts, called domains, with separate functions.</p> <p>The end part of the spidroin, called c-terminal domain, makes it form pairs. The c-terminal also starts <a href="https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001921">fibre formation when it comes into contact with acid</a>.</p> <p>So, we made a spidroin which contained only the c-terminal domain and tested its ability to form fibres.</p> <p>When we used phosphate buffer to entangle the proteins into droplets, they turned into rigid fibre instantly. When we added acid without first making droplets, fibre formation took much longer.</p> <p>This makes sense since the spidroin molecules must find each other when forming a fibre. Entangling the spidroins like spaghetti helps them rapidly assemble into silk.</p> <p>This finding tells us how the spider can instantly convert its spidroins into a solid thread. It also uncovered how nature uses the same mechanism that can make brain proteins toxic to create some of its most amazing structures.</p> <p>The surprising parallel between spider silk spinning and fibres toxic to humans could one day lead to new clues about how to fight neurodegenerative disorders.</p> <p>Scientists may use spider silk research, including what we have learned about the spider silk domains, to keep human proteins from sticking together – to stop them from becoming toxic. If spiders can learn how to keep their sticky proteins in check, perhaps so can we.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/205857/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /></p> <p><a href="https://theconversation.com/profiles/michael-landreh-1328287">Michael Landreh</a>, Researcher, Department of Microbiology, Tumor and Cell Biology, <em><a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a></em> and <a href="https://theconversation.com/profiles/anna-rising-1440132">Anna Rising</a>, Researcher in Veterinary medicine biochemistry, <em><a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a></em></p> <p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/why-understanding-how-spiders-spin-silk-may-hold-clues-for-treating-alzheimers-disease-205857">original article</a>.</em></p> <p><em>Images: Getty</em></p>

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Huge news for Alzheimer’s sufferers

<p>An experimental new drug by Eli Lilly has demonstrated an ability to slow the progression of Alzheimer’s disease, according to new study reports. </p> <p>The pharmaceutical company has said that its drug, donanemab, met each goal of their 18-month trial, successfully slowing cognitive decline by 35 per cent compared to a placebo. </p> <p>1,182 individuals in the early stages of Alzheimer’s participated in the study, with each patient receiving monthly infusions of donanemab. </p> <p>After 12 months, half of the participants showed no evidence of amyloid plaques, while 48 per cent of patients in the trial had no disease progression at 12 months, compared to 29 per cent from the placebo group.</p> <p>In the wake of the news, experts are optimistic, but still hold concerns about the risks moving forward. </p> <p>Dr Ronald Petersen, a Mayo Clinic Alzheimer research, told the ABC that “Lilly's trial is the third to show removing amyloid from the brain slows progression of the disease, which could put to rest some lingering doubts about the benefits of drugs in the class and the amyloid-lowering theory.</p> <p>"It's modest, but I think it's real and I think it's clinically meaningful."</p> <p>Washington University neurologist Dr Erik Musiek noted that mounting evidence was suggesting “that these drugs do work”. </p> <p>He also said that the findings were reminding them of the benefits of early treatment, explaining that “it really does suggest that you need to remove these plaques early, before the tau really gets going.”</p> <p>When it comes to the associated risks, Eli Lilly have said that the drug’s side effects could include brain swelling as well as bleeding, with serious swelling occurring in 1.6 per cent of patients. </p> <p>As Dr Eric Reiman, Banner Alzheimer’s Institute’s executive director, explained, “clearly one saw benefits here, but there is some risk that needs to be considered.” </p> <p>From there, Lily plan to file for US approval by the end of June, and to proceed with regulars from other countries in the time after. A spokesperson for the company is confident that a decision over approval in the US should occur by the end of 2023, or early in 2024. </p> <p>Experts in the field want to see the study’s full results, which are likely to be presented at an Amsterdam Alzheimer’s meeting later in the year. </p> <p>As for the cost, the company has not yet finalised a price point, but CEO David Ricks informed CNBC that they intend for it to be similar to other therapies in the same field. </p> <p><em>Images: Getty</em></p>

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13 things neurologists do to help prevent Alzheimer’s disease

<p><strong>Understand Alzheimer's disease</strong></p> <p>Alzheimer’s disease is the leading cause of dementia. But all dementia is not Alzheimer’s, says Dr David Knopman, a neurologist at the Mayo Clinic in Minnesota. Dementia is a general term used to describe a set of symptoms that may include memory loss and difficulties with thinking, problem-solving or language.</p> <p>Alzheimer’s is a physical disease that targets the brain, causing problems with memory, thinking and behaviour. It is also age-related (symptoms usually start at age 65) and progressive, as symptoms usually  worsen over time. Research shows that plaques and tangles two proteins that build up and block connections between nerve cells and eventually kill nerve cells in the brain, cause Alzheimer’s symptoms.</p> <p><strong>Get enough sleep</strong></p> <p>When you toss and turn all night, levels of brain-damaging proteins in the cerebrospinal fluid can rise: A 2017 study in Brain suggests that those with chronic sleep problems during middle age may increase their risk of Alzheimer’s later in life.</p> <p>“You have to commit to the importance of sleep,” says neurologist Dr Gayatri Devi. “I prioritise sleep as one of the most important activities I do – I will leave a party early in order to get a good night’s sleep.”</p> <p><strong>Stay socially active</strong></p> <p>Say yes to those social invitations! A 2019 study published in PLOS Medicine found that social activity with friends in your 60s could lower your risk of dementia by 12%. “There is something intrinsically valuable about social engagement,” says Dr Knopman.</p> <p>“It makes sense that those who are more engaged, especially socially, will think more positively and have a better outlook on life.”</p> <p><strong>Keep learning</strong></p> <p>People with advanced degrees have a lower risk of Alzheimer’s, according to 2017 research published in the BMJ. Education seems to build a ‘cognitive reserve’, which enables the brain to better resist neurological damage.</p> <p>“Higher education has a powerful effect,” says Dr Knopman. It’s never too late, check out the continuing education courses offered online or near you.</p> <p><strong>Learn a second language</strong></p> <p>Speaking more than one language can protect against Alzheimer’s disease and other types of dementia, according to 2017 research published in Clinical Interventions in Aging.</p> <p>While no one is sure why a second language helps so much, Dr Knopman theorises that the effort to communicate bilingually is like a workout for the brain, helping preserve grey matter and neurons.</p> <p><strong>Do it yourself</strong></p> <p>Challenging your brain in new ways can enhance memory as you age. Dr Devi has her own take on this: “If there is a problem with the phone or the plumbing, I will try to fix it,” she says.</p> <p>“If I try to figure out how to fix this on my own, it is good for my brain.” Right now she’s designing and building a window seat. “It is a way to keep different parts of my brain thriving.”</p> <p><strong>Stay active</strong></p> <p>Exercise is crucial to your wellness and your brain. Research published in Cureus in 2020, found that people who exercise regularly can slow cognitive decline. According to the Alzheimer’s Society, the combined results of 11 studies indicate that regular exercise can reduce the risk of developing dementia by about 30%; it drops the risk of Alzheimer’s by 45%.</p> <p>“When you are physically active, you burn more calories and you’re less likely to be obese,” explains Dr Knopman. “You’ll have better cardiovascular health because you are pushing your heart rate.”</p> <p><strong>Take care of your heart</strong></p> <p>“What is good for the heart is good for the brain,” says Dr Devi. Conditions such as high blood pressure, diabetes and high cholesterol, which increase the risk of cardiovascular disease, may also increase the risk of developing Alzheimer’s, and a 2017 study in JAMA found that middle-aged people with risk factors for heart attacks and stroke are also more likely to develop changes in the brain that can lead to the disease.</p> <p>“Anything that keeps the heart healthy is directly related to brain health,” Dr Devi says. It also reduces the risk of stroke, which can cause its own kind of dementia – vascular dementia.</p> <p><strong>Lower your stress levels</strong></p> <p>Persistent stress can take a toll on the brain, and 2018 research published in Neurobiology of Stress indicates that chronic stress can accelerate Alzheimer’s disease. When you’re stressed, your body releases cortisol, a hormone linked to memory trouble.</p> <p>In addition, experts have found that stress can lead to conditions such as depression and anxiety, which also increases the risk for dementia, according to research in Current Opinion in Psychiatry. “Eliminating stress helps reduce the amount of cortisol and optimises glucose utilisation, which your brain needs for food,” says Dr Devi.</p> <p><strong>Try the MIND diet</strong></p> <p>A combination of the Mediterranean diet and the DASH (Dietary Approaches to Stop Hypertension) diet, the MIND diet is designed specifically for brain health. (MIND is short for Mediterranean-DASH Diet Intervention for Neurodegenerative Delay.) The diet is pretty pleasant: you eat at least three servings of whole grains a day, two portions of vegetables (one of which must be a leafy green), snack on nuts, eat lean proteins like chicken and fish, berries, and have a glass of wine a day.</p> <p>According to research in Alzheimer’s &amp; Dementia, those who adhered to the diet rigorously were able to lower their risk of cognitive decline later in life. You can’t trust all diets, warns Dr Knopman, but he likes this approach: “I tell my patients that if you follow a reasonable diet with lots of fresh fruits and vegetable that balances different food groups, and avoid obesity, you will be okay.”</p> <p><strong>Get your snoring checked out</strong></p> <p>Another way to wreck your sleep without realising it is with sleep apnea. According to the US National Institutes of Health, sleep apnoea occurs when a person’s upper airway becomes blocked repeatedly during sleep, reducing or completely stopping airflow. Many factors – from obesity to large tonsils to neuromuscular disorders – can cause sleep apnoea.</p> <p>Sleep apnoea not only prevents restful sleep, but untreated it can increase the risk of developing certain health conditions. “If left untreated, sleep apnoea has significant cardiovascular consequences and consequences of mental function,” says Dr Knopman.</p> <p><strong>Protect your head</strong></p> <p>According to the Alzheimer’s Association, there is a strong link between serious head trauma and developing Alzheimer’s later in life, especially if the injury involves loss of consciousness. A 2017 review of research in PLOS One suggests head injuries that require medical attention may increase the risk of dementia and Alzheimer’s disease.</p> <p>Wear a helmet while cycling, make your home fall-proof, and always use a seat belt to help protect your noggin.</p> <p><strong>Drink a cup of tea</strong></p> <p>Green tea has loads of health benefits – including some for your brain. A 2019 systematic review in Nutrients found that green tea might reduce the risk of dementia.</p> <p>And research in the Journal of the American Chemical Society found that it’s a compound in the beverage that can disrupt the formation of toxic plaques that contribute to Alzheimer’s disease.</p> <p><em>Image credits: Getty Images</em></p> <p><em>This article originally appeared on <a href="https://www.readersdigest.com.au/healthsmart/conditions/13-things-neurologists-do-to-help-prevent-alzheimers-disease?pages=1" target="_blank" rel="noopener">Reader's Digest</a>. </em></p>

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Experimental Alzheimer’s drug shows promise

<p>The first drug that can slow the rate of decline in Alzheimer’s patients has been found. The experimental drug, called lecanemab, is an antibody that targets the toxic clumps of amyloid protein associated with the mind-robbing disease. While these results are cause for celebration, there are still significant questions about its safety and rollout.</p> <p>The full results of the phase 3 lecanemab drug trial (the final stage of testing in humans) have <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2212948">been published in the New England Journal of Medicine</a>. The trial showed that patients receiving the drug had a 27% slower disease progression than those receiving a placebo after 18 months of treatment.</p> <p>Overall, this is good news. For the first time, we have a potential treatment that has a demonstrated effect on both the symptoms and underlying pathology of Alzheimer’s disease. These results are a breakthrough in the search for treatments for this devastating disease and give a strong indication that the course of the disease can be altered.</p> <p>But the results paint a mixed picture for those with Alzheimer’s. On one hand, this is the first drug that has been shown to have any effect on slowing the progression of the disease. On the other hand, the apparent effects are slight and the risks are not inconsiderable.</p> <p>About 1,800 people with early-stage Alzheimer’s took part in the global trial. The participants were randomly assigned to receive either lecanemab or placebo intravenously every two weeks. The study was “double blind”, meaning neither the participants nor the researchers knew who was receiving the experimental drug and who was receiving the placebo until the end of the trial.</p> <p>Throughout the study, the participants’ disease progression was tracked using the clinical dementia rating scale, which scores the patient on cognition and ability to live independently. The participants’ brains were also scanned for the two proteins commonly associated with Alzheimer’s disease: amyloid and tau.</p> <p>Alzheimer’s scores in both groups worsened during the 18 months of the study, but the rate of decline was slower in those receiving the lecanemab. Also, the magnitude of the slowing, while statistically significant (not likely to be due to chance) was small – a 0.45 reduction on an 18-point scale.</p> <p>Some experts are concerned that this effect may not be clinically meaningful. In a <a href="https://www.sciencemediacentre.org/expert-reaction-to-phase-3-trial-results-of-lecanemab-for-early-alzheimers-disease/">statement to the Science Media Centre</a>, Rob Howard, professor of old age psychiatry at UCL, said that “none of the reported results, including the primary outcome, reached accepted levels of improvement to constitute a clinically meaningful treatment effect”.</p> <p>The success of lecanemab was also measured by the amount of amyloid and tau protein in those on the experimental drug compared with those receiving the placebo infusion. The results showed a reduction in these proteins in those receiving lecanemab.</p> <p>Indeed, the levels of brain amyloid were reduced to below the threshold needed for a positive Alzheimer’s diagnosis. However, markers of brain cell death were unaffected, indicating that amyloid in Alzheimer’s disease is just one mechanism in a complicated disease landscape.</p> <h2>Side-effects</h2> <p>About one in four participants (26.6%) in the lecanemab group experienced brain swelling or a bleed on the brain (which can be both minor or major). STAT, a medical news website, <a href="https://www.statnews.com/2022/10/28/patient-death-lecanemab-alzheimers-trial/">reported that a man died of a brain haemorrhage</a> after receiving lecanemab, citing a possible interaction with his blood thinning medication.</p> <p>A short while later, the <a href="https://www.science.org/content/article/second-death-linked-potential-antibody-treatment-alzheimer-s-disease">journal Science reported</a> a second death of a trial patient, also after receiving treatment for a stroke. However, the drug’s developer, Eisa, told Science: “All the available safety information indicates that lecanemab therapy is not associated with an increased risk of death overall or from any specific cause.”</p> <p>Nevertheless, given the possibility that patients may be on the drug for the rest of their lives, more research is needed on safety and interactions with existing medications.</p> <p>It’s also important to find out how long-lived the improvements in cognition are, and whether the drug continues to slow the rate of decline, or if the results plateau – or even decline.</p> <p>It should be noted that only patients who had a sufficient level of amyloid detected in the brain or spinal fluid – which requires a PET brain scan or an invasive lumbar puncture – were eligible to take part in this phase 3 trial. In the UK, Alzheimer’s is currently diagnosed via an interview with a doctor. Dr Susan Kohlhaas, director of research at Alzheimer’s Research UK, says the <a href="https://www.sciencemediacentre.org/expert-reaction-to-phase-3-trial-results-of-lecanemab-for-early-alzheimers-disease/">NHS is not ready for a new era of dementia treatment</a>.</p> <blockquote> <p>We estimate that unless there are drastic changes in how people access specialist diagnostic tests for Alzheimer’s disease, only 2% of people eligible for drugs like lecanemab will be able to access them.</p> </blockquote> <p>Restructuring NHS dementia services to provide routine and timely PET scans or lumbar punctures would be a costly and lengthy process.</p> <p>Based on previous results, Eisai applied to the US drug regulator (the Food and Drug Administration) for accelerated approval of their drug. A decision is expected by January 6 2023. If accelerated approval is granted by the regulator, these latest results will probably support an application for full approval.</p> <figure class="align-right "><figcaption></figcaption></figure> <p><em>Listen to The Conversation’s podcast series <a href="https://theconversation.com/uk/topics/uncharted-brain-decoding-dementia-128903">Uncharted Brain: Decoding Dementia</a> to find out more about the latest research unlocking clues to the ongoing mystery of how dementia works in the brain. Find all episodes via <a href="https://podfollow.com/the-anthill/view">The Anthill podcast</a>.</em><!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/195383/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p> <p><a href="https://theconversation.com/profiles/ritchie-williamson-1346959">Ritchie Williamson</a>, Director of research, Associate Professor in Therapeutics, <em><a href="https://theconversation.com/institutions/university-of-bradford-911">University of Bradford</a></em> and <a href="https://theconversation.com/profiles/stuart-dickens-1397610">Stuart Dickens</a>, Post Doctoral Research Assistant, <em><a href="https://theconversation.com/institutions/university-of-bradford-911">University of Bradford</a></em></p> <p><em>Image: Shutterstock</em></p> <p>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/experimental-alzheimers-drug-shows-promise-but-there-are-many-hurdles-still-to-overcome-195383">original article</a>.</p>

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Urine sample test: new way to detect and screen for early stages of Alzheimer’s disease

<p>When it comes to <a href="https://cosmosmagazine.com/science/alzheimers-peer-review/" target="_blank" rel="noreferrer noopener">Alzheimer’s disease</a>, an early diagnosis – one made well before signs of irreversible dementia are apparent – is key to providing effective intervention and treatment. Now early detection might be as simple as a urine test, allowing for wide-scale and early screening across large populations of the elderly.</p> <p>A collaboration of researchers in China investigated urine samples for biomarkers from a large group of patients with varying severity of Alzheimer’s disease, comparing them with healthy controls.</p> <p>A compound known as <a href="https://www.acs.org/content/acs/en/molecule-of-the-week/archive/f/formic-acid.html?cid=home_motw" target="_blank" rel="noreferrer noopener">formic acid</a> (which is also produced by some ant and bee species) was a particularly sensitive marker for cognitive decline associated with Alzheimer’s disease. Significant increases in urinary formic acid levels were found in all samples from Alzheimer’s sufferers (including those with only early-stage subjective cognitive decline) as compared with those from the healthy controls.</p> <p>“Alzheimer’s disease is a continuous and concealed chronic disease, meaning that it can develop and last for many years before obvious cognitive impairment emerges,” say the authors. “The early stages of the disease occur before the irreversible dementia stage, and this is the golden window for intervention and treatment.”</p> <p>When blood samples of the participants were analysed for Alzheimer’s biomarkers in combination with the urinary formic acid level, the researchers were able to predict to what stage of the disease the patient had progressed. Their report is in <em><a href="https://www.frontiersin.org/articles/10.3389/fnagi.2022.1046066/full" target="_blank" rel="noreferrer noopener">Frontiers in Ageing</a></em>.</p> <p>Other methods currently used to diagnose Alzheimer’s disease, such as positron emission tomography brain scans, <a href="https://cosmosmagazine.com/health/medicine/alzheimers-blood-test-developed/" target="_blank" rel="noreferrer noopener">invasive blood draws</a> and lumbar punctures, tend to be costly and invasive. Although other urinary biomarkers for Alzheimer’s disease have been found, none have been able to detect the disease at its earliest stages.</p> <p>The links between urinary formic acid and Alzheimer’s disease are still not fully understood, but this research is an important step towards developing tools to diagnose and treat this debilitating condition amongst a vulnerable group in society.</p> <p>“Urinary formic acid showed an excellent sensitivity for early Alzheimer’s screening,” said the authors. “The detection of urine biomarkers of Alzheimer’s is convenient and cost-effective, and it should be performed during routine physical examinations of the elderly.”</p> <p><!-- Start of tracking content syndication. Please do not remove this section as it allows us to keep track of republished articles --></p> <p><img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=227116&amp;title=Urine+sample+test%3A+new+way+to+detect+and+screen+for+early+stages+of+Alzheimer%E2%80%99s+disease" width="1" height="1" data-spai-target="src" data-spai-orig="" data-spai-exclude="nocdn" /></p> <p><!-- End of tracking content syndication --></p> <div id="contributors"> <p><em><a href="https://cosmosmagazine.com/health/urine-new-way-detect-alzheimers-disease/" target="_blank" rel="noopener">This article</a> was originally published on Cosmos Magazine and was written by Clare Kenyon. </em></p> <p><em>Image: Getty Images</em></p> </div>

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This is the difference between dementia and Alzheimer’s

<p>There are around 50 million people living with dementia worldwide, according to the World Health Organization. While dementia and Alzheimer's disease are often used interchangeably, there are important differences between them. Here’s what you need to know.</p> <p><strong>Dementia vs. Alzheimer’s</strong></p> <p>Here’s the first thing you need to know: how to tell the difference between dementia and Alzheimer’s disease. Dementia is an umbrella term for symptoms like impaired memory and thinking that interferes with daily living; Alzheimer’s disease is a specific type of dementia. Other types of dementia include vascular dementia, dementia with Lewy bodies, frontotemporal dementia, Parkinson’s disease, and Huntington’s disease.</p> <p>“Alzheimer’s is the most common form of dementia – about 60 to 70 per cent of the time, a patient with dementia has Alzheimer’s,” says Dr Richard Isaacson, Director of the Alzheimer’s Prevention Clinic at NewYork-Presbyterian/Weill Cornell Medical Center. The reason you hear about Alzheimer’s most often is not only because it is the most common type of dementia, but also because the science behind Alzheimer’s is the most advanced across all dementias,” explains Dr Isaacson.</p> <p><strong>Causes of dementia are vastly different</strong></p> <p>A medical illness, metabolic issue (like a nutritional or thyroid problem), vascular disease (like a stroke), or, rarely, infectious diseases can affect brain cells, causing dementia. Even mad cow disease, which is very rare, can contribute to dementia, says Dr Isaacson. A condition called depressive “pseudo” dementia is another possible source. As he explains, when levels of the neurotransmitter serotonin run low, you may have trouble paying attention. And when you’re distracted, you have trouble remembering things, which can manifest as dementia.</p> <p>On the other hand, Alzheimer’s has its own origins. It’s a brain disease marked by deposits of beta-amyloid plaques and proteins called tau that damage cells in brain regions that control functions like thinking, memory, and reasoning.</p> <p><strong>Multiple factors can be at play</strong></p> <p>There’s also what’s called mixed dementia, meaning there are multiple conditions that can come together to cause dementia. “Thirty percent of the time, patients who have Alzheimer’s also have a vascular disease that makes cognitive symptoms worse,” says Dr Isaacson. Alzheimer’s and dementia with Lewy bodies (in this disease, clumps of alpha-synuclein proteins develop in the brain) have also been found to occur together.</p> <p><strong>Symptoms can look very similar</strong></p> <p>Losing your keys – again – and forgetting where you parked are basic memory problems, so how do you know when it crosses the line to dementia or Alzheimer’s? According to the Alzheimer’s Association, in order for a person to be diagnosed with dementia, two of the following must be “significantly impaired”: memory, communication and language, the ability to focus and pay attention, reasoning and judgment, and visual perception. When it comes to Alzheimer’s, you may forget new information or find that you have to ask family members to remember important facts you should be able to keep track of yourself. (It’s not those little brain blips where you can’t remember the name of your second cousin and then it comes to you later – that’s normal). Research published in the <em>Journal of Alzheimer’s Disease</em> in 2016 also indicates that difficulty using a map may be one of the earliest warning signs of Alzheimer’s.</p> <p><strong>You may be able to prevent Alzheimer’s</strong></p> <p>“We have the Alzheimer’s Prevention Clinic, and the fact that you can talk about those words together is advanced,” says Dr Isaacson. The clinic investigates how lifestyle choices – a healthy diet, exercise, social and mentally stimulating activities, as well as everyday habits, and ample sleep can markedly reduce your risk of Alzheimer’s. In fact, in a study in 2014 published in the Lancet Neurology, reducing certain risk factors can decrease the risk of Alzheimer’s by 33 per cent. The most important ways to prevent Alzheimer’s: Control diabetes and high blood pressure, reduce weight if obese, stay active, treat depression, don’t smoke, and stay in school. The Lancet, in a 2017 article, also notes that staying social (spending time with friends and family members) and managing hearing loss have been shown to be among the controllable factors that may help prevent dementia.</p> <p><strong>Treatment options depend on the type of dementia</strong></p> <p>There are virtually no FDA-approved therapies for dementia (only one approved drug for Parkinson’s dementia), but there are four medications that target Alzheimer’s, according to Dr Isaacson. And while these drugs don’t stall disease progression (or cure the disease), they can help control symptoms. Patients of Dr Isaacson’s say these drugs may help for six to nine months, but many stay on them for the long haul because they help with behavioural symptoms such as agitation and aggression. “When you stop the medications, the psychological symptoms get worse,” he says.</p> <p>As for other types of dementia, lifestyle changes may be the best option. Treatment for vascular dementia relies on doing things that are healthy for your arteries and heart: reducing blood pressure and cholesterol, and controlling diabetes. “Managing other chronic conditions is important,” says Dr Isaacson. “Those are a great way to press the fast-forward button on dementia.”</p> <p><strong>You can find out if you’re at an increased risk of Alzheimer’s now</strong></p> <p>If you get evaluated for Alzheimer’s, your doctor can make a diagnosis based on symptoms, a clinical history, and medical tests (to rule out causes like thyroid issues or nutritional deficiencies). Brain imaging tests like a cat scan or MRI can look for beta amylase plaques gunking up brain regions.</p> <p><strong>You don’t have to be scared</strong></p> <p>Forgetting how to work the remote in your home, being afraid to leave your neighbourhood out of fear you might not get home, or misplacing your belongings so often that it hurts your ability to get out the door can all be particularly worrisome – especially if a loved one expresses concern. If you’re worried, see your doctor, says Dr Issacson. “Get educated, get informed, get evaluated,” he says. “The earlier the diagnosis, the earlier you can be treated. And the earlier you’re treated, the better you’ll do.”</p> <p><em><span id="docs-internal-guid-439d99b3-7fff-2e74-36b4-a8ac764e0b4c">Written by Jessica Migala. This article first appeared in <a href="https://www.readersdigest.com.au/healthsmart/this-is-the-difference-between-dementia-and-alzheimers" target="_blank" rel="noopener">Reader’s Digest</a>. For more of what you love from the world’s best-loved magazine, <a href="http://readersdigest.innovations.com.au/c/readersdigestemailsubscribe?utm_source=over60&amp;utm_medium=articles&amp;utm_campaign=RDSUB&amp;keycode=WRA87V" target="_blank" rel="noopener">here’s our best subscription offer.</a></span></em></p> <p><em>Image: Getty Images</em></p>

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Chris Hemsworth’s Alzheimer’s gene doesn’t guarantee he’ll develop dementia

<p>Chris Hemsworth, famous for his role as the god Thor in Marvel Cinematic Universe movies, has announced he will be <a href="https://www.theguardian.com/film/2022/nov/21/chris-hemsworth-to-take-time-off-from-acting-after-discovering-alzheimers-risk" target="_blank" rel="noopener">taking a break</a> from acting after being told he has two copies of the <a href="https://www.nia.nih.gov/news/study-reveals-how-apoe4-gene-may-increase-risk-dementia" target="_blank" rel="noopener">APOE4 gene</a>, increasing his risk of Alzheimer’s.</p> <p>Having one copy of the <a href="https://www.science.org/doi/abs/10.1126/science.8346443" target="_blank" rel="noopener">APOE4 gene</a> increases your risk for Alzheimer’s 2-3 times. Two copies increases your risk 10-15 times.</p> <p>But the key here is “risk”. Having one or more copies of the gene doesn’t guarantee Chris or anyone else in a similar situation will go on to develop Alzheimer’s, the most common form of dementia.</p> <p><strong>Sharing the news</strong></p> <p>Hemsworth’s willingness to share his concerns about developing Alzheimer’s with millions should be applauded. It’s a reminder to all of us to keep an eye on our health and reduce our risk of future illness.</p> <p>Alzheimer’s, and dementia more broadly, is <a href="https://www.dementiastatistics.org/statistics/global-prevalence/" target="_blank" rel="noopener">set to challenge</a> health-care systems worldwide.</p> <p>In Australia alone there are <a href="https://www.dementia.org.au/statistics" target="_blank" rel="noopener">up to</a> 500,000 people with dementia, supported by almost 1.6 million carers. By 2036, about <a href="https://www.dementia.org.au/sites/default/files/NATIONAL/documents/The-economic-cost-of-dementia-in-Australia-2016-to-2056.pdf" target="_blank" rel="noopener">450 people</a> are predicted to be diagnosed daily. So understanding how APOE4 alters the risk for the major cause of dementia may be pivotal in preventing cases.</p> <p>But not all people with the APOE4 gene go on to develop Alzheimer’s. This means that there may be a combination of environmental factors interplaying with the gene that lead some people to develop Alzheimer’s, while others do not.</p> <p><strong>What’s APOE4 got to do with Alzheimer’s?</strong></p> <p>Most Australians have APOE3 or APOE2 genes. In Caucasians it’s only <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5531868/" target="_blank" rel="noopener">about 15%</a>, like Hemsworth, who have inherited an APOE4 gene.</p> <p>The APOE gene types are best known for their role in modulating the metabolism of lipids (fats), such as cholesterol and triglycerides.</p> <p>They code for synthesis of different versions of the protein APOE, with subtle differences in structure. The APOE proteins become an integral part of lipoproteins in the blood. These are the fat-carrying particles your GP measures to consider your risk of heart disease.</p> <p>APOE proteins have a similar function in the brain, to modulate lipid levels. But in the context of Alzheimer’s, researchers study it for its effect on the integrity of brain cells.</p> <p>Accumulating evidence <a href="https://www.sciencedirect.com/science/article/pii/S0197458022000550" target="_blank" rel="noopener">suggests</a> APOE4, is associated with brain inflammation and cellular damage.</p> <blockquote class="twitter-tweet"> <p dir="ltr" lang="en">APOE4 is the strongest genetic risk factor for Alzheimer’s disease. A study in <a href="https://twitter.com/Nature?ref_src=twsrc%5Etfw">@Nature</a> establishes a functional link between APOE4, cholesterol, myelination and memory, offering therapeutic opportunities for Alzheimer’s disease. <a href="https://t.co/bNsmDVPfFW">https://t.co/bNsmDVPfFW</a> <a href="https://t.co/58odE1JASl">pic.twitter.com/58odE1JASl</a></p> <p>— Nature Portfolio (@NaturePortfolio) <a href="https://twitter.com/NaturePortfolio/status/1594762841487249410?ref_src=twsrc%5Etfw">November 21, 2022</a></p></blockquote> <p><strong>Can we prevent Alzheimer’s?</strong></p> <p><strong>1. Look after your capillaries</strong></p> <p>Damaged and leaky blood vessels (capillaries) in the brain lead to inflammation, the death of brain cells and cognitive impairment. In fact, in Alzheimer’s, damaged capillaries are the earliest sign of the type of brain damage that causes disease.</p> <p>The protein encoded by the APOE4 gene may be less able to support healthy capillaries in the brain. <a href="https://www.sciencedirect.com/science/article/abs/pii/S0163782709000563" target="_blank" rel="noopener">We suggested</a> APOE4 increases the abundance of specific complexes of lipoproteins and proteins in blood that silently damage brain capillaries, causing them to leak.</p> <p>We also see more brain capillary leakage in mice fed Western-style diets richer in saturated fats.</p> <p>The relationship between how the APOE proteins mediate lipid metabolism and capillary health in humans is poorly understood.</p> <p>But we have 60 years of research knowledge to say with confidence that eating foods good for the heart should also be good for the brain. This is particularly relevant for people with the APOE4 gene.</p> <p>So if you have the APOE4 gene and want to minimise your risk of Alzheimer’s, a healthy diet is a good place to start.</p> <figure class="align-center zoomable"><em><a href="https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip"><img src="https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=600&amp;h=316&amp;fit=crop&amp;dpr=1 600w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=600&amp;h=316&amp;fit=crop&amp;dpr=2 1200w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=600&amp;h=316&amp;fit=crop&amp;dpr=3 1800w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;h=397&amp;fit=crop&amp;dpr=1 754w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=754&amp;h=397&amp;fit=crop&amp;dpr=2 1508w, https://images.theconversation.com/files/497142/original/file-20221124-24-rlqyk5.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=754&amp;h=397&amp;fit=crop&amp;dpr=3 2262w" alt="Capillaries" /></a></em><figcaption><em><span class="caption">Looking after your capillaries with a healthy diet is a good place to start.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/system-many-small-capillaries-branch-out-1745173364" target="_blank" rel="noopener">Shutterstock</a></span></em></figcaption></figure> <p><strong>2. Give your brain a break</strong></p> <p>Reducing unnecessary stimuli to “give your brain a rest” may have big impact over decades of your life. The latter may be a more important consideration if you have the APOE4 gene.</p> <p>That’s because the APOE gene is also linked to how the brain uses energy, which may lead to more <a href="https://www.frontiersin.org/articles/10.3389/fnmol.2018.00216/full" target="_blank" rel="noopener">oxidative stress and damage</a>.</p> <p>While we’ve yet to collect robust data in humans, take a digital detox now and again, plan some down time, and avoid unnecessary stress if you can.</p> <p><strong>Should we test for the APOE4 gene?</strong></p> <p>Some people might be tempted to get tested for the APOE4 gene, especially if there’s a family history of Alzheimer’s.</p> <p>But unless genetic testing is going to change your treatment (for instance, by taking certain medications to slow progression of brain damage), or your behaviour to minimise your risk Alzheimer’s, then testing is not justified.</p> <p>We can’t change the genes our parents gifted us, but we can change our environment.</p> <p>Poor diet, every drop of alcohol you drink, obesity and diabetes, high blood pressure and sedentary behaviour <a href="https://www.dementia.org.au/risk-reduction" target="_blank" rel="noopener">all contribute, over time</a>, to poorer vascular health and increase your risk of dementia.</p> <p>We’re still learning about how these risk factors for Alzheimer’s interact with the APOE4 gene. But there is no reason we shouldn’t all take greater responsibility for minimising our risk of dementia now, whether we have the APOE4 gene or not.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/195094/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p> <p><em>Writen by John Mamo. Republished with permission from <a href="https://theconversation.com/chris-hemsworths-alzheimers-gene-doesnt-guarantee-hell-develop-dementia-heres-what-we-can-all-do-to-reduce-our-risk-195094" target="_blank" rel="noopener">The Conversation</a>.</em></p> <p><em>Image: Instagram</em></p>

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The surprising reason exercise improves symptoms of Alzheimer’s

<p><span style="font-weight: 400;">Though we already know that physical activity is good for us, new research has discovered that it may have even more benefits for those with Alzheimer’s disease.</span></p> <p><span style="font-weight: 400;">A team of researchers have </span><a rel="noopener" href="https://www.scimex.org/newsfeed/why-exercise-is-beneficial-for-those-with-alzheimers" target="_blank"><span style="font-weight: 400;">identified</span></a><span style="font-weight: 400;"> a potential explanation for why exercise improves brain health.</span></p> <p><span style="font-weight: 400;">Dr Kaitlin Casaletto, the study’s senior author and a neurophysiologist at the University of California’s Memory and Ageing Centre, said the study makes the link between exercise and better brain health via inflammation.</span></p> <p><span style="font-weight: 400;">“We are starting to show the ‘who of the how’: physical activity related to better cognitive outcomes via reduced brain inflammation, particularly in adults with greater Alzheimer’s disease pathology,” she told </span><span style="font-weight: 400;">OverSixty</span><span style="font-weight: 400;">. “Broadly, our study supports the dynamic</span></p> <p><span style="font-weight: 400;"> and plastic nature of the brain, even in older adults and even in the context of pathology.”</span></p> <p><span style="font-weight: 400;">The researchers monitored the activity of microglia - the brain’s immune cells -  in 167 older adults, as well as the levels of activation in brain tissue from deceased patients with Alzheimer’s. </span></p> <p><span style="font-weight: 400;">As the brain’s first line of immune defence, the cells activate to remove debris, damaged neurons, and foreign invaders. But, if the cells are too active, they can trigger inflammation, damage neurons, and interrupt signalling in the brain.</span></p> <p><span style="font-weight: 400;">This was particularly noticeable in a region of the brain responsible for processing visual information. This area is one of the regions severely impacted by Alzheimer’s disease, resulting in difficulty processing new information and remembering it later.</span></p> <blockquote class="twitter-tweet"> <p dir="ltr"><a href="https://twitter.com/hashtag/JNeurosci?src=hash&ref_src=twsrc%5Etfw">#JNeurosci</a> | New research from <a href="https://twitter.com/UCSFmac?ref_src=twsrc%5Etfw">@UCSFmac</a> shows physical activity may improve <a href="https://twitter.com/hashtag/Alzheimers?src=hash&ref_src=twsrc%5Etfw">#Alzheimers</a> by lowering brain inflammation. <a href="https://twitter.com/kbcasaletto?ref_src=twsrc%5Etfw">@kbcasaletto</a> et al. show benefits may come through decreased immune cell activation. <a href="https://t.co/ZSgCVfnPCQ">https://t.co/ZSgCVfnPCQ</a> <a href="https://t.co/oSganHTYHj">pic.twitter.com/oSganHTYHj</a></p> <p>— SfN Journals (@SfNJournals) <a href="https://twitter.com/SfNJournals/status/1462844838576017418?ref_src=twsrc%5Etfw">November 22, 2021</a></p></blockquote> <p><span style="font-weight: 400;">Physical activity was also found to have a pronounced effect in reducing inflammation in people with severe Alzheimer’s.</span></p> <p><span style="font-weight: 400;">“For instance, our study suggests that individuals at risk for Alzheimer’s related inflammation may particularly benefit from an exercise regimen,” Dr Casaletto said.</span></p> <p><span style="font-weight: 400;">But, she said it’s important to understand that exercise “may not work for everyone’s brain health”.</span></p> <p><span style="font-weight: 400;">Previous work has made the connection between exercise and reduced risks of neurodegenerative diseases such as Alzheimer’s, but Dr Casaletto said the new study is the first to show the same kinds of results in humans.</span></p> <p><span style="font-weight: 400;">“Many studies show that physical activity relates to better brain and cognitive health. Yet we still do not fundamentally understand the mechanisms linking physical activity to cognition in humans,” said Dr Casaletto.</span></p> <p><span style="font-weight: 400;">“Ours is the first human data showing that brain inflammation may be a meaningful mechanism.” </span></p> <p><span style="font-weight: 400;">The researchers also noted that exercise could be used to identify potential treatments.</span></p> <p><span style="font-weight: 400;">“Our team aims to identify biological targets that link known neuroprotective factors like physical activity to the brain,” Dr Casaletto said.</span></p> <p><span style="font-weight: 400;">“Ideally, if we can ‘bottle’ these biological mechanisms, they could be therapeutic targets for cognitive ageing and Alzheimer’s disease.”</span></p> <p><span style="font-weight: 400;">The study was published in the </span><em><a rel="noopener" href="https://www.jneurosci.org/content/early/2021/11/11/JNEUROSCI.1483-21.2021" target="_blank"><span style="font-weight: 400;">Journal of Neuroscience</span></a></em><span style="font-weight: 400;">.</span></p> <p><em><span style="font-weight: 400;">Image: Getty Images</span></em></p>

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"Dramatic result": New drug shows hope for slowing down Alzheimer's disease

<p>A trial drug has shown "significant" results in slowing down Alzheimer's disease, with Australian healthcare experts hopeful in where this breakthrough can take their research. </p> <p>The drug, known as Lecanemab, has been proven to reduce cognitive decline by 27 per cent compared to placebo, according to an overseas study. </p> <p>More than 1,700 patients with mild cognitive impairment were enrolled in the study and the results were collected over 18 months.</p> <p>"Functionally and cognitively, it seems they did better and so that is a dramatic result," Dr Lawrence Honig, one of the study investigators from Columbia University Medical Centre, said.</p> <p>The drug works by removing the build-up of amyloid plaques in the brain which is one of the hallmarks of the disease, which featured in the scans of each study participant. </p> <p>Australian experts are excited about the findings, and how this can further their research. </p> <p>"This is the first time we've seen a drug like this have these kinds of effects," Professor Sharon Naismith, Clinical Neuropsychologist & NHMRC Dementia Leadership Fellow at the University of Sydney, said.</p> <p>"The results of this trial have massive implications for our resourcing."</p> <p>Naismith warns there's a need to spend more money on better diagnosing patients with mild cognitive impairment.</p> <p>"In the past there has been a lot of reluctance from healthcare physicians to diagnose or ask about cognitive impairment, even in primary care," she said.</p> <p>She said being able to access a drug that can slow cognitive decline will change the paradigm and conversation around Alzheimer's disease. </p> <p>"I do think we're going to get a real avalanche of people coming to GPs and coming to memory clinics for that reason," she said.</p> <p>Professor Kathryn Goozee, Director of KaRa Minds at Macquarie Park said the study showed using an antibody to target amyloid in the brain can help with cognition.</p> <p>"To date there has been no disease-modifying medication so we want to be offering studies that can potentially change that trajectory," Goozee said.</p> <p>The full details of the results will be presented at an international conference of experts in the US in late November.</p> <p><em>Image credits: 9News</em></p>

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Could Alzheimer’s be an autoimmune disease?

<p>Searching for an Alzheimer’s cure is among the world’s most pressing needs. Researchers in Canada have a new theory.</p> <p>Alzheimer’s is a degenerative brain disease with no cure and no effective therapeutic treatments to  stop or slow its progression. It impacts an estimated <a href="https://cosmosmagazine.com/health/dementias-rising-pressure/" target="_blank" rel="noreferrer noopener">50 million people around the world</a>, and for those afflicted, invariably results in <a href="https://www.dementia.org.au/" target="_blank" rel="noreferrer noopener">dementia</a> and death.</p> <p><a href="https://www.healthdirect.gov.au/alzheimers-disease" target="_blank" rel="noreferrer noopener">In Australia Alzheimer’s affects up to 1 in 10 Australians over 65 years of age, and up to 3 in 10 over 85. It is not a normal part of ageing.</a></p> <p>One prevailing theory suggests that a sticky protein called beta-amyloid builds up in the brain forming clumps known as plaques, which then acts to kill brain cells, directly causing Alzheimer’s disease. However, 30 years of research into the development of medical treatments designed to target these plaques have led to failure after failure.</p> <p>Now, scientists at the Krembil Brain Institute, which is part of the University Health Network in Ontario, Canada suggest that new thinking around the disease is desperately needed.</p> <p>They are asking: “Could Alzheimer’s be an <a href="https://cosmosmagazine.com/health/medicine/autoimmune-disease-on-the-rise/" target="_blank" rel="noreferrer noopener">autoimmune disease</a>?”</p> <div class="newsletter-box"> <div id="wpcf7-f6-p215071-o1" class="wpcf7" dir="ltr" lang="en-US" role="form"> <form class="wpcf7-form mailchimp-ext-0.5.62 spai-bg-prepared init" action="/news/could-alzheimers-be-an-autoimmune-disease/#wpcf7-f6-p215071-o1" method="post" novalidate="novalidate" data-status="init"> <p style="display: none !important;"><span class="wpcf7-form-control-wrap referer-page"><input class="wpcf7-form-control wpcf7-text referer-page" name="referer-page" type="hidden" value="https://cosmosmagazine.com/health/" data-value="https://cosmosmagazine.com/health/" aria-invalid="false" /></span></p> <p><!-- Chimpmail extension by Renzo Johnson --></form> </div> </div> <p>“Yes,” says Dr. Donald Weaver, co-Director of the Krembil Brain Institute and author of <a href="https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12789" target="_blank" rel="noreferrer noopener">new research</a> published in the peer-reviewed journal, <em>Alzheimer’s &amp; Dementia</em>. “We don’t think of Alzheimer’s as fundamentally a disease of the brain. We think of it as a disease of the immune system <em>within</em> the brain.”</p> <p>The role of beta-amyloid in the brain is as an ‘immunopeptide’ – a messenger within the immune system which is involved in repairing the brain. “If we have head trauma, beta-amyloid repairs it. If a virus or a bacteria comes along, beta-amyloid is there to fight it,” explains Weaver.</p> <p>But unfortunately, beta-amyloid can become confused.</p> <p>“Beta-amyloid gets confused and can’t tell the difference between a bacteria and a brain cell,” says Weaver. “And so, it inadvertently attacks our own brain cells. This, then, becomes what we call an autoimmune disease.”</p> <p>To test these ideas, the team surveyed the disease and patient literature to develop a detailed model describing the cause and effect relationship of Alzheimer’s disease (known as a <a href="https://royalsocietypublishing.org/doi/10.1098/rsbl.2017.0660" target="_blank" rel="noreferrer noopener">mechanistic model</a>).</p> <p>This approach allowed them to step back and take a more holistic review of the workings of the disease at several different levels within the biological system — such as Alzheimer’s progression and effect on different sections of the brain’s nerve cells, and the larger immune disease response — and also to consider novel causes and inputs into the disease.</p> <p>Tangible rethinking about Alzheimer’s disease as an autoimmune disease, and beta-amyloid as a normal part of our immune system, opens the door to new avenues and approaches to develop innovative new therapies, says Dr. Weaver, who hopes that this new conceptual framework could eventually present a new way to combat this insidious and devastating disease.</p> <p><!-- Start of tracking content syndication. Please do not remove this section as it allows us to keep track of republished articles --></p> <p><img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=215071&amp;title=Could+Alzheimer%E2%80%99s+be+an+autoimmune+disease%3F" width="1" height="1" /></p> <p><!-- End of tracking content syndication --></p> <div id="contributors"> <p><em><a href="https://cosmosmagazine.com/news/could-alzheimers-be-an-autoimmune-disease/" target="_blank" rel="noopener">This article</a> was originally published on <a href="https://cosmosmagazine.com" target="_blank" rel="noopener">Cosmos Magazine</a> and was written by <a href="https://cosmosmagazine.com/contributor/clare-kenyon" target="_blank" rel="noopener">Clare Kenyon</a>. Clare Kenyon is a science journalist for Cosmos. An ex-high school teacher, she is currently wrangling the death throes of her PhD in astrophysics, has a Masters in astronomy and another in education. Clare also has diplomas in music and criminology and a graduate certificate of leadership and learning.</em></p> <p><em>Image: Getty Images</em></p> </div>

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Babysitting grandkids can ward off Alzheimer’s

<p>Good news for grandmothers! A new study finds grandchildren not only add joy to grandparents’ lives but that spending time with grandkids can ward off Alzheimer’s.</p> <p>The study, published in the journal Menopause, found post-menopausal women who spend time taking care of grandkids lower their risk of developing Alzheimer's and other cognitive disorders. However, too much time with the grandchildren – five or more days a week – wasn’t so good for grandma.</p> <p>Researchers for Women’s Health Ageing Project in Australia administered three different tests to assess the cognitive abilities of 186 women, ages 57 to 68. Among the group, 120 were grandmothers. The study found that grandmothers who helped with their grandchildren at least one day per week scored highest on the tests, while the women who spent five or more days a week with their grandkids scored significantly lower.</p> <p>Researchers found that grandmothers who helped out more often felt their own children – the parents of the grandkids – were too demanding on their time which dampened moods and impacted brain function.</p> <p>“The motivation of the present study was to expand on the current literature by examining the impact of grandparenting on cognitive function," the authors write in the new study. “To our knowledge, this is the first study to examine the relationship between grandparenting and cognition.”</p> <p><em>Image: Getty</em></p>

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Exercise and Alzheimer’s: Is it necessary?

<div> <div class="copy"> <p>It’s no real surprise that an active lifestyle is beneficial for people with <a rel="noreferrer noopener" href="https://cosmosmagazine.com/health/predictive-test-for-alzheimers-disease/" target="_blank">Alzheimer’s disease</a>. But researchers from the University of California have now added another piece to the puzzle in understanding how physical activity improves brain health and helps people with Alzheimer’s disease.</p> <p>According to their study, <a rel="noreferrer noopener" href="https://www.jneurosci.org/content/early/2021/11/11/JNEUROSCI.1483-21.2021" target="_blank">published</a> earlier this week in <em>JNeurosci</em>, exercise might play a role in decreasing immune cell activation<em>.</em></p> <p>The brain’s immune cells, called microglia, activate to clear debris and foreign invaders from the brain. But too much activation can trigger inflammation, damage neurons, and disrupt brain signalling.</p> <p>Animal studies have shown that increasing physical activity reduces abnormal microglia activation, but the link has not been established in humans.</p> <p>The researchers tracked the physical activity of 167 people, 60% of whom had Alzheimer’s disease, for almost a decade. The participants wore activity monitors 24 hours a day for up to 10 days straight before annual cognitive exams.</p> <p>They then analysed participants’ brains after their deaths, which occurred at an average of 90 years of age. After adjusting for age, sex, education, and motor performances, the researchers observed that brain immune cells were less active in those who exercised more, particularly in areas of the brain linked to Alzheimer’s disease.</p> <p>“We’ve known for a long time that midlife physical activity is associated with a reduced risk of dementia,” says Professor Amy Brodtmann, a neurologist at the Florey Institute of Neuroscience and Mental Health in Melbourne, who was not involved in the study. “But how late-life physical activity improves brain health still isn’t clear.”</p> <p>Brodtmann says past studies have looked at the effect of exercising on beta-amyloid and tau, two proteins that accumulate in the brain forming plaques and disrupting brain functioning. Muscle mass has also been associated with better brain health, while reducing cardiovascular disease and the risk of stroke in the brain through exercising contributes to lowering the risk of dementia.</p> <p>The role of brain immune cells in cognitive decline is now receiving an enormous amount of attention. “We used to think that inflammation came after the pathologies in the brain,” Brodtmann said. “But what we’re now thinking is that other events in life, particularly vascular disease, can cause increased inflammation in the brain, and this may be the primary driver of the pathology [in the brain].”</p> <p>Brodtmann says this study uncovered the positive effect of physical activity on neuroimmune modulation. “That means that at any stage in your life, you can affect your brain’s health by exercising.”</p> <p>She says that physicians should encourage patients to exercise regularly, as well as adopt a Mediterranean diet and address all other risk factors.</p> <p>“Age in itself is not a barrier to exercise,” Brodtmann says, adding that including physical activity in your routine could be as simple as going for a brisk, 30-minute walk most days of the week. Running, swimming, cycling and some gentle strength workout is also highly recommended.</p> <p>As people get older, reduced mobility might be a challenge, but Brodtmann said some level of physical activity is beneficial at any age and stage of the disease.</p> <p>“These diseases are usually the cumulative effects of a lifetime of not exercising or eating well, and this behaviour is not very easy to change.”</p> <em>Image credits: Getty Images</em></div> <div id="contributors"> <p><em>This article was originally published on <a href="https://cosmosmagazine.com/health/body-and-mind/exercise-and-alzheimers-is-it-necessary/">cosmosmagazine.com</a> and was written by Dr Manuela Callari. </em></p> </div> </div>

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Could Viagra help prevent Alzheimer’s disease?

<p>Viagra is used by millions of people each year to treat erectile dysfunction. But new research shows that it might not just be helpful in the bedroom – there’s a suggestion that Viagra may also help to prevent Alzheimer’s disease.</p> <p>Despite what it’s best known for, sildenafil – marketed as Viagra – isn’t a one-trick pony. It was <a rel="noreferrer noopener" href="https://cosmosmagazine.com/science/biology/how-i-discovered-viagra/" target="_blank">originally developed to treat angina</a> – although it didn’t make it through trials – and there’s some evidence it could <a rel="noopener" href="https://www.pasteur.fr/en/viagra-prevent-transmission-malaria-parasite" target="_blank">help </a><a rel="noreferrer noopener" href="https://www.pasteur.fr/en/viagra-prevent-transmission-malaria-parasite" target="_blank">t</a><a rel="noopener" href="https://www.pasteur.fr/en/viagra-prevent-transmission-malaria-parasite" target="_blank">reat malaria</a>. Tadalafil, a similar drug to Viagra, <a rel="noreferrer noopener" href="https://cosmosmagazine.com/health/medicine/sex-med-looks-promising-as-heart-failure-drug/" target="_blank">has been proposed</a> as a heart failure treatment.</p> <p>A <a rel="noreferrer noopener" href="https://doi.org/10.1038/s43587-021-00138-z" target="_blank">paper</a> in <em>Nature Aging </em>has expanded its potential further, using records from insurance claims to examine the link between Viagra and Alzheimer’s disease.</p> <p>The researchers, who are based in the US, examined the insurance records of 7.23 million people, alongside genetic and other biological data. They looked through the data to pull out indicators of Alzheimer’s disease, and then examined the relationship between these indicators and over 1,600 prescribed medicinal drugs.</p> <p>Viagra had the highest link to lower chance of Alzheimer’s, with its prescription being associated with a 69% reduced risk of the disease.</p> <p>The researchers point out that while this link is significant, it doesn’t establish causality: it may be that Viagra prevents Alzheimer’s, or it may be that people who have fewer biological precursors to Alzheimer’s are also more likely to recieve a Viagra prescription.</p> <p>There could also be other confounding factors at play. Sildenafil, for instance, is more likely to be prescribed to wealthy people, and wealthy people are also less likely to get Alzheimer’s disease. The sample size of Viagra users was also – unsurprisingly – mostly male.</p> <p>“Taken together, the association between sildenafil usage and decreased incidence of AD [Alzheimer’s disease] does not establish causality or its direction,” write the researchers in their paper.</p> <p>“Our results therefore warrant rigorous clinical trial testing of the treatment efficacy of sildenafil in patients with AD, inclusive of both sexes and controlled by placebo.”</p> <p><!-- Start of tracking content syndication. Please do not remove this section as it allows us to keep track of republished articles --></p> <p><img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=175427&amp;title=Could+Viagra+help+prevent+Alzheimer%E2%80%99s+disease%3F" alt="" width="1" height="1" /></p> <p><!-- End of tracking content syndication --></p> <div id="contributors"> <p><em><a rel="noopener" href="https://cosmosmagazine.com/health/medicine/viagra-prevent-alzheimers-disease-study/" target="_blank">This article</a> was originally published on <a rel="noopener" href="https://cosmosmagazine.com" target="_blank">Cosmos Magazine</a> and was written by <a rel="noopener" href="https://cosmosmagazine.com/contributor/ellen-phiddian" target="_blank">Ellen Phiddian</a>. Ellen Phiddian is a science journalist at Cosmos. She has a BSc (Honours) in chemistry and science communication, and an MSc in science communication, both from the Australian National University.</em></p> <p><em>Image: Getty Images</em></p> </div>

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Could Viagra help prevent Alzheimer’s disease?

<h1><span style="font-size: 14px;">Insurance shows a link between Viagra prescription and a lower chance of the disease. </span></h1> <div class="copy"> <p>Viagra is used by millions of people each year to treat erectile dysfunction. But new research shows that it might not just be helpful in the bedroom – there’s a suggestion that Viagra may also help to prevent Alzheimer’s disease. Insurance shows a link between Viagra prescription and a lower chance of the disease. </p> <p>Despite what it’s best known for, sildenafil – marketed as Viagra – isn’t a one-trick pony. It was <a rel="noreferrer noopener" href="https://cosmosmagazine.com/science/biology/how-i-discovered-viagra/" target="_blank">originally developed to treat angina</a> – although it didn’t make it through trials – and there’s some evidence it could <a rel="noopener" href="https://www.pasteur.fr/en/viagra-prevent-transmission-malaria-parasite" target="_blank">help </a><a rel="noreferrer noopener" href="https://www.pasteur.fr/en/viagra-prevent-transmission-malaria-parasite" target="_blank">t</a><a rel="noopener" href="https://www.pasteur.fr/en/viagra-prevent-transmission-malaria-parasite" target="_blank">reat malaria</a>. Tadalafil, a similar drug to Viagra, <a rel="noreferrer noopener" href="https://cosmosmagazine.com/health/medicine/sex-med-looks-promising-as-heart-failure-drug/" target="_blank">has been proposed</a> as a heart failure treatment.</p> <p>A <a rel="noreferrer noopener" href="https://doi.org/10.1038/s43587-021-00138-z" target="_blank">paper</a> in <em>Nature Aging </em>has expanded its potential further, using records from insurance claims to examine the link between Viagra and Alzheimer’s disease.</p> <p>The researchers, who are based in the US, examined the insurance records of 7.23 million people, alongside genetic and other biological data. They looked through the data to pull out indicators of Alzheimer’s disease, and then examined the relationship between these indicators and over 1,600 prescribed medicinal drugs.</p> <p>Viagra had the highest link to lower chance of Alzheimer’s, with its prescription being associated with a 69% reduced risk of the disease.</p> <p>The researchers point out that while this link is significant, it doesn’t establish causality: it may be that Viagra prevents Alzheimer’s, or it may be that people who have fewer biological precursors to Alzheimer’s are also more likely to receive a Viagra prescription.</p> <p>There could also be other confounding factors at play. Sildenafil, for instance, is more likely to be prescribed to wealthy people, and wealthy people are also less likely to get Alzheimer’s disease. The sample size of Viagra users was also – unsurprisingly – mostly male.</p> <p>“Taken together, the association between sildenafil usage and decreased incidence of AD [Alzheimer’s disease] does not establish causality or its direction,” write the researchers in their paper.</p> <p>“Our results therefore warrant rigorous clinical trial testing of the treatment efficacy of sildenafil in patients with AD, inclusive of both sexes and controlled by placebo.”</p> <!-- Start of tracking content syndication. Please do not remove this section as it allows us to keep track of republished articles --> <img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=175427&amp;title=Could+Viagra+help+prevent+Alzheimer%E2%80%99s+disease%3F" alt="" width="1" height="1" /> <!-- End of tracking content syndication --></div> <div id="contributors"> <p><a href="https://cosmosmagazine.com/health/medicine/viagra-prevent-alzheimers-disease-study/">This article</a> was originally published on <a href="https://cosmosmagazine.com">Cosmos Magazine</a> and was written by <a href="https://cosmosmagazine.com/contributor/ellen-phiddian">Ellen Phiddian</a>. </p> </div>

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Alzheimer’s marker found in the brain

<p><span style="font-weight: 400;">A new study has linked an area of the brainstem called the locus coeruleus (LC) to several of the main features of early Alzheimer’s disease.</span></p> <p><span style="font-weight: 400;">The team of researchers concluded that the health of the LC could be used as an indicator for early Alzheimer’s.</span></p> <p><span style="font-weight: 400;">They also suggest that monitoring the changes in this area of the brain could shed light on the possible trajectory of the disease in individual patients.</span></p> <p><span style="font-weight: 400;">“Being able to detect and measure the initial site of pathology will be critical to improve early detection and identify individuals eligible for clinical trials aimed at delaying the disease process,” they write.</span></p> <p><span style="font-weight: 400;">Affecting more than 44 million people worldwide, Alzheimer’s disease is the most common form of dementia, resulting in memory loss and declining cognitive abilities.</span></p> <p><strong>Plaques and tangles</strong></p> <p><span style="font-weight: 400;">Alzheimer’s disease is characterised by an accumulation of plaques and tangles in the brain.</span></p> <p><span style="font-weight: 400;">These two structures are believed to be responsible for damaging and killing nerve cells, which results in the symptoms of Alzheimer’s.</span></p> <p><span style="font-weight: 400;">Protein plaques are deposits of a protein fragment called beta-amyloid, which build up in between nerve cells.</span></p> <p><span style="font-weight: 400;">Another protein, called tau, can build up inside cells and its fibres can twist into tangles that are neurotoxic.</span></p> <p><span style="font-weight: 400;">Researchers have previously identified the LC as an initial site where tau builds up, but it has been unclear how this relates to the progression of the disease.</span></p> <p><span style="font-weight: 400;">This new study has found that a decline in the integrity of the LC is linked to a larger amount of tau tangles, by comparing brain scans of healthy and cognitively impaired individuals.</span></p> <p><span style="font-weight: 400;">For those individuals with poorer LC health, the team found they had more severe disease symptoms and a faster decline in memory and executive functions, including poor attention, an inability to manipulate objects, and an inability to selectively concentrate on one sense.</span></p> <p><strong>Why this matters</strong></p> <p><span style="font-weight: 400;">The research could pave the way for improved diagnosis, especially for individuals under 65 who may be diagnosed with early-onset Alzheimer’s. </span></p> <p><span style="font-weight: 400;">With no current cure for Alzheimer’s, this finding could also assist healthcare professionals monitor the progression of the disease in their patients.</span></p> <p><span style="font-weight: 400;">The study was published in </span><em><a rel="noopener" href="https://www.science.org/doi/10.1126/scitranslmed.abj2511" target="_blank"><span style="font-weight: 400;">Science Translational Medicine</span></a></em><span style="font-weight: 400;">.</span></p> <p><em><span style="font-weight: 400;">Image: Getty Images</span></em></p>

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A better test for Alzheimer’s disease

<div class="copy"> <p>Alzheimer’s disease is tricky to diagnose, and suspecting its presence in oneself or a loved one brings with it inevitable anxiety about the future. A team of Australian researchers has developed a predictive tool that may address some of this uncertainty.</p> <p>The tool revolves around examining mild cognitive impairment (MCI), which is often a precursor to Alzheimer’s disease.</p> <p>“Someone with mild cognitive impairment is usually living normally in the community and able to look after oneself, but when tested with neurocognitive tests, performing below what would be expected for this age,” according to Professor Nicolas Cherbuin, head of the Centre for Research on Ageing, Health and Wellbeing at the Australian National University, and one of the developers of the tool.</p> <p>“They might have some memory lapses or other difficulties in thinking, but generally speaking, they live normally.”</p> <p>Around one in six people aged over 60 have MCI, but it’s not always an indicator of Alzheimer’s.</p> <p>“Of those, about one in three progress to Alzheimer’s disease within 1.5 to five years,” says Cherbuin.</p> <p>“But it leaves two in three who do not progress, who either remain stable or, for a small fraction, might even return to normal cognition.”</p> <p>Currently, it’s difficult to predict an individual’s Alzheimer’s risk, because the diagnostic tools are difficult to access.</p> <p>“Some are very invasive, and therefore they’re not recommended or suitable for frequent use in a clinical setting. Some might be very expensive, and many are technically demanding,” says Cherbuin.</p> <p>Cherbuin, along with his medical student, Nicolas Darmanthéc, and colleague Dr Hossein Tabatabaei-Jafari, set out to rectify this by developing a simpler predictive tool.</p> <p>“We used data from the Alzheimer’s Disease Neuroimaging Initiative [a US-based longitudinal study], and we focused only on people who had mild cognitive impairments, for many years, with multiple assessments. So it was possible to tell at what stage they progressed from this mild cognitive impairment stage to the clinical Alzheimer’s disease stage.”</p> <p>The researchers examined the subjects’ scores from a test called the “mini-mental state examination”, which is commonly used in clinics, and a biomarker called plasma neurofilament light chains (pNFL), which can be found with a blood test.</p> <p>“When neurons in the brain are damaged or die, they start breaking apart in small pieces, and part of the scaffolding of these cells breaks into little chains,” explains Cherbuin.</p> <p>“One of these chains is called a neurofilament light chain. These fragments of neurons then make their way into the bloodstream where, if we take a blood draw, we can measure them.”</p> <p>Combined, the mini-mental state examination and the pNFL test had good predictive power for Alzheimer’s.</p> <p>“What we found is that when we combine these two measures together, we can predict with good accuracy who is at higher risk versus less risk of progressing towards Alzheimer’s disease within five years.</p> <p>“That ‘within five years’ is the important factor,” adds Cherbuin. “Studies that have predicted conversion from mild cognitive impairment to Alzheimer’s disease have not really focused on a time frame, and for use in a clinical setting, this is what is really needed.”</p> <p>People with MCI don’t just want to know their chances of developing Alzheimer’s – they want to know if it’s imminent, as well.</p> <p>“If they have a better sense earlier as to whether they’re at higher risk or not, they can plan what they want to do and how they want to be treated,” says Cherbuin.</p> <p>“They might want to write a will. And it might also provide an opportunity for the clinician to target the treatment.”</p> <p>This predictive test could be clinically available in two to three years, assuming it succeeds at spotting Alzheimer’s in a few more clinical trials. But there are two major roadblocks at the moment for it to be widely used.</p> <p>One is the data on the pNFL test. “It’s widely available for research, and it’s not particularly expensive, and it’s reliable, but it hasn’t been approved for clinical use,” says Cherbuin.</p> <p>This is likely to change in the near future, however, as a large multi-centre study on the pNFL test wraps up; according to Cherbuin, early data from the study is promising. Once approved, the test can be done easily at large pathology labs.</p> <p>The other roadblock is further trials of the predictive tool. “We’ve shown this in one very well-characterised population, but it needs to be repeated in in several other populations to confirm it behaves in the same way,” says Cherbuin.</p> <p>A paper describing the predictive tool is currently available as a <a rel="noreferrer noopener" href="https://mcusercontent.com/73b3c4bf45063d7aa04d62036/files/cac59333-152a-4993-f663-adc04760fc6d/ANU_Alzheimer_s_research_paper.pdf" target="_blank">preprint</a>, and will be published next week in <a rel="noreferrer noopener" href="https://www.j-alz.com/" target="_blank"><em>The Journal of Alzheimer’s Disease</em></a><em>.</em></p> <!-- Start of tracking content syndication. Please do not remove this section as it allows us to keep track of republished articles --> <img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=159857&amp;title=A+better+test+for+Alzheimer%E2%80%99s+disease" alt="" width="1" height="1" /> <!-- End of tracking content syndication --></div> <div id="contributors"> <p><a rel="noopener" href="https://cosmosmagazine.com/health/body-and-mind/predictive-test-for-alzheimers-disease/" target="_blank">This article</a> was originally published on <a rel="noopener" href="https://cosmosmagazine.com" target="_blank">Cosmos Magazine</a> and was written by <a rel="noopener" href="https://cosmosmagazine.com/contributor/ellen-phiddian" target="_blank">Ellen Phiddian</a>. Ellen Phiddian is a science journalist at Cosmos. She has a BSc (Honours) in chemistry and science communication, and an MSc in science communication, both from the Australian National University.</p> </div>

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Genetic link between alcoholism and Alzheimer’s risk discovered

<p><span style="font-weight: 400;">Scientists have found a genetic overlap between alcohol use disorder (AUD) and neurodegenerative disorders such as Alzheimer’s.</span></p> <p><span style="font-weight: 400;">In a </span><a rel="noopener" href="https://www.nature.com/articles/s41467-021-25392-y" target="_blank"><span style="font-weight: 400;">study</span></a><span style="font-weight: 400;"> published in </span><em><span style="font-weight: 400;">Nature Communications</span></em><span style="font-weight: 400;">, the researchers identified several genes associated with alcoholism, including two previously linked to neurodegenerative disorders.</span></p> <blockquote class="twitter-tweet"> <p dir="ltr">First of its kind study using multi-omics approach identifies large list of candidate genes associated with alcohol use disorder - study shows potential genetic link between <a href="https://twitter.com/hashtag/alcoholism?src=hash&amp;ref_src=twsrc%5Etfw">#alcoholism</a>, <a href="https://twitter.com/hashtag/Alzheimers?src=hash&amp;ref_src=twsrc%5Etfw">#Alzheimers</a> disease, &amp; other neurodegenerative disorders <a href="https://t.co/kzautcL6DN">https://t.co/kzautcL6DN</a><a href="https://twitter.com/hashtag/genetics?src=hash&amp;ref_src=twsrc%5Etfw">#genetics</a> <a href="https://t.co/nUNbvYf2L8">pic.twitter.com/nUNbvYf2L8</a></p> — Mount Sinai Genetics (@SinaiGenetics) <a href="https://twitter.com/SinaiGenetics/status/1428699409475309571?ref_src=twsrc%5Etfw">August 20, 2021</a></blockquote> <p><span style="font-weight: 400;">“Several of these genes are also associated with neurodegenerative disorders - an intriguing connection because of alcohol’s ability to prematurely age the brain,” David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) told </span><span style="font-weight: 400;">The Scientist</span><span style="font-weight: 400;">.</span></p> <p><span style="font-weight: 400;">The scientists compared the genetic data of about 700,000 families involved in the NIAAA’s </span><a rel="noopener" href="https://www.niaaa.nih.gov/research/major-initiatives/collaborative-studies-genetics-alcoholism-coga-study" target="_blank"><span style="font-weight: 400;">Collaborative Studies on the Genetics of Alcoholism</span></a><span style="font-weight: 400;"> (COGA), as well as data from the </span><a rel="noopener" href="https://www.ukbiobank.ac.uk/enable-your-research/approved-research/alcohol-consumption-and-brain-health" target="_blank"><span style="font-weight: 400;">UK Biobank</span></a><span style="font-weight: 400;">, against analyses of adult and foetal brains to determine which genes were silenced or expressed.</span></p> <p><span style="font-weight: 400;">Though the study did identify many genes associated with alcohol use, the team focused on the two genes linked to neurodegenerative disorders: </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> and </span><em><span style="font-weight: 400;">MAPT</span></em><span style="font-weight: 400;">. </span></p> <p><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> produces a protein that controls the activity of immune cells, while </span><em><span style="font-weight: 400;">MAPT</span></em><span style="font-weight: 400;"> produces a protein found throughout the nervous system called tau.</span></p> <p><strong><em>SPI1</em> linked to Alzheimer’s</strong></p> <p><a rel="noopener" href="https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-018-0277-1" target="_blank"><span style="font-weight: 400;">Previous research</span></a><span style="font-weight: 400;"> has shown that </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> influenced the likelihood of a person developing Alzheimer’s disease, with some theorising that it influences the activity of microglia, immune cells that are found in the brain.</span></p> <p><span style="font-weight: 400;">In a </span><a rel="noopener" href="https://www.nature.com/articles/s41398-019-0384-y" target="_blank"><span style="font-weight: 400;">study</span></a><span style="font-weight: 400;"> from two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and the new paper’s first author, and his team found evidence that people with AUD might have an overactive immune system - and this new paper could help explain their previous findings.</span></p> <p><span style="font-weight: 400;">The new study also found an association between the </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> gene and both heavy drinking and a diagnosis of AUD.</span></p> <p><span style="font-weight: 400;">Though alcoholism is already associated with immune dysfunction, the team found that expression of the </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> gene was higher in some foetal brains.</span></p> <p><span style="font-weight: 400;">Kapoor says this finding suggests that those genetically predisposed to AUD and heavy drinking are also predisposed to developing an overactive immune system.</span></p> <p><span style="font-weight: 400;">If this is the case, when people with particular versions of the gene drink heavily, Kapoor suggests that their immune systems could become overactivated and cause brain immune cells to alter connections between neurons.</span></p> <p><span style="font-weight: 400;">Kapoor bases this theory on a previous </span><a rel="noopener" href="https://stke.sciencemag.org/content/13/650/eaba5754" target="_blank"><span style="font-weight: 400;">study</span></a><span style="font-weight: 400;"> in mice that found that binge drinking activated brain immune cells, which selectively pruned certain synapses and caused the animals to display anxiety-like behaviours.</span></p> <p><span style="font-weight: 400;">The activation of these brain immune cells could result in the pruning of connections to neurons that produce dopamine - the chemical behind the “reward” feeling we get after drinking alcohol.</span></p> <p><span style="font-weight: 400;">As a result, people with certain versions of </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> who start drinking regularly would “have to drink more and more to get the same level of reward”, Kapoor says.</span></p> <p><span style="font-weight: 400;">“And their immune system will get more activated”, pruning more synapses.</span></p> <p><span style="font-weight: 400;">“It will become a vicious cycle,” Kapoor says.</span></p> <p><span style="font-weight: 400;">As for </span><em><span style="font-weight: 400;">MAPT</span></em><span style="font-weight: 400;">, the gene isn’t associated with AUD, but is associated with consuming more drinks per week.</span></p> <p><span style="font-weight: 400;">The tau protein it produces is thought to play a major role in neurodegenerative disorders including Alzheimer’s, Parkinson’s, frontotemporal dementia, and supranuclear palsy.</span></p> <p><span style="font-weight: 400;">However, it is still unclear how tau may factor into the consumption of alcohol.</span></p> <p><strong>Why this matters</strong></p> <p><span style="font-weight: 400;">Joel Gelernter, a geneticist and neurobiologist at Yale University School of Medicine, who was not involved in the study, says the study is “a really necessary step in unravelling the biology of alcohol intake and alcohol use disorder”.</span></p> <p><span style="font-weight: 400;">Kapoor says this work could benefit people in a few ways.</span></p> <p><span style="font-weight: 400;">First, he believes that drugs currently in development to treat neurodegenerative disorders could be repurposed to help people in reducing or stopping drinking.</span></p> <p><span style="font-weight: 400;">Second, it could be a way of reducing a person’s risk for neurodegenerative disorders.</span></p> <p><span style="font-weight: 400;">“If we can identify some group of people that are more at risk of Alzheimer’s disease, we can ask them to reduce their drinking,” he says.</span></p> <p><span style="font-weight: 400;">“That might be beneficial to them.”</span></p> <p><em><span style="font-weight: 400;">Image: Getty Images</span></em></p>

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