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Hollywood star's heartbreaking health update

<p>Gena Rowlands's son has shared his mother's heartbreaking health battle, that is reminiscent of one of her most iconic movie character's similar health issue.</p> <p>The 94-year-old Golden Globe winner who portrayed an older version of Rachel McAdam’s character, Allie, in the 2004 film<em> The Notebook</em>, has been battling Alzheimer’s disease for the past five years.</p> <p>While discussing the film's 20 year anniversary, Nick Cassavetes, the director of the movie and Rowlands’ son, revealed his mother’s diagnosis. </p> <p>“I got my mum to play older Allie, and we spent a lot of time talking about Alzheimer’s and wanting to be authentic with it, and now, for the last five years, she’s had Alzheimer’s,” Cassavetes told <em><a href="https://ew.com/the-notebook-star-gena-rowlands-has-alzheimers-8668642">Entertainment Weekly</a></em> of Rowlands’ character, who also had dementia.</p> <p>“She’s in full dementia. And it’s so crazy — we lived it, she acted it, and now it’s on us.”</p> <p>Back in 2004, Rowlands — whose mother, actress Lady Rowlands, also suffered from the disease — explained why playing Allie was “particularly hard.”</p> <p>“This last one — The Notebook, based on the novel by Nicholas Sparks — was particularly hard because I play a character who has Alzheimer’s,” she told <em><a href="https://www.oprah.com/spirit/gena-rowlands-aha-moment">O magazine</a></em>.</p> <p>“I went through that with my mother, and if Nick hadn’t directed the film, I don’t think I would have gone for it — it’s just too hard. It was a tough but wonderful movie.”</p> <p><em>Image credits: New Line Cinema/Demmie Todd/Warner Bros/Spring Creek/Kobal/Shutterstock Editorial </em></p>

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What’s the difference between Alzheimer’s and dementia?

<div class="theconversation-article-body"> <p><a href="https://theconversation.com/profiles/nikki-anne-wilson-342631">Nikki-Anne Wilson</a>, <em><a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a></em></p> <p>Changes in thinking and memory as we age can occur for a variety of reasons. These changes are <a href="https://www.nia.nih.gov/health/memory-loss-and-forgetfulness/memory-problems-forgetfulness-and-aging#changes">not always cause for concern</a>. But when they begin to disrupt daily life, it could indicate the first signs of dementia.</p> <p>Another term that can crop up when we’re talking about dementia is Alzheimer’s disease, or Alzheimer’s for short.</p> <p>So what’s the difference?</p> <h2>What is dementia?</h2> <p>Dementia is an umbrella term used to describe a range of syndromes that result in changes in memory, thinking and/or behaviour due to degeneration in the brain.</p> <p>To meet the <a href="https://alz-journals.onlinelibrary.wiley.com/doi/epdf/10.1016/j.jalz.2011.03.005">criteria</a> for dementia these changes must be sufficiently pronounced to interfere with usual activities and are present in at least two different aspects of thinking or memory.</p> <p>For example, someone might have trouble remembering to pay bills and become lost in previously familiar areas.</p> <p>It’s less-well known that dementia can also occur in <a href="https://www.childhooddementia.org/what-is-childhood-dementia">children</a>. This is due to progressive brain damage associated with more than 100 rare genetic disorders. This can result in similar cognitive changes as we see in adults.</p> <h2>So what’s Alzheimer’s then?</h2> <p><a href="https://www.alz.org/alzheimers-dementia/what-is-alzheimers">Alzheimer’s</a> is the most common type of dementia, accounting for <a href="https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12068">about 60-80%</a> of cases.</p> <p>So it’s not surprising many people use the terms dementia and Alzheimer’s interchangeably.</p> <p>Changes in memory are the most common sign of Alzheimer’s and it’s what the public <a href="https://alzres.biomedcentral.com/articles/10.1186/s13195-023-01219-4">most often</a> associates with it. For instance, someone with Alzheimer’s may have trouble recalling recent events or keeping track of what day or month it is.</p> <p>We still don’t know exactly what <a href="https://link.springer.com/article/10.1134/s002689332104004x">causes Alzheimer’s</a>. However, we do know it is associated with a build-up in the brain of two types of protein called <a href="https://www.dementiasplatform.uk/news-and-media/blog/amyloid-and-tau-the-proteins-involved-in-dementia">amyloid-β and tau</a>.</p> <p>While we all have some amyloid-β, when too much builds up in the brain it clumps together, forming plaques in the spaces between cells. These plaques cause damage (inflammation) to surrounding brain cells and leads to disruption in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468450/">tau</a>. Tau forms part of the structure of brain cells but in Alzheimer’s tau proteins become “tangled”. This is toxic to the cells, causing them to die. A <a href="https://content.iospress.com/articles/journal-of-alzheimers-disease/jad180583">feedback loop</a> is then thought to occur, triggering production of more amyloid-β and more abnormal tau, perpetuating damage to brain cells.</p> <p>Alzheimer’s can also occur with other forms of dementia, such as <a href="https://www.mayoclinic.org/diseases-conditions/vascular-dementia/symptoms-causes/syc-20378793">vascular dementia</a>. This combination is the most common example of a <a href="https://www.dementiauk.org/information-and-support/types-of-dementia/mixed-dementia/">mixed dementia</a>.</p> <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip"><img src="https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&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/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=45&amp;auto=format&amp;w=600&amp;h=456&amp;fit=crop&amp;dpr=1 600w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=30&amp;auto=format&amp;w=600&amp;h=456&amp;fit=crop&amp;dpr=2 1200w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=15&amp;auto=format&amp;w=600&amp;h=456&amp;fit=crop&amp;dpr=3 1800w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;h=573&amp;fit=crop&amp;dpr=1 754w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=30&amp;auto=format&amp;w=754&amp;h=573&amp;fit=crop&amp;dpr=2 1508w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&amp;q=15&amp;auto=format&amp;w=754&amp;h=573&amp;fit=crop&amp;dpr=3 2262w" alt="" /></a><figcaption></figcaption></figure> <h2>Vascular dementia</h2> <p>The second most common type of dementia is <a href="https://www.mayoclinic.org/diseases-conditions/vascular-dementia/symptoms-causes/syc-20378793">vascular dementia</a>. This results from disrupted blood flow to the brain.</p> <p>Because the changes in blood flow can occur throughout the brain, signs of vascular dementia can be more varied than the memory changes typically seen in Alzheimer’s.</p> <p>For example, vascular dementia may present as general confusion, slowed thinking, or difficulty organising thoughts and actions.</p> <p>Your <a href="https://www.mayoclinic.org/diseases-conditions/vascular-dementia/symptoms-causes/syc-20378793">risk of vascular dementia</a> is greater if you have heart disease or high blood pressure.</p> <h2>Frontotemporal dementia</h2> <p>Some people may not realise that dementia can also affect behaviour and/or language. We see this in different forms of frontotemporal dementia.</p> <p>The behavioural variant of <a href="https://neuro.psychiatryonline.org/doi/10.1176/appi.neuropsych.20090238#:%7E:text=The%20behavioral%20variant%20of%20frontotemporal,often%20delayed%20for%20several%20years.">frontotemporal dementia</a> is the second most common form (after Alzheimer’s disease) of <a href="https://www.healthdirect.gov.au/younger-onset-dementia">younger onset dementia</a> (dementia in people under 65).</p> <p>People living with this may have difficulties in interpreting and appropriately responding to social situations. For example, they may make uncharacteristically rude or offensive comments or invade people’s personal space.</p> <p><a href="https://www.sciencedirect.com/topics/neuroscience/semantic-dementia">Semantic dementia</a> is also a type of frontotemporal dementia and results in difficulty with understanding the meaning of words and naming everyday objects.</p> <h2>Dementia with Lewy bodies</h2> <p><a href="https://www.alz.org/alzheimers-dementia/what-is-dementia/types-of-dementia/dementia-with-lewy-bodies">Dementia with Lewy bodies</a> results from dysregulation of a different type of protein known as α-synuclein. We often see this in people with Parkinson’s disease.</p> <p>So people with this type of dementia may have altered movement, such as a stooped posture, shuffling walk, and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7428504/">changes in handwriting</a>. Other symptoms include changes in alertness, visual hallucinations and significant <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029467/">disruption to sleep</a>.</p> <h2>Do I have dementia and if so, which type?</h2> <p>If you or someone close to you is concerned, the first thing to do is to <a href="https://cdpc.sydney.edu.au/research/clinical-guidelines-for-dementia/">speak to your GP</a>. They will likely ask you some questions about your medical history and what changes you have noticed.</p> <p>Sometimes it might not be clear if you have dementia when you first speak to your doctor. They may suggest you watch for changes or they may refer you to a specialist for <a href="https://www.nia.nih.gov/health/alzheimers-and-dementia/what-dementia-symptoms-types-and-diagnosis#diagnosis">further tests</a>.</p> <p>There is no single test to clearly show if you have dementia, or the type of dementia. A diagnosis comes after multiple tests, including brain scans, tests of memory and thinking, and consideration of how these changes impact your daily life.</p> <p>Not knowing what is happening can be a challenging time so it is important to speak to someone about how you are feeling or to reach out to <a href="https://www.dementia.org.au/get-support/national-dementia-helpline">support services</a>.</p> <h2>Dementia is diverse</h2> <p>As well as the different forms of dementia, everyone experiences dementia in different ways. For example, the speed dementia progresses varies a lot from person to person. Some people will continue to <a href="https://livingwellwithdementia.org.au">live well with dementia</a> for some time while others may decline more quickly.</p> <p>There is still significant <a href="https://academic.oup.com/gerontologist/article-abstract/64/5/gnad130/7281753">stigma</a> surrounding dementia. So by learning more about the various types of dementia and understanding differences in how dementia progresses we can all do our part to create a more <a href="https://www.dementiafriendly.org.au/">dementia-friendly community</a>.</p> <hr /> <p><em>The <a href="https://www.dementia.org.au/get-support/national-dementia-helpline">National Dementia Helpline</a> (1800 100 500) provides information and support for people living with dementia and their carers. To learn more about dementia, you can take this <a href="https://www.utas.edu.au/wicking/understanding-dementia">free online course</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/225271/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><a href="https://theconversation.com/profiles/nikki-anne-wilson-342631">Nikki-Anne Wilson</a>, Postdoctoral Research Fellow, Neuroscience Research Australia (NeuRA), <a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a></em></p> <p><em>Image credits: Shutterstock</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/whats-the-difference-between-alzheimers-and-dementia-225271">original article</a>.</em></p> </div>

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Study finds new link for increased risk of Alzheimer’s

<p>A new study has found that people suffering from anxiety disorders could be more likely to develop Alzheimer's disease. </p> <p>The study, which was published by brain researchers The Florey, analysed data from 2443 older Australians from Melbourne and Perth, who are part of a cohort for dementia research.</p> <p>Study leads Dr Yijun Pan and Dr Liang Jin found that anxiety and other neurological disorders are linked to an increased likelihood of developing Alzheimer's disease.  </p> <p>"People with anxiety and neurological disorders are 1.5 and 2.5 times more likely to have Alzheimer's disease," Dr Pan said.</p> <p>"For people with anxiety, males have higher odds than females of developing Alzheimer's disease."</p> <p>They also found a few other medical conditions which were linked to a decreased risk of Alzheimer's, including arthritis, cancer, gastric complaints, and high cholesterol. </p> <p>The study leads said that the p53 protein - which causes neuron dysfunction and cell death in Alzheimer's patients - loses its function when someone has cancer, which could possibly explain the link between the two conditions. </p> <p>"We need further research to understand whether these diseases interfere with the evolution of Alzheimer's or whether there might be other reasons," Dr Pan said.</p> <p>"The medications or treatments used for these diseases may possibly contribute to this observation."</p> <p>The study however, did not find a link between  Alzheimer's and depression, falls or strokes. </p> <p>"This is the first study to assess 20 comorbidity associations with cognitive impairment using a single Australian dataset, which allowed us to fully consider how these conditions affect the likelihood of developing Alzheimer's disease," Dr Pan said. </p> <p>"We also studied whether age, gender, smoking, education, alcohol consumption, and the APOE gene – believed to be connected to Alzheimer's - affects these associations.</p> <p>"Our study indicates a new opportunity for biologists to study the links between these 20 conditions with Alzheimer's disease.</p> <p>"This work also provides valuable epidemiological evidence to clinicians, which may help them to evaluate one's risk of developing Alzheimer's disease."</p> <p><em>Image: Nine</em></p>

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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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Chris Hemsworth to slow down in Hollywood

<p>Chris Hemsworth has revealed he’s taking a break from acting following the news that he is at very high risk of developing Alzheimer’s disease later in life.</p> <p>While he may be slowing down, <em>Page Six </em>reported that the Aussie actor’s upcoming schedule is not quite so idle.</p> <p>Hemsworth has four projects in the works, including the return of his iconic <em>Thor</em> character in the highly anticipated <em>Avengers</em> sequel, and an untitled Hulk Hogan biopic. Although after those four projects, a source said, “he doesn’t plan to take on many roles because of [learning about his high risk for] Alzheimer’s.”</p> <p>Speaking to <em>Vanity Fair</em>, Hemsworth, 39, said he’s “not talking about retiring by any means,”</p> <p>The 39-year-old discovered he’s at high risk for Alzheimer’s while filming the National Geographic and Disney+ docuseries, <em>Limitless</em>.</p> <p>He told <em>Vanity Fair</em> about “the intensity [of] navigating” the test results and highlighted while it’s not a diagnosis, it’s a scary sign that the disease is more likely to develop in him than most other people.</p> <p>“Most of us, we like to avoid speaking about death,” he said. “Then to all of a sudden be told some big indicators are actually pointing to this as the route which is going to happen, the reality of it sinks in. Your own mortality.”</p> <p>He revealed learning that he’s “eight to 10 times more likely” to develop Alzheimer’s, “triggered something in me to want to take some time off.”</p> <p>“I’ve been completing the things I was already contracted to do,” he said, adding that he plans to “go home and … to have a good chunk of time off and just simplify. Be with the kids, be with my wife.”</p> <p><em>Image credit: 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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Chris Hemsworth reveals life-changing health shock

<p>Chris Hemsworth has revealed how he discovered he has a genetic predisposition to Alzheimer's disease. </p> <p>The actor revealed that while he was filming his new docuseries, titled <em>Limitless with Chris Hemsworth</em>, he discovered he has two copies of the gene APOE4, meaning he is "eight to 10 times more likely" to battle the progressive disease characterised by mental deterioration.</p> <p>"Most of us, we like to avoid speaking about death," Hemsworth told <a href="https://www.vanityfair.com/hollywood/2022/11/chris-hemsworth-exclusive-interview-alzheimers-limitless" target="_blank" rel="noopener">Vanity Fair</a>. "Then to all of a sudden be told some big indicators are actually pointing to this as the route which is going to happen, the reality of it sinks in. Your own mortality."</p> <p>Hemsworth is part of the rare two to three per cent of the population that has a copy of the APOE4 gene from both parents.</p> <p>The father-of-three noted how after his grandfather was diagnosed with Alzheimer's, he often "slips in and out of Dutch", English, in a "mash-up and then maybe some other new words as well".</p> <p>It was "confronting initially" to get news of his genetic predisposition, Hemsworth said, but he told the outlet he has turned it into a "self-deprecating sort of joke."</p> <p>"I feel like my memory's getting worse," the Aussie star revealed. "It's a placebo effect – or it's taking place! … It's my excuse now."</p> <p>Since receiving the news, Hemsworth says he has made certain lifestyle choices and is now more selective about the projects he takes on and prioritises spending "outdoorsy and adventurous" time with his family – wife Elsa Pataky, 46, daughter India, 10, and sons Sasha and Tristan, eight.</p> <p>The actor star also said he is taking preventative measures against Alzheimer's, though evidence suggests it's not completely preventable, but certain lifestyle choices can provide a greater quality of life with the disease.</p> <p>"I feel thankful that I have in my arsenal the sort of tools to best prepare myself and prevent things happening in that way," Hemsworth said. "The benefit of preventative steps is that it affects the rest of your life."</p> <p>"When you have predisposition to … anything – it's all about sleep management, stress management, nutrition, movement fitness," he continued. "It's all kind of the same tools that need to be applied in a consistent way."</p> <p>Hemsworth said he shared his story in the hopes of encouraging others to "to take better care of themselves."</p> <p><em>Image credits: Getty Images</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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How can your lifestyle affect your memory?

<p>Did you know that dementia is now the second leading cause of death in Australia? The numbers of people being diagnosed with dementia are increasing every year, instead of decreasing. Many families are now affected by dementia with having either a parent, family member or friend being diagnosed.</p> <p>Did you know that memory problems are one of the earliest symptoms of Alzheimer’s disease/dementia?</p> <p>So it makes sense that if memory problems are one of the earliest symptoms of dementia, you should not be ignoring those memory problems when they occur. They are signals for you to be proactive, find out why they are happening, and not wait till they get worse, because time is of the utmost importance.</p> <p>Our modern lifestyle plays a huge role as to why dementia numbers are increasing. I have found in my research so many causes of memory problems that I have put them into two categories – medical causes and lifestyle causes. Some of these causes may be able to be treated which may help to improve your memory.</p> <p>Here are two examples of lifestyle causes of memory problems that you should be aware of:</p> <p><strong>1. Stress</strong></p> <p>Stress is one of the major causes of memory problems<strong>. </strong>When we are stressed and produce the stress hormone cortisol, thousands of neurons (brain cells) can die off. When we are highly stressed, we seem to think less clearly and tend to forget even simple things.</p> <p>Too much cortisol causes a decline in the daily function of your brain. It also robs your brain of glucose, which is its only source of fuel. Excessive cortisol also affects your brain’s chemical messengers – your neurotransmitters – which carry your thoughts from one brain cell to the next. Many scientists now believe that too much exposure to stress can actually shrink your brain.</p> <p><strong>2. Foods to Avoid</strong></p> <p>These are the ingredients found in packaged food products. These particular ingredients have been added to many packaged food products and ‘diet’ drinks found on the supermarket shelves.</p> <p>One main ingredient to look out for and avoid as much as possible is aspartame, an artificial sweetener. Aspartame is an excito-toxin which may cause brain cells to become over-stimulated.  If they become too over-stimulated this may cause brain cells to die. Check out the packaged food products and drinks in your pantry and look at the ingredient list for Aspartame (950) or (951) and avoid them.</p> <p>Have you been getting a bit forgetful occasionally and wondered why this may be happening? You may be consuming ‘diet’ drinks as part of your lifestyle because you want to cut back on your sugar intake or are watching your weight. But these ‘diet’ drinks may be the cause of your memory problems. Try to reduce the amount of ‘diet’ drinks you consume. As a result, you may notice an improvement in your memory.</p> <p><a href="https://www.smartbrainhealthcentre.com.au/"><em>Louise Hallinan</em></a><em> is the international award-winning author of </em>Smart Brain, Healthy Brain<em>, a natural medicine practitioner and founder of the Smart Brain Health Centre which specialises in </em><em>helping Baby Boomers and Generation X mothers avoid the risk of dementia.</em></p> <p><em>Image: Getty</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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Your dog can get dementia - here’s how to prevent it

<p dir="ltr">Just like us, dogs can experience cognitive decline as they age. They can also risk developing a neurodegenerative condition called Canine Cognitive Dysfunction (CCD), a condition similar to Alzhheimer’s Disease.</p> <p dir="ltr">Like Alzheimer’s, symptoms dogs with CCD can experience include a loss of spatial awareness, memory deficiencies, disrupted sleep, and altered social interactions.</p> <p dir="ltr">Both CCD and Alzheimer’s also share symptoms found in the brain itself, including <a href="https://oversixty.com.au/health/mind/alzheimer-s-marker-found-in-the-brain" target="_blank" rel="noopener">the buildup of fragments of a protein called beta-amyloid</a> in between nerve cells.</p> <p dir="ltr">According to a new study published in the journal <em><a href="https://doi.org/10.1038/s41598-022-15837-9" target="_blank" rel="noopener">Scientific Reports</a></em>, the risk of developing CCD increases by 68 percent each year after dogs turn 10.</p> <p dir="ltr">The team studied a whopping 15,019 dogs that took part in a longitudinal study called the Dog Ageing Project. Between 2019 and 2020, the owners of participating pets completed two surveys about the health status and physical activity of their dogs. They also completed the Canine Social and Learned Behaviour survey, which tested for symptoms of CCD such as dogs failing to recognise familiar people.</p> <p dir="ltr">But, they also found that older pooches that were very active had a much smaller risk of developing the condition in comparison to less active dogs of the same breed and health - with the more sedentary dogs having a 6.47 times higher risk of having CCD.</p> <p dir="ltr">They stress that their study doesn’t show that a lack of physical activity causes CCD, and are calling for more research to determine whether CCD is caused by less physical activity or if the inactivity is caused by CCD.</p> <p dir="ltr">Because of the similarities between CCD and Alzheimer’s disease, the team argue that means that researching CCD could have implications for our understanding and treatment of Alzheimer’s, and vice versa.</p> <p dir="ltr">For example, the association between physical activity and lower risks of CCD come after numerous studies showing this relationship in rodents <a href="https://oversixty.com.au/health/mind/the-surprising-reason-exercise-improves-symptoms-of-alzheimer-s" target="_blank" rel="noopener">and in humans</a>.</p> <p dir="ltr">“These observations may reflect a variety of biologic mechanisms, including a reduction of pro-inflammatory cytokines in the brain that otherwise contribute to neural damage and death, and an increase in neural plasticity,” they write of the studies with rodents and people, adding that these mechanisms might also explain the link between physical activity and CCD risk.</p> <p dir="ltr">“Given increasing evidence of the parallels between canine and human cognitive disease, accurate CCD diagnosis in dogs may provide researchers with more suitable animal models in which to study ageing in human populations.”</p> <p><span id="docs-internal-guid-91437cc1-7fff-5a43-0a9a-bca582c47473"></span></p> <p dir="ltr"><em>Image: Getty Images</em></p>

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