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Rare coin hidden for decades to fetch eye-watering sum

Three sisters from the US who inherited a dime coin kept it in a bank vault for more than 40 years, and while they know it had some value, they didn't know just how much until a few years ago. The rare coin, struck by the US Mint in San Francisco in 1975, could be worth more than $US500,000 ($748,000), according to Ian Russell, president of GreatCollections, the auction house selling the coin. What makes the coin depicting President Franklin D. Roosevelt so valuable is that it is just one of two coins missing the "S" mint mark for San Francisco. The other dime sold for $US682,000 (over $1 million) at a 2019 auction and then again months later to a private collector. While avid coin collectors have known about the existence of these two extraordinarily rare coins, their whereabouts had remained a mystery since the late 1970s. “They were hidden for decades,” Russell said. “Most major collectors and dealers have never seen one.” The three sisters from Ohio, who want to remain anonymous, inherited one of the two dimes after the recent death of their of their brother, Russell said. They told Russell that their brother and mother bought the first error coin discovered in 1978 for $27,225, which would amount to roughly $135,000 today. Their parents, who ran a dairy farm, saw the coin as a financial safety net, and it was only until last year that one of the sisters saw the coin first-hand. Russell also said that their brother had reached out to him about seven years ago and told him about the coin, but he too kept it a secret. When Russell told one of the sisters about the potential value of the coin, she told him: “is that really possible?”. The coin, known as the “1975 ‘no S’ proof dime,” will be displayed at a coin show beginning on Wednesday in Tampa, Florida, and before <a href="https://www.greatcollections.com/Coin/1655587" target="_blank" rel="noopener">the auction</a> closes late next month, Russell said. The current highest bidder has offered $US250,000 ($374,000). Images: Great Collections/ Professional Coin Grading Services

Money & Banking

New device could help GPs detect Alzheimer's in minutes

GPs could soon be able to screen their patients for Alzheimer's Disease in a matter of minutes, using a handheld device the size of a credit card. The first-of-a-kind finger-prick blood test was developed by engineers at Melbourne's Monash University and it can detect the hallmark protein biomarkers of early Alzheimer's Disease within minutes. This could become an important tool for doctors in diagnosing patients before the symptoms progress. In Australia alone there are around 420,000 people living with dementia, with that number set to double by 2054. Associate Professor Sudha Mokkapati, from Monash Materials Science and Engineering, helped lead the development of the testing device. "Detecting very early disease in large populations could dramatically change the trajectory of this burdening disease for many patients, and shave millions off associated healthcare costs," Mokkapati said. "We've completed testing that shows the technology is highly advanced by design and capable of detecting ultra-low levels of several disease biomarkers in blood." The device also has the potential to remove the need for laboratory-based pathology tests, making diagnoses faster and cheaper. The university is currently seeking funding to complete the next stage - clinical validation, which will help bring the device one step closer to reality. "Most patients with neurodegenerative disease are typically diagnosed at advanced stages. Sadly, treatments targeting late-onset disease provide limited therapeutic benefit," Associate Professor Matthew Pase, at Monash's School of Psychological Sciences, said. "Earlier screening could change the outlook for many patients diagnosed with cognitive impairment, increasing the chance of halting or slowing symptom development and the rapid progression of the disease." Image: Monash University/ Nine

Caring

Major breakthrough holds the key to diagnosing Alzheimer's

A new study has found that a simple blood test could be key to diagnosing Alzheimer's more quickly and more accurately. The research, published on the Journal of the American Medical Association, was conducted by a team of scientists at Sweden’s Lund University, was based off 1213 patients there with the condition. They found that a blood test could correctly identify whether patients with memory problems had Alzheimer’s 90 per cent of the time – making it “significantly” more accurate than cognitive tests and CAT scans in diagnosing the condition. The test itself measures tau protein 217, which if there is an abnormal build up of both in and around brain cells, may be the cause of the disease. “Increases in p tau-217 concentrations in the blood are quite profound in Alzheimer’s disease,” study co-author, Lund University associate professor and senior consultant neurologist, Dr Sebastian Palmqvist, told CNN. “At the dementia stage of the disease, levels are more than eight times higher compared with elderly (people) without Alzheimer’s.” As part of the study, the p tau-217 test was combined with one testing for another blood biomarker for Alzheimer’s called the amyloid 42/40 ratio. Other doctors have shared their thoughts on the research findings, with Chief science officer of America’s Alzheimer’s Association, Dr Maria Carrillo, telling CNN that doctors would “love to have a blood test that can be used in a primary care physician’s office, functioning like a cholesterol test but for Alzheimer’s”. “The p tau-217 blood test is turning out to be the most specific for Alzheimer’s and the one with the most validity. It seems to be the frontrunner,” she added. Blood tests like this could “change the game in the speed in which we can conduct Alzheimer’s trials and get to the next new medication”. Dr Jason Karlawish, the co-director at the University of Pennsylvania’s Penn Memory Centre, said of the research: “Not too long ago measuring pathology in the brain of a living human was considered just impossible.” “This study adds to the revolution that has occurred in our ability to measure what’s going on in the brain of living humans.” Image: Shutterstock

Caring

Is it really possible to have Alzheimer’s yet no symptoms?

<div class="theconversation-article-body"><a href="https://theconversation.com/profiles/michael-hornberger-1507154">Michael Hornberger</a>, <a href="https://theconversation.com/institutions/university-of-east-anglia-1268">University of East Anglia</a> Some people seem to be more <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11003087/#:%7E:text=Some%20individuals%20are%20able%20to,into%20a%20widely%20debated%20concept.">resilient</a> to developing Alzheimer’s diseases, despite having the biological hallmarks of the devastating disease. For obvious reasons, scientists are very interested in studying this special group of people. Alzheimer’s disease, the most common form of dementia, is thought to start because of a build-up of two proteins in the brain: amyloid and tau. Once these proteins accumulate, for yet-to-be-determined reasons, they become toxic to brain cells (neurons) and these cells start dying. As a result, people develop symptoms such as memory loss because the brain can’t function properly with all these dead neurons. This cascade of events has been known for many years and is how the disease progresses in most people with Alzheimer’s. Most people, except a special group who are more resilient. But why are they resilient? A recent study in the journal <a href="https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-024-01760-9">Acta Neuropathologica Communications</a> investigated whether our genes might influence how resilient we are against Alzheimer’s disease symptoms when there are high levels of amyloid in our brain. The scientists conducted a study on the brains of three groups of people. The first group comprised people who had died with Alzheimer’s disease. The second were healthy people who died of natural causes. And the third comprised people who had high levels of Alzheimer’s proteins in the brain but never developed symptoms of the disease during their lifetime – or at least never had a diagnosis of Alzheimer’s disease. The last group, they considered as being resilient to Alzheimer’s disease since they had the proteins in their brains but did not have the symptoms or a diagnosis of Alzheimer’s disease during their lifetime. The scientists found that genes related to the activity of the immune system seem to have been more active in the Alzheimer’s resilient group. This would make sense as it is well established that the immune system helps clear the excess proteins from the brain, so genes that help this process might make us more resilient to developing symptoms of the disease. <h2>How to become resilient – even if you don’t have the genes</h2> This is great if you have inherited these genes from your parents, but what does it mean for the rest of us who do not have those genes? Is there a way we can make ourselves more resilient to developing Alzheimer’s disease regardless of our genes? “Yes” is the short answer. There is now good scientific evidence that <a href="https://theconversation.com/can-alzheimers-really-be-reversed-as-a-new-documentary-claims-230705">lifestyle changes</a> and drugs allow us to reduce our risk of developing Alzheimer’s disease in the future. In particular, physical activity has been shown to reduce our risk of developing Alzheimer’s, probably because it has a well-known beneficial effect on our immune system and hence helps clear those rogue proteins accumulating in our brains. This means that being more physically active might have the same effect on our Alzheimer’s resilience as those lucky people who have the “right” genes. Interestingly, we do not know how physically active the resilient people in the study were and how this might have influenced their resilience to Alzheimer’s disease. As so often in science, it is not clear whether nature (genes) or nurture (lifestyle) contributed to their resilience. The other interesting aspect is that the resilient people in the study died of another cause than Alzheimer’s disease, but they might have developed Alzheimer’s disease eventually if they had lived longer.<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/230334/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/michael-hornberger-1507154">Michael Hornberger</a>, Professor of Applied Dementia Research, <a href="https://theconversation.com/institutions/university-of-east-anglia-1268">University of East Anglia</a> Image credits: Shutterstock 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/is-it-really-possible-to-have-alzheimers-yet-no-symptoms-230334">original article</a>. </div>

Mind

"Cut this rubbish out": Channel 7's fresh "news" segment slammed

Channel 7's major bulletin shake up has not been well received by some viewers. On Friday night, they kicked off their new comedy segment with Mark Humphries, whose satirical humour was intended to be used to "cut through political spin and translate current affairs in the universal news language of taking the piss” according to appointed news director Anthony De Ceglie. Humphries’ three minutes comedy segment premiered under the banner The 6.57pm News, and was made to look like a continuation of the news. That night, they were discussing US President Joe Biden's press conference which aired earlier in the day. “His press conference was delayed for over an hour, presumably because the President was running late … or more likely waddling late,” Humphries said in the segment. “Biden who is 81 – but doesn’t look a day over 90 – spoke smoothly on a variety of issues and allayed voters fears about his age … is what I wish I could tell you. “Instead, this happened …” He then played a clip of Biden confusing Kamala Harries with Donald Trump, followed by another clip of him whispering on the lectern. “Very reassuring and not weird at all,” the comic said. <blockquote class="instagram-media" style="background: #FFF; border: 0; border-radius: 3px; box-shadow: 0 0 1px 0 rgba(0,0,0,0.5),0 1px 10px 0 rgba(0,0,0,0.15); margin: 1px; max-width: 540px; min-width: 326px; padding: 0; width: calc(100% - 2px);" data-instgrm-captioned="" data-instgrm-permalink="https://www.instagram.com/p/C9TGVSTTozZ/?utm_source=ig_embed&utm_campaign=loading" data-instgrm-version="14"> <div style="padding: 16px;"> <div style="display: flex; flex-direction: row; align-items: center;"> <div style="background-color: #f4f4f4; border-radius: 50%; flex-grow: 0; height: 40px; margin-right: 14px; width: 40px;"> </div> <div style="display: flex; flex-direction: column; flex-grow: 1; justify-content: center;"> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; margin-bottom: 6px; width: 100px;"> </div> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; width: 60px;"> </div> </div> </div> <div style="padding: 19% 0;"> </div> <div style="display: block; height: 50px; margin: 0 auto 12px; width: 50px;"> </div> <div style="padding-top: 8px;"> <div style="color: #3897f0; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: 550; line-height: 18px;">View this post on Instagram</div> </div> <div style="padding: 12.5% 0;"> </div> <div style="display: flex; flex-direction: row; margin-bottom: 14px; align-items: center;"> <div> <div style="background-color: #f4f4f4; border-radius: 50%; height: 12.5px; width: 12.5px; transform: translateX(0px) translateY(7px);"> </div> <div style="background-color: #f4f4f4; height: 12.5px; transform: rotate(-45deg) translateX(3px) translateY(1px); width: 12.5px; flex-grow: 0; margin-right: 14px; margin-left: 2px;"> </div> <div style="background-color: #f4f4f4; border-radius: 50%; height: 12.5px; width: 12.5px; transform: translateX(9px) translateY(-18px);"> </div> </div> <div style="margin-left: 8px;"> <div style="background-color: #f4f4f4; border-radius: 50%; flex-grow: 0; height: 20px; width: 20px;"> </div> <div style="width: 0; height: 0; border-top: 2px solid transparent; border-left: 6px solid #f4f4f4; border-bottom: 2px solid transparent; transform: translateX(16px) translateY(-4px) rotate(30deg);"> </div> </div> <div style="margin-left: auto;"> <div style="width: 0px; border-top: 8px solid #F4F4F4; border-right: 8px solid transparent; transform: translateY(16px);"> </div> <div style="background-color: #f4f4f4; flex-grow: 0; height: 12px; width: 16px; transform: translateY(-4px);"> </div> <div style="width: 0; height: 0; border-top: 8px solid #F4F4F4; border-left: 8px solid transparent; transform: translateY(-4px) translateX(8px);"> </div> </div> </div> <div style="display: flex; flex-direction: column; flex-grow: 1; justify-content: center; margin-bottom: 24px;"> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; margin-bottom: 6px; width: 224px;"> </div> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; width: 144px;"> </div> </div> <p style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; line-height: 17px; margin-bottom: 0; margin-top: 8px; overflow: hidden; padding: 8px 0 7px; text-align: center; text-overflow: ellipsis; white-space: nowrap;"><a style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: normal; line-height: 17px; text-decoration: none;" href="https://www.instagram.com/p/C9TGVSTTozZ/?utm_source=ig_embed&utm_campaign=loading" target="_blank" rel="noopener">A post shared by Mark Humphries (@humphriesmark)</a> </div> </blockquote> Humphries then tried to make a joke out of it saying that Biden was suffering from a condition called “that guy old” with symptoms including confusing names, long pauses, “and keeping your mouth just that little bit open with that slightly disappointed look like Bunnings just told you the sausage sizzle is closed”. “But if you think that’s bad, wait till you find out the condition the other candidate has ‘that guy convicted felon’,” he concluded. While some Channel 7 viewers "loved" it and thought it was “better than The Project,” a few others were less impressed. “This was an appalling segment … hire, rather than sack, journos,” read one comment on social media. “It was a deplorable segment that has no place in a news bulletin,” another added. "It was absolutely ridiculous. I hope channel 7 cut this rubbish out," wrote a third. "This was cringe," another said. Images: Instagram

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

<div class="theconversation-article-body"> <a href="https://theconversation.com/profiles/nikki-anne-wilson-342631">Nikki-Anne Wilson</a>, <a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a> 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. Another term that can crop up when we’re talking about dementia is Alzheimer’s disease, or Alzheimer’s for short. So what’s the difference? <h2>What is dementia?</h2> 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. 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. For example, someone might have trouble remembering to pay bills and become lost in previously familiar areas. 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. <h2>So what’s Alzheimer’s then?</h2> <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. So it’s not surprising many people use the terms dementia and Alzheimer’s interchangeably. 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. 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>. 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. 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>. <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=45&auto=format&w=1000&fit=clip"><img src="https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=45&auto=format&w=754&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&q=45&auto=format&w=600&h=456&fit=crop&dpr=1 600w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=30&auto=format&w=600&h=456&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=15&auto=format&w=600&h=456&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=45&auto=format&w=754&h=573&fit=crop&dpr=1 754w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=30&auto=format&w=754&h=573&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/592838/original/file-20240508-18-6msd4.png?ixlib=rb-4.1.0&q=15&auto=format&w=754&h=573&fit=crop&dpr=3 2262w" alt="" /></a><figcaption></figcaption></figure> <h2>Vascular dementia</h2> 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. 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. For example, vascular dementia may present as general confusion, slowed thinking, or difficulty organising thoughts and actions. 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. <h2>Frontotemporal dementia</h2> Some people may not realise that dementia can also affect behaviour and/or language. We see this in different forms of frontotemporal dementia. 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). 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. <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. <h2>Dementia with Lewy bodies</h2> <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. 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>. <h2>Do I have dementia and if so, which type?</h2> 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. 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>. 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. 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>. <h2>Dementia is diverse</h2> 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. 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>. <hr /> 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>.<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" /> <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> Image credits: Shutterstock 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>. </div>

Mind

Study finds new link for increased risk of Alzheimer’s

A new study has found that people suffering from anxiety disorders could be more likely to develop Alzheimer's disease. 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. 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. "People with anxiety and neurological disorders are 1.5 and 2.5 times more likely to have Alzheimer's disease," Dr Pan said. "For people with anxiety, males have higher odds than females of developing Alzheimer's disease." 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. 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. "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. "The medications or treatments used for these diseases may possibly contribute to this observation." The study however, did not find a link between Alzheimer's and depression, falls or strokes. "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. "We also studied whether age, gender, smoking, education, alcohol consumption, and the APOE gene – believed to be connected to Alzheimer's - affects these associations. "Our study indicates a new opportunity for biologists to study the links between these 20 conditions with Alzheimer's disease. "This work also provides valuable epidemiological evidence to clinicians, which may help them to evaluate one's risk of developing Alzheimer's disease." Image: Nine

Caring

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

<a href="https://theconversation.com/profiles/steve-macfarlane-4722">Steve Macfarlane</a>, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a> 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. 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. Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s. 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. <h2>What’s CJD got to do with Alzehimer’s?</h2> 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. 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. <h2>Human growth hormone used to come from donated organs</h2> Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue. 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>. 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. 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. <h2>What are the latest findings about Alzheimer’s disease?</h2> The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission. 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. They considered other explanations for the findings but concluded donated hGH was the likely cause. 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. 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. 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. <h2>When was this process used in Australia?</h2> 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. <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. 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. 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. <h2>The risk is very low – and you can’t ‘catch’ it like a virus</h2> 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. 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. 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.<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" /> <a href="https://theconversation.com/profiles/steve-macfarlane-4722">Steve Macfarlane</a>, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, <a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a> Image credits: Getty Images 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>.

Mind

Harry and Meghan named "2023's biggest losers"

Prince Harry and Meghan Markle have been crowned "the biggest losers of 2023" by highly influential entertainment magazine The Hollywood Reporter. The publication released its annual list of winners and losers, with celebrities like Taylor Swift, Margot Robbie and Greta Gerwig making the winners list. The Duke and Duchess of Sussex on the other hand topped this year's list of losers, which included Twitter/X/Elon Musk, and the streaming series Yellowstone. The publication wrote that this year's list reflected "some of the industry’s biggest success stories — and most embarrassing missteps." Royal commentator Victoria Arbiter said that this is a huge blow for the royal couple, as The Hollywood Reporter is considered an "industry bible that people pay attention to". "It is humiliating in Meghan's home town and they refer to the couple's - and I quote this - 'whiney documentary', that 'whiney biography' and the horrible South Park episode," she said in an interview with Nine's Today. Despite being crowned this year's biggest losers, Arbiter said that the couple are looking forward to a better year ahead. "It is time to leave the royal family behind and really establish what it is they want to do and make positive steps forward if they plan to be successful in 2024," she said. "We've been promised a number of different things via rumours over the past year, with talk of Meghan's website The TIG relaunching and she was going to launch a lifestyle brand similar to Gwyneth Paltrow's Goop. "Netflix paid $3 million pounds for rights to a book Harry and Meghan said they would turn into a rom-com, however we haven't had further development on those plans." The royal commentator added that Harry and Meghan will need to build consumer trust and avoid "negative, scandalous headlines that follow them everywhere", as they approach the new year. "Hollywood doesn't do well with negativity," she said. Check out the full list <a href="https://www.hollywoodreporter.com/movies/movie-news/hollywood-winners-losers-2023-1235712279/" target="_blank" rel="noopener">here</a>. Image: Getty

7 things you never knew about MAS*H

Did you know M*A*S*H ran more than three times longer than the actual Korean War? It may have graced our screens for 11 years, but you might not know all there is to know about the classic TV series, M*A*S*H. <ol> <li>No one wanted a laugh track – Despite pleas from the show’s producers, the network (CBS) went ahead and added in canned laughter. You might have noticed the laugh track growing quieter and quieter as the years progressed, and in the UK, the laugh track was removed entirely.</li> <li>CBS banned an “unpatriotic” episode – An idea for an episode was shot down by the network for being “unpatriotic”. It involved soldiers standing outside in the freezing cold to make themselves sick enough to be sent home – a tactic actually used during the war.</li> <li>The writers got back at complaining cast members – If ever an actor complained about their script (or asked for changes), the writing team would change the script to make it “parka weather”, making the cast swelter in jackets through days in excess of 32°C on their Florida film set.</li> <li>Patients were named after sports teams – After running out of names for patients visiting the hospital, the writers turned to baseball teams. In season six, four Marines are named after California Angels infielders, while in season seven, they named patients after the 1978 Los Angeles Dodgers.</li> <li>M*A*S*H hosted some big-name stars – Guest appearances on the show include Ron Howard, Leslie Nielsen, Patrick Swayze, Laurence Fishburne and Rita Wilson.</li> <li>The series finale broke records – The two-and-a-half-hour 1983 series finale, “Goodbye, Farewell and Amen,” was watched by a staggering 121.6 million people in the US alone – back then, that was 77 per cent of households with TV sets. It remains the most-watched episode of a TV show in US history.</li> <li>The time capsule didn’t stay buried long – In the series’ second-last episode, the M*A*S*H gang bury a time capsule. When the show wrapped up, the land used as the show’s set was sold, and a construction worker found the capsule just months later. After getting in contact with Alan Alda to return it, Alda told the worker he could keep it.</li> </ol> Image credits: Getty Images

"Finally!": 2023’s Sexiest Man Alive crowned

Patrick Dempsey has been named People’s Sexiest Man Alive for 2023! The 57-year-old actor known for his role as Derek "McDreamy" Shepherd on Grey's Anatomy snagged the title from last year's winner, Marvel heart-throb Chris Evans. In his interview with the publication, the actor said that he will use his new-found status to promote “something positive”. “I’m glad it’s happening at this point in my life,” he said. “It’s nice to have the recognition, and certainly my ego takes a little bump, but it gives me the platform to use it for something positive.” When asked about his reaction to finding out he was 2023's Sexiest Man Alive the actor joked that it was a long-time coming. “I was completely shocked, and then I started laughing, like, this is a joke, right? I’ve always been the bridesmaid!” he joked. “I’d completely forgotten about it and never even contemplated being in this position. So my ego is good.” <blockquote class="twitter-tweet"> Introducing PEOPLE’s 2023 <a href="https://twitter.com/hashtag/SexiestManAlive?src=hash&ref_src=twsrc%5Etfw">#SexiestManAlive</a>, Patrick Dempsey. 🔥 <a href="https://t.co/4eYnCAG1Zr">https://t.co/4eYnCAG1Zr</a> <a href="https://t.co/5V0xVblnaE">pic.twitter.com/5V0xVblnaE</a> — People (@people) <a href="https://twitter.com/people/status/1722114648638394482?ref_src=twsrc%5Etfw">November 8, 2023</a></blockquote> The father-of-three also joked about how his children, Talula, 21, and 16-year-old twins Sullivan and Darby, will react to this news. “They’re just going to make fun of me and pick on me and figure out every reason why I shouldn’t be,” he said. “Which is good, they keep me young.” Funnily enough, his newfound status was also met with confusion, mostly from the younger generation who have no idea who he is. “Who the hell is Patrick Dempsey?” one confused Gen Zer wrote. “You all are making up new people every day; who is Patrick Dempsey?” another commented. This left many Millennials feeling old. “People ... not knowing who Patrick Dempsey is making me feel like a grandma. What do you mean you didn’t grow up watching Grey’s Anatomy, and you weren’t obsessed with Derek Sheppard since you were 10,” one commented. “There is an is actual difference in being 26 vs. being 23! Because I am seeing 23 yr olds not know who Patrick Dempsey is,” another added. And not everyone who is a Millennial agreed with People's choice. "I mean… yes back in the day. But seriously? How is it not someone who is hot right now? I haven’t even seen/heard him mentioned in years," commented one person. Is it 2005?” another wrote. “Um, he is so 2007,” a third commented. Regardless, Dempsey has aged like fine wine and many have said it's about time. “Finally! Ain’t nobody under this post showed me a white man finer!" Image: People Magazine/ X

Beauty & Style

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

<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> 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>. 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. 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? <h2>What the study did and found</h2> 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. 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. 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. <h2>Important considerations</h2> 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. 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. 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. 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. 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. <h2>What does other evidence say?</h2> <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. 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. 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. <h2>Why the link?</h2> There are several potential pathways through which stress, anxiety and depression could increase the risk of dementia. 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. 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>. 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.<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" /> <a href="https://theconversation.com/profiles/yen-ying-lim-355185">Yen Ying Lim</a>, 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> Image credits: Getty Images 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>.

Mind

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

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. Scientists and researchers are celebrating this groundbreaking development, viewing it as a tremendous opportunity to transform the landscape of Alzheimer's treatment. 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">New York Post</a>. 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. 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 JAMA. 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 Fierce Biotech. 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. 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. 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. 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. 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. 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. 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. 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." 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. Image: Shutterstock

Mind

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

<a href="https://theconversation.com/profiles/michael-landreh-1328287">Michael Landreh</a>, <a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a> and <a href="https://theconversation.com/profiles/anna-rising-1440132">Anna Rising</a>, <a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a> 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. The fascinating properties of spider silk make it no wonder that scientists have been trying to unravel its secrets for decades. 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>. <figure><iframe src="https://www.youtube.com/embed/zNtSAQHNONo?wmode=transparent&start=0" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe></figure> 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. 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. <h2>Weaving a web</h2> 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. 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>. 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. 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. In Alzheimer’s disease, an abnormal form of tau builds up and clings to the normal tau proteins, creating “tau tangles”. 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. <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img src="https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&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&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/528217/original/file-20230525-25-p40y48.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" alt="Beautiful spider web with water drops close-up" /></a><figcaption>The trick spiders use to speed up their spinning process can be used to spin better artificial silk. <a class="source" href="https://www.shutterstock.com/image-photo/beautiful-spider-web-water-drops-close-155560781">Aastels/Shutterstock</a></figcaption></figure> 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. 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. 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. 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. <h2>Silky science</h2> 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. 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. 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>. So, we made a spidroin which contained only the c-terminal domain and tested its ability to form fibres. 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. 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. 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. 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. 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" /> <a href="https://theconversation.com/profiles/michael-landreh-1328287">Michael Landreh</a>, Researcher, Department of Microbiology, Tumor and Cell Biology, <a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a> and <a href="https://theconversation.com/profiles/anna-rising-1440132">Anna Rising</a>, Researcher in Veterinary medicine biochemistry, <a href="https://theconversation.com/institutions/karolinska-institutet-1250">Karolinska Institutet</a> 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>. Images: Getty

Body

Huge news for Alzheimer’s sufferers

An experimental new drug by Eli Lilly has demonstrated an ability to slow the progression of Alzheimer’s disease, according to new study reports. 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. 1,182 individuals in the early stages of Alzheimer’s participated in the study, with each patient receiving monthly infusions of donanemab. 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. In the wake of the news, experts are optimistic, but still hold concerns about the risks moving forward. 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. "It's modest, but I think it's real and I think it's clinically meaningful." Washington University neurologist Dr Erik Musiek noted that mounting evidence was suggesting “that these drugs do work”. 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.” 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. 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.” 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. 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. 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. Images: Getty

Caring

"With Jock in our hearts": Channel 10's big MasterChef announcement

The 15th season of Masterchef Australia will be broadcast as planned, Channel 10 have confirmed. The season, otherwise known as Masterchef: Secrets & Surprises, was initially sent into limbo when fan-favourite host and <a href="https://www.oversixty.com.au/news/news/shattered-hearts-culinary-world-mourns-tragic-death-of-jock-zonfrillo">chef Jock Zonfrilllo passed away unexpectedly</a>, reportedly in a Melbourne hotel room. But now, the network behind the hit cooking competition series have confirmed that after a one-week delay and <a href="https://www.oversixty.com.au/entertainment/tv/huge-broadcast-blunder-sees-new-footage-of-late-jock-zonfrillo-mistakenly-aired">an unfortunate streaming blunder</a>, Masterchef will return to screens across Australia, and likely the rest of the world in the coming months. The network made the announcement through social media, sharing a statement that assured audiences the decision had come with “the full support of Jock Zonfrillo’s family”. “Masterchef Australia Judge Jock Zonfrillo took great pride in challenging and coaching the contestants and of course inspiring a nation of home cooks,” it continued, before going on to note that they would be keeping the late Zonfrillo close to their hearts over the course of the upcoming season, and beyond. It concluded with the news that “the show will honour Jock by reflecting on his personal and professional life in a celebration of his incredible achievements”, with some fans declaring in the comments that this was the “best way to honour his work”. <blockquote class="twitter-tweet"> The new season of <a href="https://twitter.com/hashtag/MasterChefAU?src=hash&ref_src=twsrc%5Etfw">#MasterChefAU</a> begins 7.30pm Sunday on 10 and 10 Play. <a href="https://t.co/CnENu2UpUO">pic.twitter.com/CnENu2UpUO</a> — Channel 10 (@Channel10AU) <a href="https://twitter.com/Channel10AU/status/1653667970303033344?ref_src=twsrc%5Etfw">May 3, 2023</a></blockquote> The official Masterchef Australia account shared the same statement, and was met with a similar response from supporters of the show. “I’ll look forward to watching this with a whisky in hand, give it up for Jock,” one wrote. “I look forward to watching it. I think that viewing Jock’s final season together with all other MasterChef fans will be a fitting way for us to remember what an amazing person, chef and inspirational mentor he was,” another said. “A difficult decision,” one noted, “however the opportunity to see the great chef live on and do what it seemed he loved and was so very good at, making people love cooking.” The idea that it could not have been an easy decision to reach for one shared by a large portion of fans, with another likely speaking for all of them when they wrote that “this must have been a really emotionally tough decision for Jock's family. I think I'll need a box of tissues for this one.” “As long as Jock's family are OK with this, we can respect Channel 10's decision,” another decided. “I personally will find it very hard to watch the series in light of what's happened, but I'll think of it as a wonderful tribute to a fantastic man and beautiful soul.” Meanwhile, one fan had another idea for honouring the late chef, asking Masterchef Australia, “would you consider changing the name of the trophy the winner gets to the Jock Zonfrillo trophy?” Images: Twitter

Second MAS*H star to pass away in just one month

Actress Eileen Saki, best known for her role as bar owner Rosie in the hit series M*A*S*H has died. The 79-year-old had been fighting pancreatic cancer, and “passed away peacefully in Los Angeles” on May 1, according to PEOPLE. Eileen’s <a href="https://oversixty.com.au/entertainment/tv/m-a-s-h-star-passes-away" target="_blank" rel="noopener">fellow M*A*S*H star, Judy Farrell, had died</a> just one month prior on April 2. Eileen’s manager, Camilla Fluxman Pines confirmed the devastating news in a statement to the publication, writing that “she was diagnosed with pancreatic cancer in January. "She was a lung cancer survivor in 2004.She got a second chance at auditioning and working in the industry that she loved so much - she shot a couple big commercials shortly before her diagnosis. "She was often recognized by face or even just voice by people who knew they knew her 'from somewhere' - and loved talking to young actors about the journey." Suki’s former co-star Jeff Maxwell, who brought the character Igor Straminsky to life on M*A*S*H, honoured his late friend with a social media post, sharing the news of her passing on the official page for his MASH Matters podcast. “Our sweet Eileen. Our sassy Rosie,” he wrote, before going on to extend his appreciation - as well as that of her husband, Bob - to Eileen’s devoted fans and followers who offered her their love and their support in her final days, before promising to share more on Eileen as the day went on, and encouraging others to do the same. “Our sweet, sweet Eileen. How we love you,” he concluded. “How we will miss you.” <iframe style="border: none; overflow: hidden;" src="https://www.facebook.com/plugins/post.php?href=https%3A%2F%2Fwww.facebook.com%2Fmashmatterspodcast%2Fposts%2Fpfbid0LmjyFaQF6dHNoWfZKNqRpBEqzgyNKSsf41AZxkg9kjKCuSJaisowUawFowusyacyl&show_text=true&width=500" width="500" height="719" frameborder="0" scrolling="no" allowfullscreen="allowfullscreen"></iframe> True to his word, Jeff went on to post a few favourite Eileen moments, from her most recent work in advertisements, to time on screen with the likes of Mickey Rooney and Dom Deluise, and last - but certainly not least - as “a scene with a certain sassy bartender”. <iframe style="border: none; overflow: hidden;" src="https://www.facebook.com/plugins/video.php?height=314&href=https%3A%2F%2Fwww.facebook.com%2Fmashmatterspodcast%2Fvideos%2F1531503437375801%2F&show_text=false&width=560&t=0" width="560" height="314" frameborder="0" scrolling="no" allowfullscreen="allowfullscreen"></iframe> Saki had actually been the third actress to portray Rosie, having taken over from Frances Fong and Shizuko Hoshi for her eight episode stint. In the end, she was the final and longest-running owner of Rosie’s Bar, and remains dear to her co-workers and fans for it. “You will forever be in our hearts!” one commented, in a sentiment shared by many. “Sorry to hear of her passing. Great memories at Rosie’s,” said another. “She was the best Rosie of them all and such a great actress,” one declared. “So sorry to hear she passed on.” “One of the finest roles ever played,” someone agreed, before requesting that she “say hello to Col. Blake, Trapper, Major Burns”. And as one said on behalf of them all, “you fought the great fight, Eileen. Now, rest easy, for your burdens and struggles are behind you. Love and strength to the entire family during these hard days ahead.” Images: Facebook

Caring

MAS*H star passes away

M*A*S*H star Judy Farrell has passed away at the age of 84, her son has confirmed to TNZ. The actress, who is best known around the world for her portrayal of Nurse Able, died in hospital nine days after suffering a stroke which left her unable to communicate. However, TNZ have reported that Judy was conscious still and able to squeeze the hands of her loved ones. While Judy’s son Michael - whom she shared with fellow M*A*S*H actor Mike Farrell - has not yet spoken publicly about her mother’s passing, her former co-star Loretta Swift spoke to Fox News Digital about losing “family”. “Judy was a most beautiful woman - inside and out. We grew up together," the actress behind Major Margaret ‘Hot Lips’ Houlihan said. "She was family. This has been a painful loss, but we will always have the beauty of her memory. “Rest in peace, Nurse Able." Farrell starred as Nurse Able in eight episodes of the hit series, and was the only actress to ever be credited as the character. Initially, Nurse Able was a minor role - often just a placeholder for the instances where a background nurse had a line - and from Seasons 2-11 she was played by no fewer than 11 different people. By the fourth season, the role progressed so that she became involved in the show’s plot. It was in the sixth season that Judy Farrell secured her place in television history as Nurse Able, taking over for the character’s final appearances on screen in Seasons 6-11 for eight episodes. During her time on the show, Farrell starred alongside the likes of Loretta Swift, Alan Alda, and ex-husband Mike Farrell. The latter joined M*A*S*H’s cast in 1975, replacing Wayne Rogers, and remained until the 1983 finale. The couple had married in 1963, but went on to divorce 20 years later, in the same year that M*A*S*H bid farewell to its audience. Their split was reportedly amicable, with the two going on to remarry and co-parent their children, son Michael and daughter Erin. And as Farrell’s loved ones mourn her loss, fans and followers of the actress have taken to social media to share their grief, and to honour her work, sharing some of their fondest memories of her time bringing their beloved Nurse Able to life. “RIP Nurse Able. I was so thrilled to have known you, Judy Farrell,” wrote comedian Murray Valeriano. “Condolences to the Farrell and MASH families,” one fan said. And for another, it came as a tragic opportunity to share a clip of Farrell’s work, showcasing the actress alongside some of her former co-stars, with Classic MASH writing “Sad news today.” <blockquote class="twitter-tweet"> Sad news today. Judy Farrell has passed away. <a href="https://twitter.com/hashtag/ClassicMASH?src=hash&ref_src=twsrc%5Etfw">#ClassicMASH</a> <a href="https://t.co/hCfSpL7c0W">pic.twitter.com/hCfSpL7c0W</a> — Classic MASH 🍸 (@ClassicMASH) <a href="https://twitter.com/ClassicMASH/status/1643275688017903616?ref_src=twsrc%5Etfw">April 4, 2023</a></blockquote> Images: Getty, Twitter, MASHFandom.com

13 things neurologists do to help prevent Alzheimer’s disease

Understand Alzheimer's disease 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. 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. Get enough sleep 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. “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.” Stay socially active 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. “It makes sense that those who are more engaged, especially socially, will think more positively and have a better outlook on life.” Keep learning 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. “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. Learn a second language 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. 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. Do it yourself 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. “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.” Stay active 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%. “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.” Take care of your heart “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. “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. Lower your stress levels 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. 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. Try the MIND diet 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. According to research in Alzheimer’s & 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.” Get your snoring checked out 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. 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. Protect your head 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. Wear a helmet while cycling, make your home fall-proof, and always use a seat belt to help protect your noggin. Drink a cup of tea 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. 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. Image credits: Getty Images 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>.

Mind

Experimental Alzheimer’s drug shows promise

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. 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. 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. 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. 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. 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. 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. 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”. 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. 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. <h2>Side-effects</h2> 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. 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.” 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. 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. 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>. <blockquote> 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. </blockquote> Restructuring NHS dementia services to provide routine and timely PET scans or lumbar punctures would be a costly and lengthy process. 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. <figure class="align-right "><figcaption></figcaption></figure> 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>.<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" /> <a href="https://theconversation.com/profiles/ritchie-williamson-1346959">Ritchie Williamson</a>, Director of research, Associate Professor in Therapeutics, <a href="https://theconversation.com/institutions/university-of-bradford-911">University of Bradford</a> and <a href="https://theconversation.com/profiles/stuart-dickens-1397610">Stuart Dickens</a>, Post Doctoral Research Assistant, <a href="https://theconversation.com/institutions/university-of-bradford-911">University of Bradford</a> Image: Shutterstock 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>.

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