tag:theconversation.com,2011:/us/topics/herpes-simplex-37547/articlesHerpes simplex – The Conversation2022-11-17T11:06:20Ztag:theconversation.com,2011:article/1947732022-11-17T11:06:20Z2022-11-17T11:06:20ZUnlocking new clues to how dementia and Alzheimer’s work in the brain – Uncharted Brain podcast series<p>This week on <a href="https://theconversation.com/uk/topics/the-conversation-weekly-98901">The Conversation Weekly</a> podcast we’re running a three-part series called <em>Uncharted Brain: Decoding Dementia</em>, which delves into new research searching for answers to how dementia works in the brain and the damage it leaves behind. Hosted by Paul Keaveny and Gemma Ware, it was initially published via <a href="https://theconversation.com/uk/topics/the-anthill-podcast-27460">The Anthill</a> podcast from the team at The Conversation in the UK. </p>
<h2>Part 1: a lifelong study unlocks clues to Alzheimer’s</h2>
<p>In the first episode, we explore how a study which began just after the end of the second world war is discovering clues to Alzheimer’s. </p>
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<p>Based on a representative sample of 5,362 babies all born in the same week in the UK in 1946, the National Survey of Health and Development began as a one-off investigation of the cost of childbirth and the quality and efficiency of obstetric services. From there it became the longest continuously running study of health over the human life course in the world – also known as the British 1946 birth cohort. </p>
<p>Since 2016, the brains of some of its participants are revealing new insights into the risk factors for Alzheimer’s disease. We find out more from Marcus Richards and Jon Schott, two of the researchers from UCL in the UK behind the study, and David Ward, one of the study participants whose brain is being studied as part of the dementia research. </p>
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Read more:
<a href="https://theconversation.com/weve-been-studying-the-same-people-for-76-years-this-is-what-weve-found-out-about-alzheimers-disease-183949">We've been studying the same people for 76 years – this is what we’ve found out about Alzheimer’s disease</a>
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<h2>Part 2: the family trauma of dementia from sports injuries</h2>
<p>In the second episode, we explore chronic traumatic encephalopathy (CTE), a form of dementia that athletes from a whole range of sports can develop. We hear about the toll it can take on family members, who are often unaware of what’s happening to their loved ones.</p>
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<p>CTE is now at the centre of a number of legal challenges involving sports from <a href="https://www.theguardian.com/sport/2022/jul/25/case-against-rugby-union-governing-bodies-on-dementia-destined-for-courts">rugby</a> to <a href="https://www.nytimes.com/2013/08/30/sports/football/judge-announces-settlement-in-nfl-concussion-suit.html">American football</a>.</p>
<p>After Lisa McHale’s husband Tom, a former NFL player, died in 2008, she received a request from researchers at Boston University School of Medicine to study his brain for signs of CTE – and was told he had quite a severe case. She says that learning more about the disease has been extremely helpful in processing what happened to her husband. </p>
<p>Today, McHale is director of family relations at the US-based Concussion Legacy Foundation, which works with family members who lost loved ones after they developed CTE. Matt Smith, a sports psychologist at the University of Winchester, recently led a research project interviewing some of these family members about their experiences. We talk to them both in part two of the series. </p>
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Read more:
<a href="https://theconversation.com/sport-induced-traumatic-brain-injury-families-reveal-the-hell-of-living-with-the-condition-172828">Sport-induced traumatic brain injury: families reveal the 'hell' of living with the condition</a>
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<h2>Part 3: the role viruses may play in Alzheimer’s</h2>
<p>There are many competing theories about what causes Alzheimer’s disease. For more than 30 years, Ruth Itzhaki has been accumulating evidence that viruses are involved in its development in the brain. We investigate this evidence in the third and final episode. </p>
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<p>Itzhaki, a neurobiologist and visiting professorial fellow at the University of Oxford, believes the common cold sore virus (herpes simplex 1 or HSV1) could be playing a vital role in Alzheimer’s. But she has faced years of hostility from many within the scientific community who didn’t take the theory seriously. Now, though, it seems the tide of opinion is at last turning in Itzhaki’s favour.</p>
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Read more:
<a href="https://theconversation.com/my-work-investigating-the-links-between-viruses-and-alzheimers-disease-was-dismissed-for-years-but-now-the-evidence-is-building-184201">My work investigating the links between viruses and Alzheimer’s disease was dismissed for years – but now the evidence is building</a>
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<p><em>Uncharted Brain: Decoding Dementia</em> is reported by Paul Keaveny, investigations editor at The Conversation in the UK for the <a href="https://theconversation.com/uk/insights">Insights team</a>, which published articles linked to each of the episodes in this podcast series. The series is produced and written by Tiffany Cassidy with sound design by Eloise Stevens. The executive producer and co-host is Gemma Ware. The Conversation Weekly theme music is by Neeta Sarl. </p>
<p>You can find us on Twitter <a href="https://twitter.com/TC_Audio">@TC_Audio</a>, on Instagram at <a href="https://www.instagram.com/theconversationdotcom/">theconversationdotcom</a> or <a href="mailto:podcast@theconversation.com">via email</a>.</p><img src="https://counter.theconversation.com/content/194773/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Marcus Richards receives funding from the UK Medical Research Council. Jonathan M Schott receives funding from Alzheimer's Research UK, Medical Research Council, Alzheimer's Association, Selfridge's Group Foundation, Brain Research UK, the Wolfson Foundation and the National Institute for Health Research University College London Hospitals Biomedical Research Centre. He is Chief Medical Office for Alzheimer's Research UK and Clinical Advisor to UK Dementia Research Institute. Matthew Smith is affiliated with CLF-UK and has a role as research lead for Patient and Family Services. The aim of this role is to develop research that helps understand the experiences, and support patients and family members. </span></em></p><p class="fine-print"><em><span>Ruth Itzhaki is currently working with David Kaplan and Dana Cairns at Tufts University on the effects of infection on their 3D brain model. Also with Professors Ken Muir and Curtis Dobson and Dr Artitaya Lophatananon at Manchester University on epidemiological aspects of HSV1 and Alzheimer's. Dana Cairns does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment. D. P. Devanand has received research grants from the National Institute on Aging and Alzheimer's Association that are funding his clinical trials on valacyclovir treatment of Alzheimer's disease and mild cognitive impairment, respectively.</span></em></p>The world’s longest running cohort study reveals risk factors for dementia. Families of athletes with early-onset dementia tell their stories. Could viruses cause Alzheimer’s? Listen to the Uncharted Brain: Decoding Dementia podcast series.Gemma Ware, Editor and Co-Host, The Conversation Weekly Podcast, The ConversationPaul Keaveny, Investigations Editor, Insights, The ConversationLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1942112022-11-16T00:16:26Z2022-11-16T00:16:26ZDo viruses play a role in the development of Alzheimer’s? Uncharted Brain podcast part 3<figure><img src="https://images.theconversation.com/files/494687/original/file-20221110-5951-1ev6rd.jpg?ixlib=rb-1.1.0&rect=5%2C716%2C3846%2C2367&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The herpes virus: could it play a role in Alzheimer's disease? </span> <span class="attribution"><a class="source" href="https://www.alamy.com/stock-photo-negatively-stained-transmission-electron-micrograph-tem-of-numerous-30199519.html?imageid=3FB2D82E-CE7E-4AEC-85D3-FB486D05A2DD&p=9949&pn=1&searchId=3caeb13d53fa71294990d14ccdd45a53&searchtype=0">Scott Camazine / Alamy Stock Photo</a></span></figcaption></figure><p>There are many competing theories about what causes Alzheimer’s disease. For more than 30 years, Ruth Itzhaki has been accumulating evidence that viruses are involved in its development in the brain.</p>
<p>We investigate this evidence in the third episode of <em>Uncharted Brain: Decoding Dementia</em>, a new podcast series available via <a href="https://theconversation.com/uk/topics/the-anthill-podcast-27460">The Anthill</a> podcast. </p>
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<p>Itzhaki, a neurobiologist and Visiting Professorial Fellow at the University of Oxford, believes the common cold sore virus (herpes simplex 1 or HSV1) could be playing a vital role in Alzheimer’s. But she has faced years of hostility from many within the scientific community who didn’t take the theory seriously.</p>
<p>Reflecting on a career dedicated to one of the more controversial lines of research, she told us:</p>
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<p>There are just so many people who have Alzheimer’s or other forms of dementia, and of course it’s going to get worse as people live longer … This is another reason why I feel so angry that people are not willing to look, not just at our work but at other outside views which could hold the key – or one of the keys. They should be much more open-minded.</p>
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<p>Now, though, it seems the tide of opinion is at last turning in Itzhaki’s favour. More researchers have begun developing the research she pioneered, with an <a href="https://bmjopen.bmj.com/content/10/2/e032112">anti-viral trial</a> for Alzheimer’s – the first ever – now taking place at Columbia University Medical Center in the US. The leader of that trial, D.P. Devanand told us:</p>
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<p>I think what happens is a particular idea or theory gains momentum so everybody follows that … [and] loses track of the fact that there may be other things that you need to consider. And to some extent that did happen in the field of Alzheimer’s, but at least now I think it’s a much broader approach. </p>
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<p>Listen to the full episode to hear more about the role that viruses may play in Alzheimer’s, from some of the scientists at the forefront of this research. You can also <a href="https://theconversation.com/my-work-investigating-the-links-between-viruses-and-alzheimers-disease-was-dismissed-for-years-but-now-the-evidence-is-building-184201">read an article that Ruth Itzhaki</a> wrote about her research as part of The Conversation’s <a href="https://theconversation.com/uk/insights">Insights project</a>. </p>
<p><em>Uncharted Brain: Decoding Dementia</em> is hosted by Paul Keaveny, investigations editor at The Conversation in the UK, and Gemma Ware, co-host of The Conversation Weekly podcast. The series is produced and written by Tiffany Cassidy, with sound design by Eloise Stevens. The executive producer is Gemma Ware.</p>
<p>All episodes of the series are available on <a href="https://podfollow.com/the-anthill/view">The Anthill</a> podcast channel. </p>
<p>You can find us on Twitter <a href="https://twitter.com/TC_Audio">@TC_Audio</a>, on Instagram at <a href="https://www.instagram.com/theconversationdotcom/">theconversationdotcom</a> or <a href="mailto:podcast@theconversation.com">via email</a>. You can also sign up to The Conversation’s <a href="https://theconversation.com/newsletter">free daily email here</a>.</p><img src="https://counter.theconversation.com/content/194211/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Dana Cairns does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment. D. P. Devanand has received research grants from the National Institute on Aging and Alzheimer's Association that are funding his clinical trials on valacyclovir treatment of Alzheimer's disease and mild cognitive impairment, respectively.</span></em></p><p class="fine-print"><em><span>Ruth Itzhaki is currently working with Dr David Kaplan and Dr Dana Cairns at Tufts University on the effects of infection on their 3D brain model. Also with Professors Ken Muir and Curtis Dobson and Dr Artitaya Lophatananon at Manchester University on epidemiological aspects of HSV1 and Alzheimer's.</span></em></p>Listen to the third episode of our series Uncharted Brain: Decoding Dementia via The Anthill podcast.Paul Keaveny, Investigations Editor, Insights, The ConversationGemma Ware, Editor and Co-Host, The Conversation Weekly Podcast, The ConversationLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1842012022-11-15T22:10:56Z2022-11-15T22:10:56ZMy work investigating the links between viruses and Alzheimer’s disease was dismissed for years – but now the evidence is building<figure><img src="https://images.theconversation.com/files/488130/original/file-20221004-20-g8x1ub.jpeg?ixlib=rb-1.1.0&rect=1454%2C531%2C2728%2C2647&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/brain-mind-spiritual-soul-freedom-hope-2098703830">Shutterstock/Jorm S</a></span></figcaption></figure><p><em>This article is part of the Insights Uncharted Brain series. There are many competing theories about what causes Alzheimer’s disease. Here, Ruth Itzhaki reflects on a career dedicated to one of the more controversial lines of research.</em></p>
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<p>Life is not easy for any of us. But what of that? We must have perseverance and above all confidence in ourselves. We must believe that we are gifted for something and that this thing must be attained. — Marie Curie</p>
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<p>When I was about seven or eight, I asserted that I wanted to be a scientist, or so my parents told me years later, even though I would have had little idea of what that word meant. In my mind, I was perhaps associating it with making momentous discoveries that were immediately recognised and applauded by the whole world. Soon after, I avidly read <a href="https://www.goodreads.com/en/book/show/341166.Madame_Curie%20%22%22">Madame Curie</a>, the book by Eve Curie about her mother Marie and how she overcame poverty and the many challenges faced by women in the late 19th and early 20th century to become a Nobel prize-winning scientist. Marie Curie became my lodestar for the future and thanks to my parents’ support and self-sacrifice, I did eventually become a scientist.</p>
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<img alt="Black and white image of woman standing up" src="https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=984&fit=crop&dpr=1 600w, https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=984&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=984&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1236&fit=crop&dpr=1 754w, https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1236&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/488127/original/file-20221004-14-ebba22.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1236&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Marie Curie won two Nobel Prizes in 1903 for Physics and in 1911 for Chemistry.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/marie-curie-18671934-polishfrench-physicist-who-242816158">Shutterstock/Everett Collection</a></span>
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<p>Many years later, I found myself confronting what seemed like insuperable odds just as Curie did, though in very different circumstances. I have been an independent researcher since the age of 26 when I completed my PhD. My subsequent research in a Cambridge University department on <a href="https://www.nature.com/scitable/definition/chromatin-182/">chromatin</a> (a complex of DNA and proteins) went well. Then, after eight years, my husband and I moved to Manchester where the head of the institute where I worked for 12 years decided to end my contract, leaving me jobless and lab-less. </p>
<p>In the decades that followed, my research into viruses as a possible cause of Alzheimer’s disease was greeted with much hostility, and almost all my funding applications were refused: a hostility that has continued for 25 years and which has only recently abated, thanks to <a href="https://pubmed.ncbi.nlm.nih.gov/?term=Viral+role+Alzheimer%27s">mounting evidence</a>.</p>
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<p><strong><em>This story is part of Conversation Insights</em></strong>
<br><em>The Insights team generates <a href="https://theconversation.com/uk/topics/insights-series-71218">long-form journalism</a> and is working with academics from different backgrounds who have been engaged in projects to tackle societal and scientific challenges.</em></p>
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<p>I, along with my tiny research group, survived only through the award of a few small grants from more open-minded charities and companies interested in new approaches. Once I even managed to swap a business class ticket to the US (that was provided for me to speak at a conference) for economy class, so I could use the several thousand-dollar surplus for my lab instead.</p>
<p>But, after years of struggle, there is finally hope for this line of research. An <a href="https://bmjopen.bmj.com/content/10/2/e032112">anti-viral trial</a> for Alzheimer’s – the first ever – is now taking place at Columbia University. This study is building on the years of work done by my team. Meanwhile, our <a href="https://content.iospress.com/articles/journal-of-alzheimers-disease/jad220287">latest research</a> is looking into the way infectious illnesses increase the risk of Alzheimer’s.</p>
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<iframe id="noa-web-audio-player" style="border: none" src="https://embed-player.newsoveraudio.com/v4?key=x84olp&id=https://theconversation.com/my-work-investigating-the-links-between-viruses-and-alzhei[…]dismissed-for-years-but-now-the-evidence-is-building-184201&bgColor=F5F5F5&color=D8352A&playColor=D8352A" width="100%" height="110px"></iframe>
<p><em>You can listen to more articles from The Conversation, narrated by Noa, <a href="https://theconversation.com/us/topics/audio-narrated-99682">here</a>.</em></p>
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<h2>Dementia brought home</h2>
<p>Career and academic challenges can always be balanced with the help of a support network: a family. I was always lucky with mine. During many of these years, my husband, Shaul Itzhaki, a retired academic who had worked on nucleic acid biochemistry, supported my struggles and never once suggested that I change to a safer, more conventional and non-contentious topic. He was always touchingly happy with any successes I had, and I will always remember our celebratory days when I was awarded a <a href="https://en.wikipedia.org/wiki/Beit_Memorial_Fellowships_for_Medical_Research">Beit Memorial Fellowship</a> for Medical Research, and later a Newnham College Fellowship, during our years in Cambridge.</p>
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Read more:
<a href="https://theconversation.com/alzheimers-disease-mounting-evidence-that-herpes-virus-is-a-cause-104943">Alzheimer's disease: mounting evidence that herpes virus is a cause</a>
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<p>Sadly, he died in April 2022, after suffering for about ten years from vascular dementia (a dementia distinct from Alzheimer’s disease but with many similar symptoms) and latterly, from a fractured femur that disabled him. The last four or so years were particularly hard to endure as he became increasingly aware of his failing memory. The term “brain fog” is often used in this context, but to me, it seemed more like a mist through which he could very dimly see or perceive
what he was struggling to recall; the frustration – desperation, perhaps – that he felt at his inability to grasp, hold, then voice these elusive thoughts was pitiful.</p>
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<img alt="A woman in front of lab specimens." src="https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=628&fit=crop&dpr=1 600w, https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=628&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=628&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=789&fit=crop&dpr=1 754w, https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=789&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/488126/original/file-20221004-20-stf61r.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=789&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">The author in her laboratory.</span>
<span class="attribution"><span class="license">Author provided</span></span>
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<p>I often took him to talks on topics such as the climate, migration, history and ageing, hoping to keep his mind occupied. He seemed to understand many of them, but afterwards, he was quite unable to discuss them, as his memory and ability to speak were declining inexorably. Communication of any type between us was slowly becoming impossible, although he was the person with whom I had once shared my thoughts and hopes, just as he had done with me, and it became particularly sad and unsettling, as we had had so many interests in common. Eventually came the realisation that I had “lost” him. It was a bereavement – the loss of him as a person, loss of a mind, not the death of a body; he was existing but not really living.</p>
<p>Another common feature of dementia – sudden changes of mood – affected him during these years. He had been a generally gentle, courteous person. But when, at times, the illness overcame his natural traits, he became violently angry, often for no obvious reason. Part of the problem was that his sense of location had faltered and often during the evenings he became convinced that we were about to leave and go “home” to Manchester, a place we had left in 2013. He would ask repeatedly and anxiously when we had to leave to catch the train to get there. Television programmes, even those on historical events, which would have been of particular interest to him, had to be vetted as he lost himself within them. So that after watching one that dealt with, say, the horrors of war, he thought that he was actually living in that frightening world.</p>
<p>Of course, there are so many families going through what my family went through. And there will be many more. That fact has provided one of the main motives for my pursuing my research, despite all the difficulties that have come with it.</p>
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<img alt="Uncharted Brain, podcast series" src="https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/494827/original/file-20221111-22-1t5f3l.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<p><em>This article is accompanied by a podcast series called <a href="https://theconversation.com/uk/topics/uncharted-brain-decoding-dementia-128903">Uncharted Brain: Decoding Dementia</a> which examines new research unlocking clues to the ongoing mystery of how dementia works in the brain. Listen to the full series via <a href="https://podfollow.com/the-anthill/view">The Anthill podcast</a>.</em></p>
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<h2>Early challenges</h2>
<p>During the last five years, studies supporting the idea of a viral role in Alzheimer’s disease have <a href="https://pubmed.ncbi.nlm.nih.gov/?term=viral+role+alzhiemers">greatly increased</a>. Despite this, there is still much opposition to the concept, while many in the field still ignore it.</p>
<p>I am often asked why there has been such hostility. A charitable explanation is that the possible role of a virus in dementia is difficult for others to assess because it straddles two very different topics: virology and Alzheimer’s disease. Also, many cannot grasp the concept that people can be infected but not affected (asymptomatic, when the virus resides in the brain without causing symptoms) so they dismiss the data. Either way, I have always stressed that many possible factors lead to Alzheimer’s disease – a viral role is just one of them.</p>
<p>My interest in this particular area began, rather unpromisingly, in 1978 when the aforementioned head of institute ended my work contract. The reason he cited was that my research on chromatin, and on the effects of carcinogens on chromatin, was “rather individualistic”. I thought this was an extraordinarily inept criticism, as I had generally been acknowledged as being an innovative researcher, and innovation is surely the key to good research. The funding body offered me a post in Glasgow, but that would have meant leaving my husband and children in Manchester. </p>
<p>Luckily, I was immediately given a home in the lab of a medical virologist friend, Richard Sutton. Sutton was an eccentric and pioneering man. He was dogged and wiley, in an endearing way. It was Sutton who first suggested to me the possibility of viral involvement in Alzheimer’s disease.</p>
<p>The argument for the role of the cold sore virus, herpes simplex type 1 (HSV1), in Alzheimer’s disease was first suggested by American neuropathologist <a href="https://pubmed.ncbi.nlm.nih.gov/7116237/">Melvyn
Ball</a> in 1984. But he did not pursue the idea in any practical way. Sutton and I carried out what was probably the first convincing experiment seeking the DNA of HSV1 in the human brain. We had predicted that it might be detectable in the brain of immunosuppressed patients because in the absence of an adequate immune system to keep it under control, the virus would be able to multiply. We did indeed find it, and published our
<a href="https://pubmed.ncbi.nlm.nih.gov/3016195/">results</a> in 1986.</p>
<h2>The central concept</h2>
<p><a href="https://www.who.int/news-room/fact-sheets/detail/herpes-simplex-virus">HSV1</a> is mainly transmitted by oral-to-oral contact, causing oral herpes (cold sores).
Globally, an estimated 3.7 billion people under age 50 (67%) have HSV1 infection. Most infections are asymptomatic.</p>
<p>Over the years, the supportive data we gathered for the key role of HSV1 in Alzheimer’s led me to propose a central concept: that HSV1 is a major cause of Alzheimer’s disease; that in many people, the virus travels to the brain, probably in middle age, and remains present there in latent (dormant) form, but is frequently activated by episodes of stress, head injury, immuno-
suppression and infections. These “reactivations” lead to productive HSV1 infection and inflammation (and consequent damage to the brain) over the years. The accumulated damage leads eventually to the development of the disease.</p>
<p>The possible role of HSV1, specifically, was proposed for three main reasons. The locations of the damage the virus causes in the brain during the rare but extremely serious acute disease herpes simplex encephalitis (HSE) – caused by HSV1 – are precisely the main sites of damage found in the brains of patients with Alzheimer’s disease.</p>
<p>The other reasons for implicating HSV1 were that it is very common, affecting <a href="https://www.nuffieldhealth.com/conditions/herpes">at least 80%</a> of the population (in earlier decades more probably 90%), and its ability to remain dormant in the body for years.</p>
<p>These features meet two main characteristics of Alzheimer’s disease: that it is all too common, and that it almost always waits until old age to strike its victims. Certain other infectious agents are probably involved too, perhaps individually or in combination, but so far these have been less well studied than HSV1.</p>
<h2>The laboratory work</h2>
<p>I was offered a more long-term prospect for my research in a department of the University of Manchester’s Institute of Science and Technology. The head of the department, John Cronley Dillon, was a larger-than-life character, a <em>bon viveur</em> and art lover, full of novel ideas and wild enthusiasm. He encouraged me to build up a research group (minuscule though it was) and eventually we started the research on HSV1 and Alzheimer’s.</p>
<p>It was known that when a person is infected with HSV1, the virus resides lifelong in the peripheral nervous system (PNS) – the part of the nervous system that doesn’t include the brain and the spinal cord — in a latent state. It is dormant until it is activated by events such as stress. In 1989 we decided to look for HSV1 in the brain, using the technique of polymerase chain reaction, or PCR. We used
<a href="https://pubmed.ncbi.nlm.nih.gov/1653719/">PCR</a> to examine DNA extracted from autopsy specimens of Alzheimer’s disease patients.</p>
<p>This was the first time PCR, then a new technique, had been used for this purpose. The principle of PCR is to detect a specific sequence in the target DNA by chemically amplifying it, thereby making it vastly more sensitive than the methods used in the previous few studies seeking HSV1 DNA in the brain. However, this method was prone to contamination and could produce spurious data. This meant that my poor PhD student, Gordon Jamieson, spent many frustrating months trying to get it to work satisfactorily. So we were overjoyed when <a href="https://pubmed.ncbi.nlm.nih.gov/18647689/">we
detected</a>, unambiguously, the DNA of the virus in the brain in 1991.</p>
<p>This was the first microbe to be detected in the human brain (in controls, in the absence of a disease). We were puzzled, though, as to why the virus was present in a high proportion of brains – both control brain specimens (people who had not been diagnosed with Alzheimer’s) as well as the brains of patients who had died with the disease. This near equality of prevalence does not undermine the role of HSV1 in Alzheimer’s, as some in the field have asserted. Many of the control brains were, in fact, infected with HSV1 but were asymptomatic.</p>
<p>So people can be infected but be asymptomatic, indicating that infection alone is
not sufficient to cause disease. A very relevant example is that of cold sores which afflict only a proportion (ranging from 20-40%) of those infected with HSV1. The other 60-80% are asymptomatic. Clearly, another factor determines the degree of damage caused by the virus.</p>
<h2>Other supporting factors</h2>
<p>That was something we identified in 1997 when <a href="https://pubmed.ncbi.nlm.nih.gov/9014911/">we discovered</a> that the virus confers a high risk of
Alzheimer’s disease when in the brains of people who carry a specific genetic factor. We were extremely excited by this finding, but also apprehensive about adverse reactions of some in the field, as had occurred before when we discovered HSV1 DNA in elderly brains.</p>
<p>So we were even more excited when, after I’d suggested examining cold sore sufferers (via a small blood sample), to find what variant of the specific genetic factor they carried, we discovered that it was the same variant as for Alzheimer’s. In other words, the same variant of the genetic factor conferred a risk of damage in the peripheral nervous system, as well as the central nervous system.</p>
<p>Of course, the question arose as to what it is doing, if anything, in the brain. Is it residing there merely as a passenger, doing little or nothing, or does it cause damage?</p>
<p>We <a href="https://pubmed.ncbi.nlm.nih.gov/29689721/">investigated this</a> by examining cerebrospinal fluid (the liquid that bathes the brain) looking for antibodies to the virus. We detected these antibodies in most samples of cerebrospinal fluid, again, consistently, in both Alzheimer’s patients and those in the age-matched control groups. This showed that indeed the virus was not just a passive fellow traveller.</p>
<p>We then decided to find if there were direct links between the effects of HSV1 infection and Alzheimer’s. Very hesitantly, like explorers in a new continent, we infected human brain cells with HSV1, then stained the cells with antibodies to the specific abnormal proteins seen in Alzheimer’s brains – <a href="https://theconversation.com/uk/topics/beta-amyloid-plaques-45872">amyloid</a> and <a href="https://www.alz.org/media/Documents/alzheimers-dementia-tau-ts.pdf">tau</a>.</p>
<p>To our surprise and delight we saw accumulations of both types of protein. Also, we found amyloid deposition in the brains of infected mice. However, getting the results published was a Sisyphean task and journal reviewers’ comments were often incredulous.</p>
<p>We subsequently used a very complex technique (in-situ PCR) which revealed that in tissue sections of brain, most of the viral DNA was located very specifically within amyloid plaques. This suggested that amyloid might act to cage the virus, thereby inactivating it. All this work provided strong support for a major role of HSV1 in Alzheimer’s, and much has since been extended by <a href="https://pubmed.ncbi.nlm.nih.gov/?term=herpes+simplex+Alzheimer%27s">other labs</a>.</p>
<p><a href="https://pubmed.ncbi.nlm.nih.gov/15602731/">We also discovered</a> that anti-herpes treatment was protective because it substantially reduced the damage level in the cell cultures we were testing. This further supported a role for the virus in the disease – and pointed to a potential treatment.</p>
<h2>A heretic shunned</h2>
<p>But a viral role in the development of Alzheimer’s was still seen as heretical by many researchers, so our papers continued to be rejected by one journal after another.</p>
<p>For academics, having research published in top journals is often central to keeping your job and career progression because of the perceived value to universities (related to university league table rankings, supposed research quality and performance management).</p>
<p>Similarly, almost all of our grant applications over that 25 years were refused, too, which was even more serious as without funding, the people in my lab couldn’t be paid nor materials bought. I was very fortunate in having three successive post-doctoral researchers, Woan-Ru Lin, Curtis Dobson, and especially Matthew Wozniak, who were so dedicated that they were willing to continue to work even when on repeated short-term contracts (sometimes for less than 12 months).</p>
<p>So most of my time was taken up in writing research proposals and filling in application forms, interspersed with writing and submitting articles to journals, and when rejected, trying another. I had to face derision and hostile rants unaccompanied by any meaningful, scientific criticism from reviewers. A typical example was: “This grant essentially centres on a question of belief; are viruses
important in Alzheimer’s disease, in my view they are not.”</p>
<p>Each rejection seemed like the end of the world. It was a heart-stopping moment when opening the envelope or email from the funding body and scanning the lines in the hope of finding the words, “I’m pleased to tell you …” – though all too
often, I found the words, “I regret to tell you”. I hid, weeping tears of despair, while a part of my brain questioned whether the work really was nonsensical and whether the ideas were just wild fantasies. </p>
<p>At conferences, I was often shunned by prominent people in the field. My poster presentations were too (posters were the poor man’s alternative to giving a talk, a privilege I was rarely given). Although, hearteningly, I found that younger people were interested and excited by the research.</p>
<p>Later, I benefited from the generosity of a colleague, <a href="https://www.researchgate.net/profile/Janus-Kulikowski">Janusz
Kulikowski</a>. Kulikowski was another eccentric who lived an upside-down life, working at night and either sleeping during the day or else amusing himself by lobbing provocative remarks at colleagues. He was really interested in our research, despite working in the totally different field of vision research.</p>
<p>I do realise of course that many others have suffered refusals of grant applications, and I understand how especially heartbreaking it is for those at the start of their career, as it usually means the end of all their hopes and dreams of becoming a scientist. I realise too that I had been exceptionally lucky in being able to do such utterly engrossing work – a continuous, totally fascinating puzzle and challenge – and in having a loving family.</p>
<p>But after each rejection my fear that the work would end was overwhelming. When I did get a grant – any grant – I was elated: the world sparkled. I was so happy and exuberant, not just with the funding but with the fact that some people in the field were supportive of, or at least willing to consider, a possible role for HSV1. I felt so encouraged, vindicated and ready to face any challenge in my work or from fellow scientists, and brimming over with ideas for new approaches.</p>
<p>Quite often in the later years, some strongly supported our central concept. But there was a huge divide between them and its opponents. And the hostility continues to this day. In 2019, an application by a colleague to a US funding body for a clinical trial of an antiviral for Alzheimer’s was refused. I was involved as an adviser because it was based on my lab’s research, though I was not an applicant.</p>
<p>One reviewer said: “This application is peripherally related to the idea that Human Herpes Virus (HHV) infection could play a role in Alzheimer’s disease pathogenesis … the evidence is weak, the supporting data are weak.” The second reviewer proclaimed: “The novelty of this approach appears to be quite lacking. The suggestion of latent microbe-based activation by (unknown)
factors coincident with a ‘deteriorating immune system’ as the cause for Alzheimer’s seems like hand waving”: poetic perhaps, but hardly a brilliant display of scientific disputation. In fact, no adverse comments had ever been supported by any scientific argument, despite a public assertion once by a senior government official that the HSV1/Alzheimer’s work had been refuted (though when challenged, he was unable to cite any such article).</p>
<p>Most researchers acknowledge that new, surprising and challenging ideas should be viewed with caution. But ideas should not be dismissed without any deliberation.
Perhaps another major reason for the hostility is that many people in the field have been working for several decades on amyloid as a cause, and so are understandably distressed on learning that it might not be a direct cause, except in rare familial cases. This occurs despite our repeatedly stressing that numerous factors contribute to Alzheimer’s and amyloid is clearly an important feature.</p>
<h2>Exciting developments</h2>
<p>But, as the Columbia University study shows, attitudes to the topic of Alzheimer’s and HSV1 are slowly, but steadily, improving. Of course, I am very happy about this, for the sake of patients and their carers. And I have to admit that recognition of the work on HSV1 is personally gratifying as, like most people, I am heartened to know that my work has achieved something. </p>
<p>I am pleased that the research that I and others are carrying out is now moving forwards in even more exciting directions, including the use of a 3D bioengineered human <a href="https://now.tufts.edu/2020/05/06/3d-brain-tissue-model-links-alzheimers-disease-herpes">brain model</a> which, when infected with HSV1, displays many Alzheimer’s-like characteristics.</p>
<p>We are now investigating the effects of <a href="https://content.iospress.com/articles/journal-of-alzheimers-disease/jad220287">infectious diseases</a> and a possible role for vaccinations. This follows an explanation I <a href="https://pubmed.ncbi.nlm.nih.gov/12137067/">published</a> with my then-senior post-doctoral associate, Curtis Dobson, to account for <a href="https://pubmed.ncbi.nlm.nih.gov/11762573/">the finding</a> that certain vaccines decreased the risk of Alzheimer’s disease. We suggested that infections might reactivate latent HSV1 in the brain and that vaccines might decrease the consequent risk of Alzheimer’s disease by reducing the occurrence of such infectious diseases.</p>
<p>For example, in the case of shingles – which is caused by another type of herpes virus, varicella zoster virus (VZV) – <a href="https://pubmed.ncbi.nlm.nih.gov/35754275/">a recent study</a> I carried out with Manchester University epidemiologists showed that vaccination against the disease
may protect against the development of Alzheimer’s. Two subsequent studies showed the same result. However, much further work needs to be done to elucidate the findings that certain types of vaccine appear to reduce the risk of Alzheimer’s.</p>
<figure class="align-center ">
<img alt="Colorised microscopic view of virus cells." src="https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/489196/original/file-20221011-13-dk95d3.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=424&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Scraping of a skin lesion showing characteristic giant cells in a patient with chicken pox (Varicella Zoster Virus), a type of herpes.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/cytology-scraping-skin-lesion-tzanck-smear-763028299">Shutterstock/David A Litman</a></span>
</figcaption>
</figure>
<p>I, along with researchers at Tufts University, then <a href="https://www.ox.ac.uk/news/2022-08-02-viral-role-alzheimers-disease-discovered-0">decided to find out</a> if VZV (which also causes chickenpox) plays a role similar to HSV1 in causing brain damage leading to the development of Alzheimer’s.</p>
<p><a href="https://content.iospress.com/articles/journal-of-alzheimers-disease/jad220287">Our results</a> showed that VZV infection of the cells does not lead to the formation of the main characteristic Alzheimer’s features in the brain. However, VZV infection does result in certain other Alzheimer’s-like features, including increased inflammation. And – importantly – VZV was seen to reactivate the latent HSV1 infection in the brain model, with the consequent occurrence of Alzheimer’s-like characteristics. This is consistent with our suggestion that infections reactivate latent HSV1 in the brain.</p>
<p>The <a href="https://www.science.org/doi/10.1126/science.abj8222">recent evidence</a> that another herpes virus, Epstein Barr, is a cause of another brain disease (multiple sclerosis) strengthens the likelihood of viral involvement in certain other such diseases.</p>
<p>We now plan to find out if other infections cause HSV1 reactivation from latency. If they do, the obvious corollary would be to try to limit infections by vaccination, and by improving standards of hygiene and living conditions – a particular need in developing countries – to reduce microbial transmission.</p>
<p>In addition, we now have some exciting preliminary findings suggesting that percussive brain injury (for example, concussion) can cause HSV1 reactivation. This is a very different type of injury from infection and the results suggest that the virus might be pivotal in the brain’s response to diverse types of damage. </p>
<p>This is an exciting field of study and I hope bright young scientists will enter it. Nobody said being a scientist was easy, but with the right encouragement from family, friends and open-minded peers, it is amazing what challenges can be overcome.</p>
<hr>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=112&fit=crop&dpr=1 600w, https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=112&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=112&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=140&fit=crop&dpr=1 754w, https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=140&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/313478/original/file-20200204-41481-1n8vco4.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=140&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"></span>
</figcaption>
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<p class="fine-print"><em><span>Ruth Itzhaki is currently working with Dr David Kaplan and Dr Dana Cairns at Tufts University on the effects of infection on their 3D brain model. Also with Professors Ken Muir and Curtis Dobson and Dr Artitaya Lophatananon at Manchester University on epidemiological aspects of HSV1 and Alzheimer's.</span></em></p>Ruth Itzhaki has spent more than 30 years researching whether certain common viruses play a role in the development of Alzheimer’s. But for years her research was greeted with hostility.Ruth Itzhaki, Professor Emeritus of Molecular Neurobiology at the University of Manchester and a Visiting Professorial Fellow, University of OxfordLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1049432018-10-19T11:32:35Z2018-10-19T11:32:35ZAlzheimer’s disease: mounting evidence that herpes virus is a cause<figure><img src="https://images.theconversation.com/files/241054/original/file-20181017-41153-xdfg3e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/677117257?src=3Oj1RFnuQ7e4qarYGHLYIQ-1-43&size=medium_jpg">Atthapon Raksthapu/Shutterstock.com</a></span></figcaption></figure><p>More than 30m people worldwide suffer from Alzheimer’s disease – the most common form of dementia. Unfortunately, there is no cure, only drugs to ease the symptoms. However, my <a href="https://www.frontiersin.org/articles/10.3389/fnagi.2018.00324/full">latest review</a>, suggests a way to treat the disease. I found the strongest evidence yet that the herpes virus is a cause of Alzheimer’s, suggesting that effective and safe antiviral drugs might be able to treat the disease. We might even be able to vaccinate our children against it.</p>
<p>The virus implicated in Alzheimer’s disease, herpes simplex virus type 1 (HSV1), is better known for causing cold sores. It infects most people in infancy and then remains dormant in the peripheral nervous system (the part of the nervous system that isn’t the brain and the spinal cord). Occasionally, if a person is stressed, the virus becomes activated and, in some people, it causes cold sores.</p>
<p>We discovered in <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Jamieson+and+J.+Med+Virol+33%2C1991">1991</a> that in many elderly people HSV1 is also present in the brain. And in <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=itzhaki+lancet+349%2C+241%2C244">1997</a> we showed that it confers a strong risk of Alzheimer’s disease when present in the brain of people who have a specific gene known as APOE4. </p>
<p>The virus can become active in the brain, perhaps repeatedly, and this probably causes cumulative damage. The likelihood of developing Alzheimer’s disease is 12 times greater for APOE4 carriers who have HSV1 in the brain than for those with neither factor. </p>
<p>Later, <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=wozniak+neurosci+lett+429+2007">we</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=zambrano+alzheimers+disease+14+2008">others</a> found that HSV1 infection of cell cultures causes beta-amyloid and abnormal tau proteins to accumulate. An accumulation of these proteins in the brain is characteristic of Alzheimer’s disease. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/241053/original/file-20181017-41140-1uaoy0y.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Most people are infected with the herpes simplex virus by the time they reach old age.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/521894017?src=fnwEdT5ejIK3D1uVHO8KmA-1-4&size=medium_jpg">Spectral-Design/Shutterstock.com</a></span>
</figcaption>
</figure>
<p>We believe that HSV1 is a major contributory factor for Alzheimer’s disease and that it enters the brains of elderly people as their immune system declines with age. It then establishes a latent (dormant) infection, from which it is reactivated by events such as stress, a reduced immune system and brain inflammation induced by infection by other microbes. </p>
<p>Reactivation leads to direct viral damage in infected cells and to viral-induced inflammation. We suggest that repeated activation causes cumulative damage, leading eventually to Alzheimer’s disease in people with the APOE4 gene. </p>
<p>Presumably, in APOE4 carriers, Alzheimer’s disease develops in the brain because of greater HSV1-induced formation of toxic products, or less repair of damage. </p>
<h2>New treatments?</h2>
<p>The data suggest that antiviral agents might be used for treating Alzheimer’s disease. The main antiviral agents, which are safe, prevent new viruses from forming, thereby limiting viral damage. </p>
<p>In an earlier study, we <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=wozniak+PLOS+ONE+6+e25152">found</a> that the anti-herpes antiviral drug, acyclovir, blocks HSV1 DNA replication, and reduces levels of beta-amyloid and tau caused by HSV1 infection of cell cultures. </p>
<p>It’s important to note that all studies, including our own, only show an association between the herpes virus and Alzheimer’s – they don’t prove that the virus is an actual cause. Probably the only way to prove that a microbe is a cause of a disease is to show that an occurrence of the disease is greatly reduced either by targeting the microbe with a specific anti-microbial agent or by specific vaccination against the microbe. </p>
<p>Excitingly, successful prevention of Alzheimer’s disease by use of specific anti-herpes agents has <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=tzeng+and+neurotherapeutics+15">now been demonstrated</a> in a <a href="https://content.iospress.com/articles/journal-of-alzheimers-disease/jad180266">large-scale population study</a> in Taiwan. Hopefully, information in other countries, if available, will yield similar results.</p><img src="https://counter.theconversation.com/content/104943/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ruth Itzhaki does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>New review finds that over 150 papers strongly support the view that herpes simplex plays a role in Alzheimer’s disease.Ruth Itzhaki, Professor Emeritus of Molecular Neurobiology, University of ManchesterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/866352017-11-02T12:16:17Z2017-11-02T12:16:17ZIs it safe to use makeup testers in cosmetics stores?<figure><img src="https://images.theconversation.com/files/192872/original/file-20171101-19845-bta0c8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Viral vectors.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/429526483?src=_o5Ws1gfKVNqHSMtV_3eiQ-1-38&size=medium_jpg">VTT Studio/Shutterstock</a></span></figcaption></figure><p>A woman in the US is suing a cosmetics store because she claims that she <a href="http://www.tmz.com/2017/10/30/sephora-sued-woman-herpes-lipstick-samples/">caught herpes from their lipstick tester</a>. In case you’re wondering if this is even possible, as a microbiologist, I can tell you that it most certainly is. And it’s not just herpes that can lurk in makeup.</p>
<p>But let’s look at herpes first. </p>
<p>This very common virus is mainly spread by skin-to-skin contact, kissing and sex, but it can also be transmitted in droplets of spit left by an infected person on towels, cups, cutlery and, yes, lipstick. Globally, it’s estimated that <a href="http://who.int/mediacentre/news/releases/2015/herpes/en/">67% of people are infected with the Herpes simplex virus (HSV-1)</a>. But it’s a hidden enemy – a person doesn’t need to have visible signs of the virus to spread the infection. The virus lives in facial tissues where it can shed and spread. </p>
<p>It doesn’t always show up on the skin as a blister immediately after it has infected a person, instead it can stay hidden and appear after a few months. Because of this, it’s impossible to say with certainty if the American woman caught herpes from this particular store tester, or elsewhere. </p>
<p>Herpes causes blisters on the lips and around the mouth that can last up to ten days. Lipsticks and makeup brushes that touch these parts of the face can then spread the infection to other people. </p>
<p>Fortunately, herpes is a fragile virus and typically only survives outside the body for ten seconds. But it can survive longer in warm and moist environments, such as in sweat. It can also survive between two to four hours on plastic, chrome and water, so there are lots of ways the virus can spread. </p>
<p>There is no cure for a herpes infection, although treatments are available that will reduce the length of infection.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=375&fit=crop&dpr=1 600w, https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=375&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=375&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=471&fit=crop&dpr=1 754w, https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=471&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/193000/original/file-20171102-26448-1rj3q51.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=471&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Herpes blisters.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/317192864?src=pkZUIXuzGEd2PmbqE8wMGA-1-1&size=medium_jpg">Cherries/Shutterstock</a></span>
</figcaption>
</figure>
<h2>An old problem</h2>
<p>Microbiologists have known about the link between beauty products and pathogens since the mid-1940s when talcum powder contaminated with <em>Clostridium tetani</em> bacteria <a href="https://www.omicsonline.org/open-access/comparative-microbiological-study-between-traditional-and-modern-cosmetics-in-saudi-arabia-2329-6674-1000146.pdf">caused the death of a newborn baby</a>. Since the 1960s, contamination linked to other opportunistic pathogens, including <a href="https://www.omicsonline.org/open-access/comparative-microbiological-study-between-traditional-and-modern-cosmetics-in-saudi-arabia-2329-6674-1000146.php?aid=71067"><em>Salmonella</em>, <em>Klebsiella pneumoniae</em> and <em>Pseudomonas aeruginosa</em></a>, has been reported by microbiologists across the globe. </p>
<p>Cosmetic products contain preservatives to help slow down the growth of microbes, but they can become contaminated if people use non-sterile applicators or fingers to apply products, or if the products are poorly handled and stored; for example, products stored in warm and humid or damp conditions such as the bathroom.</p>
<p>Makeup brushes also have the potential to act as suitable homes for bacteria to thrive. Often, beauty blenders and brushes are dampened to help the application of eyeshadows or foundation. But this environment has the potential to promote rapid bacterial growth. </p>
<p>In 2015, it was reported that a <a href="http://www.medicaldaily.com/mrsa-bacteria-borrowed-makeup-brush-paralyzes-27-year-old-woman-328836">27-year-old Australian woman became paralysed after contracting an MRSA infection</a> that attacked her spine. She used a brush to apply makeup that belonged to a friend who had a <em>Staphylococcus</em> infection on her face, and became contaminated with the organism.</p>
<p><em>Staphylococcus</em> is a common bacteria that doesn’t typically cause harm and lives on the skin or in the nose. However, MRSA (Methicillin-resistant Staphylococcus aureus) is an antibiotic-resistant strain of <em>Staphylococcus.</em> </p>
<h2>Irreversible blindness</h2>
<p>Mascara wands and eyeliners not only beautify the eyes, but can cause irritation and conjunctivitis, caused by both bacteria and viruses, including herpes simplex. Studies have revealed that <a href="https://www.researchgate.net/publication/18171778_Microbial_Contamination_in_Ocular_Cosmetics">43% of eyeliners and mascara wands contain contaminants</a>. I know many friends who have been left with a “pink eye” after sharing mascara or using ancient mascara that has been sitting in their makeup bags. </p>
<p>Symptoms of pink eye include redness, watery discharge and, in extreme cases, irreversible blindness. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=425&fit=crop&dpr=1 600w, https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=425&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=425&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=534&fit=crop&dpr=1 754w, https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=534&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/193002/original/file-20171102-26478-159by18.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=534&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Eyelashes trap dirt and bacteria.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/w/index.php?curid=608771">Steve Jurvetson/Wikimedia Commons</a></span>
</figcaption>
</figure>
<p>Lashes aren’t just there to make us look pretty, they serve to block out dirt and bacteria, and using products on the eyes can cause contamination of the product. With time, bacteria can build up in the cosmetic container increasing the risk of eye infection every time the product is used. </p>
<p>If all of these horror stories tell us one thing, it’s stay away from sharing makeup products, both among your friends and especially in cosmetic stores. You just don’t know what infections other people could be carrying on their skin. </p>
<p>Always keep your own cosmetic products clean and use single applicators where possible. You wouldn’t share your toothbrush with strangers, so why make an exception with your cosmetics?</p><img src="https://counter.theconversation.com/content/86635/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Amreen Bashir does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>A range of pathogens might be lurking in makeup testers, from the mild to the deadly.Amreen Bashir, Lecturer in Biomedical Science, Aston UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/756012017-04-06T10:00:24Z2017-04-06T10:00:24Z‘The Mountain’ Hafþór Júlíus Björnsson has Bell’s palsy – here’s what it means<figure><img src="https://images.theconversation.com/files/164093/original/image-20170405-14603-8f9728.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The Mountain.</span> <span class="attribution"><a class="source" href="https://commons.wikimedia.org/w/index.php?curid=43038054">Ellen Finch</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>Icelandic strongman, Hafþór Júlíus Björnsson, known for his role as The Mountain in Game of Thrones and for being “Europe’s strongest man”, recently announced that he is suffering from Bell’s palsy. He joins a list of famous people who have suffered from the condition, reportedly including <a href="http://www.bbc.co.uk/news/magazine-20123449">George Clooney</a> and <a href="http://www.bbc.co.uk/news/magazine-20123449">Sylvester Stallone</a>. </p>
<p><div data-react-class="InstagramEmbed" data-react-props="{"url":"https://www.instagram.com/p/BSUFQOkAEgL/?taken-by=thorbjornsson","accessToken":"127105130696839|b4b75090c9688d81dfd245afe6052f20"}"></div></p>
<p>Bell’s palsy is a – usually – self-limiting condition that causes paralysis to one side of a person’s face. The condition occurs when the <a href="http://teachmeanatomy.info/head/cranial-nerves/facial-nerve/">facial nerve</a> becomes inflammed. As with almost every nerve, the facial nerve is connected to the brain to either carry information from the brain to control muscles or return information to the brain relating to sensory information. For these nerves to do this, they must pass through a passage of bone near the upper jaw. If the facial nerve is inflammed it can interfere with the signals that the brain sends to muscles in the face, causing one side of the face to become paralysed.</p>
<p>People with Bell’s palsy can find it difficult to close their eyelid on the affected side. They may also drool and find it difficult to chew food. Taste can also be affected. Some people also experience headaches, jaw ache and tinnitus (ringing in the ears).</p>
<p><a href="http://www.nhs.uk/Conditions/Bells-palsy/Pages/Introduction.aspx">Bell’s palsy</a> is one of a group of conditions that can cause paralysis of the facial nerve. Bell’s palsy is the most common form of facial nerve paralysis and encompasses cases where the cause of the paralysis cannot be identified. The condition is named after the 19th-century Scottish anatomist and surgeon <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3101348/">Sir Charles Bell</a> who used three cases to describe the palsy (paralysis) that was named after him.</p>
<p>Although the causes of Bell’s palsy are not always known, it is thought that, in some cases, the <a href="https://www.ncbi.nlm.nih.gov/pubmed/20113184">herpes simplex</a> virus plays a role. The <a href="http://www.sciencedirect.com/science/article/pii/S1808869415304213">varicella zoster</a> virus (the virus that causes chickenpox and shingles) has also been named as a suspect. But neither of these causes has been proved.</p>
<p>We do know, however, that some forms of facial nerve paralysis can be caused by the bacteria <em>Borrelia burgdorferi</em> in people with <a href="http://www.nhs.uk/Conditions/Lyme-disease/Pages/Introduction.aspx">Lyme disease</a> – a disease spread by ticks.</p>
<p>Other known causes of paralysis are tumours. These tumours arise from a <a href="http://www.sciencedirect.com/science/article/pii/S2211568413002155">variety of structures</a>, such as the cells that surround the nerves and look after them, or structures that the nerve passes through, such as the parotid gland in the cheek, which produces saliva.</p>
<figure class="align-right ">
<img alt="" src="https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=882&fit=crop&dpr=1 600w, https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=882&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=882&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1109&fit=crop&dpr=1 754w, https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1109&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/164099/original/image-20170405-14603-elq711.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1109&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">A man with Bell’s palsy.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/w/index.php?curid=11520707">James Heilman</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>Regardless of the cause, the resulting inflammation results in compression of the nerve in the facial canal and the loss of function of muscles involved in chewing.</p>
<p>Rather than develop facial nerve damage, some people are born with it as part of rare syndromes, such as <a href="https://ghr.nlm.nih.gov/condition/moebius-syndrome">Mobius syndrome</a> (a neurological disease). And some babies have it as a result of a <a href="http://jamanetwork.com/journals/jamaotolaryngology/fullarticle/410281">traumatic</a> natural birth, or where forceps were used to assist in delivery. The symptoms usually <a href="https://www.ncbi.nlm.nih.gov/pubmed/2293714">clear up</a> within three to four weeks of the child being born, unless the nerve has been completely cut.</p>
<h2>Time is the best healer</h2>
<p>Most cases of facial nerve paralysis that have an unknown cause are classed as Bell’s palsy. For these cases, doctors may prescribe <a href="https://www.ncbi.nlm.nih.gov/pubmed/27428352">corticosteroids</a> to reduce the inflammation and thus ease the pressure on the squeezed nerve. Some doctors advocate <a href="https://www.ncbi.nlm.nih.gov/pubmed/24132718">surgery</a>, but surgery carries risks, including damaging important structures in the face.</p>
<p>Some studies have looked at the benefit of <a href="https://www.ncbi.nlm.nih.gov/pubmed/26559436">anti-viral</a> therapies to treat Bell’s palsy, but these have proved to be no better than placebo, although they do have some positive effects when used with corticosteroids, in that they increase the number of people with the most severe cases of Bell’s palsy who go on to make a complete recovery.</p>
<p>However, treatment usually isn’t necessary. Bell’s palsy often clears up within a month or two, without treatment. And, for most people, it doesn’t stop them going about their daily business. It certainly didn’t stop The Mountain from winning his third Europe’s Strongest Man title this month.</p><img src="https://counter.theconversation.com/content/75601/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Adam Taylor is affiliated with the Anatomical Society
</span></em></p>It certainly didn’t stop him picking up his third Europe’s strongest man title this month.Adam Taylor, Director of the Clinical Anatomy Learning Centre & Senior Lecturer in Anatomy, Lancaster UniversityLicensed as Creative Commons – attribution, no derivatives.