tag:theconversation.com,2011:/us/topics/frontotemporal-dementia-6502/articlesFrontotemporal dementia – The Conversation2023-11-17T17:18:16Ztag:theconversation.com,2011:article/2174042023-11-17T17:18:16Z2023-11-17T17:18:16ZNew blood tests for dementia announced, but what can they tell us and who will benefit?<figure><img src="https://images.theconversation.com/files/559949/original/file-20231116-28-b88a0l.jpg?ixlib=rb-1.1.0&rect=27%2C18%2C6104%2C4063&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-photo/lab-assistant-medical-scientist-chemistry-researcher-2248148893">Pickadook/Shutterstock</a></span></figcaption></figure><p>A five-year, £5 million initiative has just been launched to investigate the feasibility of using new blood tests in the diagnosis of Alzheimer’s disease. Alzheimer’s Research UK and the Alzheimer’s Society are working with the National Institute for Health and Care Research to <a href="https://www.alzheimersresearchuk.org/a-five-year-project-to-bring-alzheimers-blood-tests-to-the-nhs/">use these blood tests in the NHS</a>.</p>
<p>This funding, hot on the heels of <a href="https://theconversation.com/experimental-alzheimers-drug-shows-promise-but-there-are-many-hurdles-still-to-overcome-195383">recent drug trials</a> for Alzheimer’s disease, continues a wave of breathless excitement in a field that has traditionally found good news stories hard to come by. </p>
<p>Of those seen by specialists in memory services, the vast majority are <a href="https://www.alzheimers.org.uk/about-dementia/symptoms-and-diagnosis/dementia-diagnosis/dementia-tests">given a diagnosis</a> of dementia based on their symptoms alongside cognitive tests, blood tests to rule out other explanations (such as hormone imbalances), and sometimes an MRI brain scan. </p>
<p>A small percentage, particularly those who are younger or who have more complex symptoms, may be offered a more detailed investigation to look for some proteins (amyloid and tau) that can build up in the brain. </p>
<p>At the moment, this would involve a lumbar puncture (placing a needle into the spine and removing some of the fluid) or a specialist brain scan called a PET scan. If simple blood tests can tell us the same information, with enough accuracy, then this will be preferable for this small group of people.</p>
<p>So far, so good. But what about those people who don’t need a lumbar puncture or PET scan? Will they see meaningful benefits from these new blood tests? It is far from certain. </p>
<p>Some argue that more “precision” in the diagnosis will help people understand what the coming years will entail. But this assumes that we can confidently place all people with dementia into the <a href="https://www.alzheimers.org.uk/about-dementia/types-dementia">various disease categories</a> (such as Alzheimer’s, vascular dementia, Lewy body dementia, frontotemporal dementia) based on the pathologies we find in their brains, and that we can then accurately predict how things will unfold for that person. </p>
<p>Unfortunately, we can’t. Instead, data show that many pathologies (disease-causing abnormalities such as protein build-up or damage to blood vessels) are linked to dementia, and most people with dementia have <a href="https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(23)00019-3/fulltext#seccestitle140">more than one</a>. This mixed disease is a big part of what makes researching the syndrome of dementia so complex. </p>
<p>The other suggested benefit is that the tests will tell us if the patient is eligible for the new drugs approved in the US (and currently being considered by UK and European regulators). But beyond the headlines, the current crop of new drugs <a href="https://theconversation.com/new-alzheimers-drugs-dont-deserve-the-hype-heres-why-211842">don’t stand up to scrutiny</a>.</p>
<h2>Beyond the amyloid theory</h2>
<p>The theory on which they are based (that the build-up of the amyloid protein is the trigger for everything that comes after) is increasingly <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9997141/#:%7E:text=Taken%20together%2C%20the%20evidence%20is,initiation%20and%20progression%20of%20dementia">challenged</a> by <a href="https://academic.oup.com/brain/article-abstract/146/10/3969/7162122?redirectedFrom=fulltext&login=false">experts</a>. We need to better understand the complex biology of dementia. </p>
<p>In the past, this has been heavily focused on amyloid even though evidence has told us to <a href="https://mitpress.mit.edu/9780262546010/how-not-to-study-a-disease/#:%7E:text=Herrup%20presents%20a%20new%20and,of%20the%20Alzheimer%27s%20disease%20research">also look elsewhere</a>. </p>
<p>The ultimate frontier that many seek is screening people who have no symptoms but who would, if tested, be found to have raised protein levels. They hope that by detecting people at this stage, drugs could not just slow down the disease but prevent it altogether. </p>
<figure class="align-center ">
<img alt="Person receiving a lumbar puncture." src="https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/559961/original/file-20231116-19-knacv6.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">Person receiving a lumbar puncture.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/demonstration-simulator-lumbar-puncture-epidural-anesthesia-1946628973">Kittipong Somklang/Shutterstock</a></span>
</figcaption>
</figure>
<p>A recent trial tested this, in which people with raised amyloid but no symptoms took the amyloid-clearing drug <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2305032">solazenumab</a> for more than four years. It had no effect on cognitive function compared with a placebo, confirming that this ambition is, sadly, not close. </p>
<p>It may not ever be realised for such a complex disease. The most significant problem is that many of those who have raised brain amyloid but no symptoms <a href="https://alz-journals.onlinelibrary.wiley.com/doi/10.1016/j.jalz.2018.03.005">will die without developing dementia</a>. Therefore, most symptom-free people with a positive blood test have nothing to gain and can only experience harm – from anxiety, further tests, or treatments. Importantly, the focus of this new initiative is not people without symptoms. </p>
<h2>New initiative</h2>
<p>Several studies of new blood tests have been carried out already in people with dementia symptoms, showing they are almost as good as PET scans or lumbar punctures at detecting protein levels. But the people in these studies were typically younger (in their 60s and 70s), with minimal brain pathologies (except amyloid) and other disorders, and minimal ethnic and socioeconomic diversity. </p>
<p><a href="https://www.alzheimersresearchuk.org/wp-content/uploads/2023/05/Blood-Biomarker-Challenge-Request-for-Application.pdf">This initiative</a> will test how well these emerging blood tests perform for those with suspected dementia in the NHS. Most people in the UK who develop dementia are <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)61570-6/fulltext">in their 80s</a>, have mixed brain pathologies, commonly have other diseases (for example, kidney disease, which may <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2800717#:%7E:text=Kidney%20function%20might%20influence%20the,of%20the%20disease%20are%20multifactorial.">affect the accuracy of the blood tests</a>, and rates are higher among poorer groups and those <a href="https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12774">from some minority ethnic backgrounds</a>. </p>
<p>The results of this new initiative will tell us how well the new blood tests perform in these older, more complex people. The most important question, though, will be: do the results of protein tests change the way we look after people with dementia, resulting in a better quality of life?</p><img src="https://counter.theconversation.com/content/217404/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sebastian Walsh receives funding from the NIHR</span></em></p><p class="fine-print"><em><span>Edo Richard receives funding from The Netherlands Organisation for Health Research and Development (ZonMW) - public funding </span></em></p><p class="fine-print"><em><span>Carol Brayne 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>The NHS will trial a new blood test for dementia, which could be widely available in five years.Sebastian Walsh, NIHR Doctoral Fellow in Public Health, University of CambridgeCarol Brayne, Professor of Public Health Medicine, University of CambridgeEdo Richard, Professor of Neurology, Radboud UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2168642023-11-07T16:51:27Z2023-11-07T16:51:27ZFrontotemporal dementia: we discovered a brain fold that may delay onset of symptoms<figure><img src="https://images.theconversation.com/files/557829/original/file-20231106-270141-ib5avf.jpg?ixlib=rb-1.1.0&rect=5%2C5%2C3936%2C2854&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Bruce Willis's frontotemporal diagnosis was revealed earlier this year.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/bruce-willis-arriving-good-day-die-131400650">Featureflash Photo Agency/ Shutterstock</a></span></figcaption></figure><p>Few people had probably heard of frontotemporal dementia until earlier this year, when the family of <a href="https://theconversation.com/bruce-willis-has-frontotemporal-dementia-heres-what-we-know-about-the-disease-200188">actor Bruce Willis</a> announced the 68-year-old had been diagnosed with the condition.</p>
<p>Frontotemporal dementia is a rare disease – thought to account for only <a href="https://www.alzheimersresearchuk.org/dementia-information/types-of-dementia/frontotemporal-dementia/#:%7E:text=Frontotemporal%20dementia%2C%20also%20known%20as,younger%20or%20older%20than%20this.">one in every 20</a> cases of dementia. Symptoms usually develop in a person’s late 50s, first affecting their behaviour, personality and language ability. Unlike other forms of dementia, memory only becomes impaired in the late stages of the disease.</p>
<p>People diagnosed with frontotemporal dementia usually die within eight years of their diagnosis. While around 30% of cases <a href="https://pubmed.ncbi.nlm.nih.gov/31119452">are inherited</a>, the cause of frontotemporal dementia is largely unknown. This also means there are no cures available or treatments to slow its progression.</p>
<p>But <a href="https://academic.oup.com/braincomms/article/5/5/fcad264/7303258">recent research</a>, I have published with colleagues at Lund University, may have brought us one step closer in our understanding of how frontotemporal dementia develops and progresses. We discovered that the way your brain looks may determine your resilience to the condition.</p>
<h2>Brain folds</h2>
<p>During pregnancy, as a foetus’s brain grows within the womb, it develops its distinctive folds while expanding within the skull. These brain folds play an important role in our later <a href="https://www.livescience.com/62892-why-brains-have-folds.html">cognitive function</a>. </p>
<p>The <a href="https://academic.oup.com/cercor/article-abstract/5/1/56/329572">folds that form</a> early in foetal development are found in both sides of the brain in every person. But there’s one fold that sometimes develops later on in the process. It’s called the <a href="https://pubmed.ncbi.nlm.nih.gov/34192698/#:%7E:text=Apes%20and%20Humans-,The%20Paracingulate%20Sulcus%20Is%20a%20Unique%20Feature%20of%20the%20Medial,Brain%20Behav%20Evol.">paracingulate sulcus</a> – and not everyone has it. In those that do have it, it can either be present on just one side of the brain or both sides. </p>
<p>The paracingulate sulcus is interesting, as its presence can make a significant difference to <a href="https://academic.oup.com/cercor/article/32/18/3937/6509010">cognitive ability</a>. For example, research has shown that people with a left but not a right paracingulate sulcus have a <a href="https://academic.oup.com/cercor/article/14/4/424/286436">cognitive advantage</a> – performing better on tasks involving control and even memory. </p>
<p>Given the link between the paracingulate sulcus and cognitive function, our research team at Lund University – alongside colleagues in the US and Amsterdam – began studying this brain fold’s role in dementia. </p>
<p>To really understand what role the paracingulate sulcus plays, the team decided to focus on a type of dementia where brain damage occurs in the same region as this brain fold. The obvious choice for this research was frontotemporal dementia. This aggressive form of early-onset dementia primarily attacks the frontal lobes of the brain – particularly the central portions surrounding the paracingulate sulcus.</p>
<figure class="align-center ">
<img alt="A picture of a brain made our of puzzle pieces. One piece is missing." src="https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C6000%2C3988&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/557714/original/file-20231106-15-8e5xwv.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">Only some people have a paracingulate sulcus.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/brain-shaped-white-jigsaw-puzzle-on-1944850117">mapush/ Shutterstock</a></span>
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</figure>
<p>Our team studied <a href="https://academic.oup.com/braincomms/article/5/5/fcad264/7303258">MRI brain images</a> of 186 people who had been diagnosed with frontotemporal dementia. We excluded participants who had frontotemporal dementia with a genetic cause. Around 57% of participants had a paracingulate sulcus on the right side of their brain.</p>
<p>We discovered that in participants who had this extra fold on the right side of their brain, their dementia symptoms began on average two and a half years later. This might mean that the paracingulate sulcus may delay the onset of symptoms. These findings were statistically significant – showing they weren’t due to chance or other factors. </p>
<p>This two-and-a-half-year delay in symptoms may not sound like much, but considering the poor prognosis of the condition and the burden of symptoms, this is an extremely meaningful amount of time for patients and their relatives. </p>
<h2>Cognitive reserve</h2>
<p>That said, after the symptoms do begin, patients with this extra brain fold became sicker at a faster rate and survived for a shorter length of time than patients who do not have the fold. So despite the delay in symptoms, patients with and without this extra brain fold still died at a similar age. </p>
<p>Although it may sound strange that a factor can both delay symptoms and later speed them up, this paradox is a key feature of a principle referred to in neuroscience as “<a href="https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1016/j.jalz.2018.07.219?casa_token=NmBv2BCHXykAAAAA%3APLfoP3DZzMREV0rAmSyRjuMijmoQlKees7-dBYF9okesGGqWCW-62zefj_nUsKM9lRfpaub8pQdZUw">brain reserve</a>”. Brain reserve describes a structure in the brain which provides resilience to a disease before symptoms develop.</p>
<p>Critically, there becomes a point at which the disease overcomes these protective mechanisms, and the patient develops symptoms. After this critical point, people with high brain reserve decline rapidly – faster than people with low brain reserve. </p>
<p>For example, high brain reserve explains why <a href="https://www.thelancet.com/article/S1474-4422(12)70191-6/fulltext">Alzheimer’s disease</a> starts later in highly educated people – though the disease progresses faster for them when symptoms start. According to our research, the paracingulate sulcus operates by a similar principle – first protecting people from symptoms, then progressing rapidly when symptoms do start. </p>
<p>Our research is the first to identify a protective structure in the brain which delays the onset of symptoms in people with frontotemporal dementia. If we can now uncover a way of preserving this protective quality, it could lead to the development of treatments which can help keep symptoms – and the disease – at bay.</p><img src="https://counter.theconversation.com/content/216864/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Luke Harper receives funding from The Schörling foundation. and the Swedish federal government under the Avtal om Läkarutbildning och Forskning (ALF) agreement</span></em></p>Our study found that people born with a with a particular fold in their brain develop frontotemporal dementia symptoms on average two and a half years later than others.Luke Harper, PhD Student. Neurologist, Lund UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2128522023-09-25T20:07:31Z2023-09-25T20:07:31ZIs it normal to forget words while speaking? And when can it spell a problem?<figure><img src="https://images.theconversation.com/files/547138/original/file-20230908-25-8gkxww.jpg?ixlib=rb-1.1.0&rect=15%2C0%2C5160%2C3880&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">mimi thian/unsplash</span></span></figcaption></figure><p>We’ve all experienced that moment mid-sentence when we just can’t find the word we want to use, even though we’re certain we know it. </p>
<p>Why does this universal problem among speakers happen? </p>
<p>And when can word-finding difficulties indicate something serious? </p>
<p>Everyone will experience an occasional word-finding difficulty, but if they happen very often with a broad range of words, names and numbers, this could be a sign of a neurological disorder.</p>
<h2>The steps involved in speaking</h2>
<p>Producing spoken words involves several <a href="https://doi.org/10.1093/oxfordhb/9780190672027.013.19">stages of processing</a>. </p>
<p>These include:</p>
<ol>
<li><p>identifying the intended meaning</p></li>
<li><p>selecting the right word from the “mental lexicon” (a mental dictionary of the speaker’s vocabulary)</p></li>
<li><p>retrieving its sound pattern (called its “form”) </p></li>
<li><p>executing the movements of the speech organs for articulating it. </p></li>
</ol>
<p>Word-finding difficulties can potentially arise at each of these stages of processing.</p>
<p>When a healthy speaker can’t retrieve a word from their lexicon despite the feeling of knowing it, this is called a “tip-of-the-tongue” phenomenon by language scientists. </p>
<p>Often, the frustrated speaker will try to give a bit of information about their intended word’s meaning, “you know, that thing you hit a nail with”, or its spelling, “it starts with an <em>H</em>!”. </p>
<p>Tip-of-the-tongue states are relatively common and are a type of speech error that occurs primarily during retrieval of the sound pattern of a word (step three above).</p>
<h2>What can affect word finding?</h2>
<p>Word-finding difficulties occur at all ages but they do happen more often as we get older. In older adults, they can cause frustration and anxiety about the possibility of developing dementia. But they’re not always a cause for concern. </p>
<p>One way researchers investigate word-finding difficulties is to ask people to keep a diary to record how often and in what context they occur. <a href="https://www.frontiersin.org/articles/10.3389/fpsyg.2015.01190/full">Diary studies</a> have shown that some word types, such as names of people and places, concrete nouns (things, such as “dog” or “building”) and abstract nouns (concepts, such as “beauty” or “truth”), are more likely to result in tip-of-the-tongue states compared with verbs and adjectives. </p>
<p>Less frequently used words are also more likely to result in tip-of-the-tongue states. It’s thought this is because they have weaker connections between their meanings and their sound patterns than more frequently used words. </p>
<p>Laboratory studies have also shown tip-of-the-tongue states are more likely to occur under <a href="https://www.tandfonline.com/doi/full/10.1080/13825585.2019.1641177">socially stressful</a> conditions when speakers are told they are being evaluated, regardless of their age. Many people report having experienced tip-of-the-tongue problems during job interviews.</p>
<h2>When could it spell more serious issues?</h2>
<p>More frequent failures with a broader range of words, names and numbers are likely to indicate more serious issues. </p>
<p>When this happens, language scientists use the terms “anomia” or “<a href="https://www.aphasia.com/aphasia-library/aphasia-types/anomic-aphasia/">anomic aphasia</a>” to describe the condition, which can be associated with brain damage due to stroke, tumours, head injury or dementia such as Alzheimer’s disease.</p>
<p>Recently, the actor Bruce Willis’s family <a href="https://edition.cnn.com/2023/02/16/health/frontotemporal-dementia-definition-symptoms-wellness/index.html">revealed</a> he has been diagnosed with a degenerative disorder known as primary progressive aphasia, for which one of the earliest symptoms is word-finding difficulties rather than memory loss. </p>
<p>Primary progressive aphasia is typically associated with frontotemporal or Alzheimer’s dementias, although it can be associated with other <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637977/">pathologies</a>.</p>
<p>Anomic aphasia can arise due to problems occurring at different stages of speech production. An assessment by a clinical neuropsychologist or speech pathologist can help clarify which processing stage is affected and how serious the problem might be. </p>
<p>For example, if a person is unable to name a picture of a common object such as a hammer, a clinical neuropsychologist or speech pathologist will ask them to describe what the object is used for (the individual might then say “it’s something you hit things with” or “it’s a tool”). </p>
<p>If they can’t, they will be asked to gesture or mime how it’s used. They might also be provided with a cue or prompt, such as the first letter (<em>h</em>) or syllable (<em>ham</em>).</p>
<p>Most people with anomic aphasia benefit greatly from being prompted, indicating they are mostly experiencing problems with later stages of retrieving word forms and motor aspects of speech. </p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1699457147673682242"}"></div></p>
<p>But if they’re unable to describe or mime the object’s use, and cueing does not help, this is likely to indicate an actual loss of word knowledge or meaning. This is typically a sign of a more serious issue such as primary progressive aphasia. </p>
<p><a href="https://en.wikipedia.org/wiki/Neuroimaging">Imaging studies</a> in healthy adults and people with anomic aphasia have shown different areas of the brain are responsible for their word-finding difficulties.</p>
<p>In <a href="https://direct.mit.edu/jocn/article-abstract/35/1/111/113588/Neural-Correlates-of-Naturally-Occurring-Speech">healthy adults</a>, occasional failures to name a picture of a common object are linked with changes in activity in brain regions that control motor aspects of speech, suggesting a spontaneous problem with articulation rather than a loss of word knowledge. </p>
<p>In anomia due to primary progressive aphasia, brain regions that process word meanings show a loss of nerve cells and connections or <em><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0148707">atrophy</a></em>. </p>
<p>Although anomic aphasia is common after strokes to the left hemisphere of the brain, the associated word-finding difficulties do not appear to be distinguishable by <a href="https://www.sciencedirect.com/science/article/pii/S0010945215003299">specific areas</a>.</p>
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Read more:
<a href="https://theconversation.com/what-is-aphasia-the-condition-bruce-willis-lives-with-180399">What is aphasia, the condition Bruce Willis lives with?</a>
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<p>There are <a href="https://www.tandfonline.com/doi/abs/10.1080/02687030244000563">treatments</a> available for anomic aphasia. These will often involve speech pathologists training the individual on naming tasks using different kinds of cues or prompts to help retrieve words. The cues can be various meaningful features of objects and ideas, or sound features of words, or a combination of both. <a href="https://www.sciencedirect.com/science/article/pii/S002199241730014X">Smart tablet</a> and phone apps also show promise when used to complement therapy with home-based practice.</p>
<p>The type of cue used for treatment is determined by the nature of the person’s impairment. Successful treatment is associated with changes in activity in <a href="https://www.sciencedirect.com/science/article/pii/S0093934X14000054">brain regions</a> known to support speech production. Unfortunately, there is no effective treatment for primary progressive aphasia, although <a href="https://www.tandfonline.com/doi/full/10.1080/13607863.2019.1617246">some studies</a> have suggested speech therapy can produce temporary benefits.</p>
<p>If you’re concerned about your word-finding difficulties or those of a loved one, you can consult your GP for a referral to a clinical neuropsychologist or a speech pathologist. </p>
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<strong>
Read more:
<a href="https://theconversation.com/in-a-chatty-world-losing-your-speech-can-be-alienating-but-theres-help-121943">In a chatty world, losing your speech can be alienating. But there's help</a>
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<img src="https://counter.theconversation.com/content/212852/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Greig de Zubicaray receives funding from the Australian Research Council and National Health and Medical Research Foundation. </span></em></p>We’ve all forgotten the word we need mid-sentence, and know the feeling of it being just on the tip of our tongue. But when can this be more serious?Greig de Zubicaray, Professor of Neuropsychology, Queensland University of TechnologyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2002102023-02-22T12:54:03Z2023-02-22T12:54:03ZHow frontotemporal dementia, the syndrome affecting Wendy Williams, changes the brain – research is untangling its genetic causes<figure><img src="https://images.theconversation.com/files/511473/original/file-20230221-16-3xvr3l.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C1732%2C1732&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Some of the same genetic mutations can lead to FTD, ALS or symptoms of both.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/illustration/brain-lp-pr-royalty-free-illustration/1164761753">antoniokhr/iStock via Getty Images Plus</a></span></figcaption></figure><p>Around <a href="https://www.who.int/news-room/fact-sheets/detail/dementia">55 million people worldwide</a> suffer from dementia such as Alzheimer’s disease. On Feb. 22, 2024, it was revealed that former talk show host <a href="https://www.npr.org/2024/02/22/1233172648/wendy-williams-aphasia-frontotemporal-dementia-diagnosis">Wendy Williams</a> had been diagnosed with <a href="https://www.theaftd.org/what-is-ftd/disease-overview/">frontotemporal dementia, or FTD</a>, a rare type of dementia that typically affects people <a href="https://www.alzheimers.gov/alzheimers-dementias/frontotemporal-dementia">ages 45 to 64</a>. <a href="https://apnews.com/article/what-is-frontotemporal-dementia-bruce-willis-fbfdbfca4793bb65ef3f38f31e31bd68">Bruce Willis</a> is another celebrity who was diagnosed with the syndrome, according to his family. In contrast to Alzheimer’s, in which the major initial symptom is memory loss, FTD typically involves changes in behavior.</p>
<p>The <a href="https://www.nia.nih.gov/health/what-are-frontotemporal-disorders">initial symptoms of FTD</a> may include changes in personality, behavior and language production. For instance, some FTD patients exhibit inappropriate social behavior, impulsivity and loss of empathy. Others struggle to find words and to express themselves. This insidious disease can be especially hard for families and loved ones to deal with. There is no cure for FTD, and there are no effective treatments.</p>
<p><a href="https://www.theaftd.org/genetics-of-ftd/">Up to 40% of FTD cases</a> have some family history, which means a genetic cause may run in the family. Since researchers identified the first genetic mutations that cause FTD in 1998, <a href="https://doi.org/10.15252%2Fembj.201797568">more than a dozen genes</a> have been linked to the disease. These discoveries provide an entry point to determine the mechanisms that underlie the dysfunction of neurons and neural circuits in the brain and to use that knowledge to explore potential approaches to treatment.</p>
<p><a href="https://profiles.umassmed.edu/display/130139">I am a researcher</a> who studies the development of FTD and related disorders, including the motor neuron disease <a href="https://www.als.org">amyotrophic lateral sclerosis, or ALS</a>. ALS, also known as Lou Gehrig’s disease, results in progressive muscle weakness and death. Uncovering the similarities in pathology and genetics between FTD and ALS could lead to new ways to treat both diseases.</p>
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<figcaption><span class="caption">Wendy Williams’ care team announced her diagnosis of frontotemporal dementia on Feb. 22, 2024.</span></figcaption>
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<h2>Genetic causes of FTD</h2>
<p>Genes contain the instructions cells use to make the proteins that carry out functions essential to life. Mutated genes can result in mutated proteins that lose their normal function or become toxic. </p>
<p>How mutated proteins contribute to FTD has been under intense investigation for decades. For instance, one of the key proteins in FTD, called <a href="https://doi.org/10.1016%2Fj.neuron.2011.04.009">tau</a>, helps stabilize certain structures in neurons and can form clumps in diseased brains. Another key protein, <a href="https://doi.org/10.1038%2Fnrn.2017.36">progranulin</a>, regulates cell growth and a part of the cell called the lysosome that breaks down cellular waste products.</p>
<p>Remarkably, the most common genetic mutation in FTD – in a gene called C9orf72 – <a href="https://doi.org/10.15252%2Fembj.201797568">also causes ALS</a>. In fact, apart from the mutations in genes that encode for tau and progranulin, most genetic mutations that cause FTD <a href="https://doi.org/10.15252%2Fembj.201797568">also cause ALS</a>. Another protein, <a href="https://doi.org/10.15252/embj.201797568">TDP-43</a>, forms clumps in the brains of over 95% of ALS cases and almost half of FTD cases. Thus, these disorders share close links in genetics and pathology.</p>
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<figcaption><span class="caption">Frontotemporal dementia typically affects people under 60.</span></figcaption>
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<h2>Modifier genes</h2>
<p>The same genetic mutation can cause FTD in one patient, ALS in another or symptoms of both FTD and ALS at the same time. Remarkably, some people who carry these genetic mutations may have no obvious symptoms for decades.</p>
<p>One reason the same mutation can cause both FTD and ALS is that, in addition to <a href="https://theconversation.com/als-is-only-50-genetic-identifying-dna-regions-affected-by-lifestyle-and-environmental-risk-factors-could-help-pinpoint-avenues-for-treatment-179169">lifestyle and environmental factors</a>, other genes may also influence whether mutated genes lead to disease. Identifying these <a href="https://doi.org/10.1016%2Fj.neuron.2020.08.022">modifier genes</a> in FTD, ALS and other neurodegenerative diseases could lead to new treatment approaches by boosting the activity of those that protect against disease or suppressing the activity of those that promote disease. </p>
<p>Modifier genes have long been a focus of research in <a href="https://www.umassmed.edu/fen-biaogaolab/">my laboratory</a> at the University of Massachusetts Chan Medical School. When my laboratory was still in San Francisco, we collaborated with neurologist <a href="https://profiles.ucsf.edu/bruce.miller">Bruce Miller</a> and generated the first stem cell lines from FTD patients with mutations in <a href="https://doi.org/10.1016%2Fj.celrep.2012.09.007">progranulin</a> and <a href="https://doi.org/10.1007%2Fs00401-013-1149-y">C9orf72</a>. These stem cells can be turned into neurons for researchers to study in a petri dish. My team also uses fruit flies to identify modifier genes and then test how they influence disease in neurons from patients with FTD or ALS.</p>
<p>For instance, in close collaboration with cell biologist <a href="https://www.stjude.org/directory/t/j-paul-taylor.html">J. Paul Taylor</a>, my laboratory was among the first to discover a small <a href="https://doi.org/10.1038%2Fnature14974">subset of modifier genes</a> that help transport molecules into or out of the nucleus of a neuron. We also <a href="https://doi.org/10.1016%2Fj.neuron.2016.09.015">discovered</a> <a href="https://doi.org/10.1073%2Fpnas.1901313116">modifier genes</a> that encode for some proteins that help repair damaged DNA. Targeting these modifier genes using <a href="https://doi.org/10.1089%2Fnat.2018.0725">gene-silencing techniques</a> developed by Nobel laureate <a href="https://www.nobelprize.org/prizes/medicine/2006/mello/facts/">Craig Mello</a> and other researchers at UMass Chan could offer potential treatments.</p>
<h2>Treating behavioral changes in FTD</h2>
<p>Because the brain is an extremely complex organ, it can be very difficult to understand what causes personality and behavioral changes in FTD patients. </p>
<p>Over the years, my team has used mice to study the causes of these changes. For instance, we found that the reduced social interaction we observed in mice engineered to have FTD is linked to <a href="https://doi.org/10.1038%2Fnm.3717">two different</a> <a href="https://doi.org/10.1038%2Fs41593-019-0397-0">disease proteins</a> in the same part of the brain, suggesting that this symptom may be caused by defects in the same neural circuit. These deficits could be reversed by injecting a molecule called <a href="https://doi.org/10.1038%2Fnm.3717">microRNA-124</a> into the prefrontal cortex, the part of the brain that controls social behaviors.</p>
<p>Moreover, with my longtime collaborator neuroscientist <a href="https://www.upstate.edu/psych/faculty.php?empID=yaow">Wei-Dong Yao</a>, our labs found that mice with FTD have <a href="https://doi.org/10.1038%2Fnm.3717">defects at</a> <a href="https://doi.org/10.1038%2Fs41593-019-0397-0">the synapses</a> in this part of the brain. Synapses are areas where neurons are in contact with each other and play an important role in transporting information in the nervous system. Recently, he found that <a href="https://doi.org/10.1016/j.neuron.2022.12.027">lack of empathy</a> in another mouse model of FTD could be reversed by increasing activity in the prefrontal cortex. </p>
<p>Further research to understand the molecular mechanisms and brain circuitry behind FTD offer hope that its devastating symptoms, including behavioral and personality changes, will be treatable in the future.</p>
<p><em>This is an updated version of an article originally published on Feb. 22, 2023.</em></p><img src="https://counter.theconversation.com/content/200210/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Fen-Biao Gao receives and has previously received funding from the NIH, The Muscular Dystrophy Association, The Association for FTD, Target ALS Foundation, The ALS Association, The Tau Consortium, The Consortium for Frontotemporal Dementia Research, The Ricico Fund, The Cellucci Fund, Merck, and Stealth BioTherapeutics.
He works for the NIH as a member of its CMND study section, for The Muscular Dystrophy Association as a member of its Research Advisory Council and for The Association for FTD as a member of its Scientific Review Panel. </span></em></p>FTD leads to changes in personality and behavior. Understanding its genetic and molecular causes could lead to new ways to treat neurodegenerative diseases.Fen-Biao Gao, Professor of RNA Therapeutics, Governor Paul Cellucci Chair in Neuroscience Research, Founding Director of Frontotempral Dementia Research Center, UMass Chan Medical SchoolLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2001882023-02-20T16:59:51Z2023-02-20T16:59:51ZBruce Willis has frontotemporal dementia – here’s what we know about the disease<p>American actor Bruce Willis has frontotemporal dementia, his family <a href="https://www.theaftd.org/mnlstatement23/?utm_source=Instagram&utm_medium=Social&utm_campaign=MNL23">has announced</a>. </p>
<p>In 2022, the 67-year-old action movie star was diagnosed with aphasia - difficulty with language and speech. Aphasia can occur for a variety of reasons (most commonly stroke) but for Willis, it is now clear that these speech problems were the early signs of this particularly devastating form of dementia.</p>
<p>Frontotemporal dementia is an umbrella term for any disease that causes gradual loss of brain tissue in the frontal and temporal lobes – the front and sides of the brain. Although relatively rare, it is one of the <a href="https://www.sciencedirect.com/science/article/abs/pii/S0140673615004614?casa_token=lhrMHpWtzX8AAAAA:RnIiGCV4kTZvK8B_wTahB6zSfbDDkInhein8Q0c6hOxBYwt1IfERPE9a81azNeMMruA-X3BDwg">most common causes of dementia in people under the age of 65</a>, accounting for around <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0039-1683379">40% of early-onset cases</a>. </p>
<p>The condition – which goes by other names, such as Pick’s disease, frontal dementia, semantic dementia and primary progressive aphasia – tends to develop slowly, over several years. </p>
<p>A build-up of abnormal proteins affects critical brain areas, leading to changes in behaviour, personality and speech. Unlike other forms of dementia, such as Alzheimer’s disease, memory is often only affected later in the disease’s progression.</p>
<p>There are three different variants of frontotemporal dementia: the “behavioural variant”, “non-fluent variant primary aphasia” and “semantic variant primary aphasia”. Each of these will initially present differently and can be mistaken for other conditions. </p>
<p>The earliest signs of the behavioural variant include changes in how a person acts, particularly in social situations. They may become tactless or make rash decisions. Or they may behave inappropriately, for example, by making sexual advances. Some may develop obsessive ritualistic behaviour, or lose all sense of empathy and caring. </p>
<p>These symptoms reflect damage to the frontal lobes, an area of the brain involved in directing our behaviour, controlling our impulses, managing our emotions and generating speech and movement. </p>
<p>When they stop working, people tend to lack insight into their own behaviour or how they have changed. Their relatives find it particularly hard because they can’t have frank conversations with their loved ones as they can’t see what the problem is.</p>
<p>Diagnosis can be difficult because these symptoms also occur in other conditions where the frontal lobes are injured, such as strokes and tumours, so a full medical history and brain scans play an important role. To make things even more tricky for doctors, there is also significant overlap with several psychiatric disorders – for example, depression, schizophrenia and <a href="https://www.mind.org.uk/information-support/types-of-mental-health-problems/obsessive-compulsive-disorder-ocd/about-ocd/">obsessive-compulsive disorder</a>. This can lead to <a href="https://academic.oup.com/brain/article/143/6/1632/5780435?login=false&casa_token=s3qwRZP0lPUAAAAA:KvqHOebNUZ2Qw_nxSFVcM9kRAsVqW5C4WUW73adScVC6BN307oEVsJsNATi0PIt9vO3uIRKX_pdgnrc">misdiagnosis or a missed diagnosis</a>, especially in the early stages of the disease. </p>
<figure class="align-center ">
<img alt="Doctors looking at brain scans" src="https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=425&fit=crop&dpr=1 754w, https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=425&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/511129/original/file-20230220-28-rrg7c0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=425&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">Brain scans can detect signs of dementia and help identify which parts of the brain are most affected.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/control-room-doctor-radiologist-discuss-diagnosis-1243953511">Gorodenkoff/Shutterstock</a></span>
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<p>We don’t know which variant Willis has been diagnosed with, but his family has reported that his earlier symptoms relate to difficulties with speech, a feature that is typically seen at the onset of the other two variants. In these cases, there is a gradual loss in the ability to speak and understand language. </p>
<p>As the disease progresses, brain cells across the frontal and temporal lobes are destroyed. And, regardless of the variant, people will eventually experience many of the symptoms above. This is accompanied by increasing difficulty with walking and moving. By the end, most struggle to eat and swallow.</p>
<p>Frontotemporal dementia is a devastating and life-changing disease for which we have no cure and little in the way of treatment. For now, the focus is on managing symptoms and maximising quality of life. This may involve helping people develop ways to manage their emotions and behaviour, or drugs such as antidepressants and antipsychotics.</p>
<h2>Genes provide clues</h2>
<p>There is some room for hope. In recent years, scientists <a href="https://discovery.ucl.ac.uk/id/eprint/10073844/3/Warren%20Sivasathiaseelan_SemNeurol_FINAL.pdf">have made progress</a> in understanding more about which brain cells are being affected. One in eight sufferers will have frontotemporal dementia in the family, and important clues about the disease process are emerging from <a href="https://www.nature.com/articles/s41582-019-0231-z">detailed analysis of the genetics</a>. </p>
<p>The key now is to translate this research into earlier and better diagnosis, and ultimately to develop drugs that will halt or reverse this devastating disease.</p><img src="https://counter.theconversation.com/content/200188/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Catherine Loveday 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>In March 2022, it was announced that Willis had aphasia. The latest diagnosis is sadly worse.Catherine Loveday, Professor, Neuropsychology, University of WestminsterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1762482022-02-17T19:05:12Z2022-02-17T19:05:12ZDo we really ‘lose our filter’ as we age?<figure><img src="https://images.theconversation.com/files/446661/original/file-20220215-13-1ofytjq.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C5991%2C3979&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">Eduardo Barrios/Unsplash</span>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>Many of us will have experienced some unexpected honesty from the older people in our lives. Whether it’s grandma telling you your outfit is unflattering or grandpa saying he doesn’t like the meal you’ve prepared, we often explain it away by saying “Oh, don’t mind grandpa, he’s just lost his filter”. </p>
<p>But do we really have a “filter”, and do we lose it as we get older?</p>
<h2>What do we mean when we say ‘filter’?</h2>
<p>When someone has no “filter”, it means they say things without thinking about their audience. They may blurt out something rude, inappropriate, or unkind, without considering the likely consequences.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=900&fit=crop&dpr=1 600w, https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=900&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=900&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1131&fit=crop&dpr=1 754w, https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1131&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/446659/original/file-20220215-19-1bzf1j9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1131&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
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<span class="caption">‘Darling, these taste like crap.’ Sometimes Granny is a bit too honest.</span>
<span class="attribution"><span class="source">Andres Molina/Unsplash</span></span>
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<p>“Filters” are an important part of our everyday social interactions. A brief Monday morning chat with your boss is more complex than it may seem. For example, you might stop yourself from telling them they smell awful after their morning bike ride into the office and should’ve showered before your meeting. You might consider telling them about the fungal infection you discovered on your toenail over the weekend but decide against it. Of course, what you do or do not say also depends on how well you know them and what’s considered socially acceptable in your workplace. </p>
<p>Your “filter” relies on cognitive processes such as inhibitory control, which stops you from saying the first thing that pops into your mind. It also relies on social cognition, which refers to the ability to understand and predict other people’s behaviours, thoughts, and intentions. This helps us to recognise what behaviour is appropriate in a particular social setting and to adapt our behaviour based on this. </p>
<p>The prefrontal cortex, which is located within the frontal lobes of our brains, acts as our “filter”, helping us say and do things in a socially appropriate way. When this part of the brain isn’t functioning properly, we might act as though we’ve lost our “filter”.</p>
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Read more:
<a href="https://theconversation.com/five-common-myths-about-the-ageing-brain-and-body-67699">Five common myths about the ageing brain and body</a>
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<h2>What happens to our ‘filter’ as we age?</h2>
<p>As we get older, our brains start to shrink. This is a normal part of the ageing process known as brain atrophy. It affects how well our brain cells can communicate with one another. Importantly, brain atrophy doesn’t happen to all areas of the brain at once. It is particularly noticeable in the <a href="https://pubmed.ncbi.nlm.nih.gov/20298790/">frontal lobes</a>. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/446663/original/file-20220215-21-1j5q35z.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"></a>
<figcaption>
<span class="caption">The area of the brain that controls our social cognition shrinks as we age.</span>
<span class="attribution"><span class="source">Tim Kilby/Unsplash</span>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>Researchers have linked age-related shrinking in the frontal lobes with declines in <a href="https://link.springer.com/article/10.3758/s13415-015-0378-z">inhibitory control</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341664/">social cognition</a>. Studies have also found older adults respond differently to <a href="https://pubmed.ncbi.nlm.nih.gov/19290759/">socially awkward situations</a> than younger adults. </p>
<p>For example, older adults have more difficulty recognising when someone’s said something embarrassing or <a href="https://pubmed.ncbi.nlm.nih.gov/21280951/">tactless</a>, and show poorer understanding of <a href="https://pubmed.ncbi.nlm.nih.gov/33220614/">sarcasm</a>.</p>
<p>So as we get older, normal ageing processes in our brains may make it much easier for things to slip out through our “filters”.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/whats-happening-in-our-bodies-as-we-age-67931">What's happening in our bodies as we age?</a>
</strong>
</em>
</p>
<hr>
<h2>What if it’s more than just a few slip-ups?</h2>
<p>In some rare cases, losing your “filter” can be a sign of something more serious, such as damage to the frontal lobes due to a brain injury or stroke, or a neurodegenerative condition such as <a href="https://www.dementia.org.au/information/about-dementia/types-of-dementia/frontotemporal-dementia">frontotemporal dementia</a>.</p>
<p>People with frontotemporal dementia present with striking changes in their personality and social behaviour. This could involve losing their normal inhibitions, disregarding social conventions and other socially inappropriate or embarrassing behaviour. </p>
<p>However, these changes are completely out of character and are typically accompanied by other symptoms such as rigidity, loss of empathy, apathy, difficulties with reasoning and judgement, overeating or unusual food preferences and declines in self-care and personal hygiene. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/explainer-how-is-frontotemporal-dementia-different-and-what-are-the-warning-signs-95436">Explainer: how is frontotemporal dementia different and what are the warning signs?</a>
</strong>
</em>
</p>
<hr>
<h2>What other things could be at play?</h2>
<p>Aside from changes in the brain that impact inhibitory control and social cognition, it could simply be that as we get older, we care less about what others think.</p>
<p>Compared to younger adults, older adults are <a href="https://pubmed.ncbi.nlm.nih.gov/28006977/">less self-conscious</a>, reporting fewer experiences of emotions such as shame, guilt, and embarrassment. They also have higher overall levels of <a href="https://pubmed.ncbi.nlm.nih.gov/27561149/">happiness and life satisfaction</a>. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Man in top hat" src="https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=402&fit=crop&dpr=1 600w, https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=402&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=402&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=505&fit=crop&dpr=1 754w, https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=505&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/446662/original/file-20220215-4191-1gd1xpq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=505&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Older people are also just more comfortable in their own skin.</span>
<span class="attribution"><span class="source">Freddy Kearney/Unsplash</span>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>Perhaps we learn to let go of our “filters” and embrace the social awkwardness as we get older. Perhaps grandpa really didn’t like your cooking, and feels secure enough to tell you.</p>
<p>So, what does this mean for those of us who seem to be losing our “filter”?</p>
<p>Based on what we know about the brain and ageing, blurting out a remark without thinking isn’t necessarily something to be alarmed about. And if you’re on the receiving end, try not to take it too personally. If these remarks seem out of character or extreme, however, consider raising this with other family members or a doctor.</p><img src="https://counter.theconversation.com/content/176248/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Stephanie Wong receives funding from the National Health and Medical Research Council.</span></em></p><p class="fine-print"><em><span>Hannah Keage 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>Sometimes Granny can be a bit too honest. This is a normal part of ageing.Stephanie Wong, Lecturer/Research Fellow in Psychology, Flinders UniversityHannah Keage, Associate Professor of Psychology, University of South AustraliaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1141352019-03-27T18:25:51Z2019-03-27T18:25:51ZAn unexpected pathway to treating neurodegenerative diseases<figure><img src="https://images.theconversation.com/files/266160/original/file-20190327-139349-1h40qtz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">An MRI image of the brain.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/mri-image-head-showing-brain-344282432">SpeedKingz/Shutterstock.com</a></span></figcaption></figure><p>Scientific success stories can sometimes occur when therapies being studied for one disease can be used to treat another.</p>
<p>In the case of the drug we have been <a href="https://ken-kosik.mcdb.ucsb.edu">studying in my lab</a>, this is especially important because it could be used to develop a drug for Alzheimer’s. This cancer drug, lonafarnib, may be able to rid the cell of abnormal tau proteins and the clumps of tau protein called tangles that, together with other abnormal proteins called senile plaques, are the <a href="https://www.nia.nih.gov/health/alzheimers">hallmarks of Alzheimer’s disease</a>. Plaques and tangles are two structures easily observed under the microscope in the brains of deceased Alzheimer’s patients. </p>
<p><a href="https://ken-kosik.mcdb.ucsb.edu/people/kenneth-kosik">I am neurologist</a> and a <a href="https://www.ncbi.nlm.nih.gov/pubmed?term=kosik%20ks">neurobiologist</a> and have been interested in the diseases associated with the tau protein for nearly three decades, first while I worked at the Harvard Medical School and Brigham and Women’s Hospital and now at the University of California, Santa Barbara, where I co-direct the <a href="https://www.nri.ucsb.edu">Neuroscience Research Institute</a>. </p>
<p>We used mice engineered to develop tau tangles, and showed in my lab that lonafarnib <a href="http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aat3005">prevents their formation</a>. This approach, called repurposing, is the use of a drug originally invented to treat one disease, but is unexpectedly effective in another. Because tau in the neurofibrillary tangles is a critical feature of Alzheimer’s, a disease that has risen to <a href="https://doi.org/10.1016/j.jalz.2018.06.3063">pandemic proportions worldwide</a>, I believe this repurposed drug should be a high priority for testing in clinical trials. </p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/0GXv3mHs9AU?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">A simple explainer on Alzheimer’s and the tau and A-beta proteins.</span></figcaption>
</figure>
<h2>Preventing tangles</h2>
<p>The key component of neurofibrillary tangles is the tau protein, a normal brain protein that in the course of the disease aggregates into long rope-like structures and ultimately strangles neurons in disease. This transition from a normal protein to an aggregate is the focus of our research and using a repurposed drug was a useful way to probe the transition.</p>
<p>One thing that is exciting about repurposing this cancer drug is that testing has clearly demonstrated its safety in humans. Society does not currently have any medication that can modify or prevent Alzheimer’s – which underscores the importance of following our results from mice to patient testing. However, many details need to be worked out before a trial can proceed and the most appropriate study subjects chosen.</p>
<p>Nevertheless, it is now a good time to move promising drugs to the clinic given the <a href="https://www.statnews.com/2019/03/21/biogen-eisai-alzheimer-trial-stopped/">recent failures</a> of many drug trials for Alzheimer’s disease.</p>
<p>So how did we link a cancer drug with the tau protein? </p>
<p>The first step before even being aware of the cancer drug was a difficult and risky experiment we conducted that had a surprising outcome. We collected skin cells from patients with a form of dementia called <a href="https://www.nia.nih.gov/health/topics/frontotemporal-disorders">frontotemporal dementia</a> that has only neurofibrillary tangles but no senile plaques. In the absence of senile plaques, we cannot call this disease Alzheimer’s even though neurofibrillary tangles made of tau are a shared feature. </p>
<p>This disease simplified our quest because we didn’t have to worry about the plaques. But we believe the findings will certainly be relevant to Alzheimer’s disease especially as researchers increasingly appreciate the importance of the tangles in causing the dementia. </p>
<p>Furthermore, in the cases we studied, we knew the specific cause of the patients’ dementia; these patients all had mutations in their tau gene. We sampled and grew their skin cells in the lab using a specialized technique and then compared them with skins cells from patients with normal tau. We detected a gene, and the protein it produced – Rhes – that was abnormally turned on in the cells from patients with the tau mutations but not in the control cells. That was the ah-ha moment because the Rhes protein belongs to a family of proteins targeted by the cancer drug, lonafarnib.</p>
<p>Then came the mental leap, which makes science exciting. </p>
<h2>Targeting tau for the trash compactor</h2>
<p>Like most proteins, this one, Rhes, has multiple functions, and deciding which specific function to pursue requires both savvy and luck. In our case, we found a drug that lowered the level of the Rhes protein and enabled the abnormal tau protein to get directed into a cell compartment that degrades proteins. This compartment is called the lysosome, and it acts like a trash compactor. This organelle destroys tau before it can form tangles. </p>
<p>To test this drug we used genetically engineered mice that develop human tau tangles and then dementia. Such animals often run in circles. But when we fed these animals lonafarnib, the drug blocked the formation of the tau tangles in the brain and the abnormal behavior. </p>
<p>When tau tangles disrupt the normal brain activity, the mice are unable to build nests. But the mice receiving the drug proceeded with nest-building and other normal behaviors. Mice that were untreated all developed dementia. </p>
<p>Seeing these results and then replicating them several times were exhilarating moments and is the reward for many experiments that do not work. However, any student considering doing this type of research should have a comfort level with the long game.</p><img src="https://counter.theconversation.com/content/114135/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Kenneth S. Kosik owns shares in ADRx and Minerva Pharmaceuticals. He receives funding from the NIH, The Edward N. & Della L. Thome Memorial Foundation and the Larry H. Hillblom Foundation.
</span></em></p>Not all drug development needs to start from scratch. Sometimes researchers discover that a drug developed for one disease can be used for another. Here a cancer drug may show promise for dementia.Kenneth S. Kosik, Professor of Neuroscience, University of California, Santa BarbaraLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/954362018-05-17T02:06:28Z2018-05-17T02:06:28ZExplainer: how is frontotemporal dementia different and what are the warning signs?<figure><img src="https://images.theconversation.com/files/219148/original/file-20180516-155573-186kstn.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Not all types of dementia start in the elderly, or with memory loss.</span> <span class="attribution"><span class="source">from www.shutterstock.com</span></span></figcaption></figure><p>When most people hear about dementia, they picture older people with memory loss. But not all types of dementia start with memory loss. </p>
<p>In the same way cancer can be classified as melanoma, prostate cancer or bowel cancer, dementia can also be classified into many different types. The most common type is Alzheimer’s disease, which affects the parts of the brain responsible for memory.</p>
<p>In other types of dementia, the first symptoms may include changes in personality and behaviour. These types of symptoms are prominent in <a href="https://www.dementia.org.au/information/about-dementia/types-of-dementia/frontotemporal-dementia">frontotemporal dementia</a>. </p>
<p>Frontotemporal dementia is a common cause of dementia in people under the age of 65. New research from <a href="https://sydney.edu.au/brain-mind/our-research/healthy-ageing-and-neurodegeneration/forefront-ageing-and-neurodegeneration-team/frontier-frontotemporal-dementia-research-group.html">our clinic</a> has helped us to understand the common symptoms.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/we-can-change-our-brain-and-its-ability-to-cope-with-disease-with-simple-lifestyle-choices-91699">We can change our brain and its ability to cope with disease with simple lifestyle choices</a>
</strong>
</em>
</p>
<hr>
<h2>Symptoms</h2>
<p>Individuals with frontotemporal dementia have atrophy (or shrinkage) of the frontal lobes of the brain. The frontal lobes are important for controlling voluntary behaviour, emotions and complex thought.</p>
<p>One carer described how her husband would inappropriately approach young women, often interrupt conversations and make offensive remarks about other people’s appearances. This was completely out of character for him.</p>
<p>The symptoms are diverse and can differ from person to person. </p>
<p>Currently there is no diagnostic test for frontotemporal dementia. So, to diagnose frontotemporal dementia we rely on careful assessment of a person’s symptoms. Six key symptoms are recognised, and individuals must show a combination of these symptoms to be diagnosed.</p>
<ol>
<li><p>Some people make impulsive decisions (also known as disinhibition). People with frontotemporal dementia often overspend, gamble or buy items for which they have little use. This makes them <a href="https://www.sciencedirect.com/science/article/pii/S002839321730310X?via%3Dihub">particularly susceptible</a> to financial scams or exploitation. In one instance, a man sent large sums of money to what he thought was a charitable organisation, to the point where he needed to withdraw from his superannuation and sell his house to cover the enormous debt he had incurred.</p></li>
<li><p>Other people become apathetic or lose motivation or interest in doing things. If left to their own devices, a person with frontotemporal dementia will often sit in front of the television, unable to initiate any purposeful behaviour. They show a loss of interest in activities or hobbies they previously enjoyed, and require prompting to engage with others. <a href="https://www.sciencedirect.com/science/article/pii/S001094521830100X?via%3Dihub">Research in frontotemporal dementia</a> has linked apathy to damage in key areas of the brain that process rewards.</p></li>
<li><p>Some individuals show reduced empathy, which refers to the ability to understand and share how somebody else is feeling. Carers often report their loved ones no longer respond appropriately to other people’s emotions. This apparent lack of concern can sometimes be misinterpreted as self-centeredness. Our new research found people with frontotemporal dementia have difficulty interpreting <a href="https://www.sciencedirect.com/science/article/pii/S0010945218300613">facial information that is vital for recognising emotions</a>.</p></li>
<li><p>Changes in eating behaviour can occur in people with frontotemporal dementia. They will often overeat or show an increased preference for sugary foods (in one example, eating two tubs of ice-cream every night). These changes in eating behaviour have been linked with disruptions to the brain’s <a href="https://jamanetwork.com/journals/jamaneurology/fullarticle/2484444">endocrine, autonomic and reward-processing systems</a>.</p></li>
<li><p>Some people with frontotemporal dementia show patterns of repetitive or ritualistic behaviour. Examples include obsessions with counting and clock-watching, restricted interests in leisure activities or hobbies, and rigid adherence to certain daily routines or food preferences.</p></li>
<li><p>People with frontotemporal dementia often have problems with complex thinking. Tasks such as planning a trip to the doctor or working out how much change to expect from the cashier can be challenging.</p></li>
</ol>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/how-australians-die-cause-3-dementia-alzheimers-57341">How Australians Die: cause #3 – dementia (Alzheimer's)</a>
</strong>
</em>
</p>
<hr>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/219147/original/file-20180516-155584-13qd1sm.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"></a>
<figcaption>
<span class="caption">Some people with frontotemporal dementia make impulsive decisions such as overspending or gambling.</span>
<span class="attribution"><span class="source">from www.shutterstock.com</span></span>
</figcaption>
</figure>
<h2>Causes</h2>
<p>Family members of patients with frontotemporal dementia often find these behavioural changes more distressing and difficult to deal with than memory loss. Because these changes seem so diverse and unrelated, current research and clinical practice tend to treat each symptom separately. And the available treatments are limited in their effectiveness.</p>
<p>In our <a href="https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awy123/4995212">recent review article</a>, we identified a common thread that links these seemingly unrelated behavioural symptoms. It appears that disinhibition, apathy, reduced empathy, overeating and repetitive actions can all be traced back to shrinking of brain areas that control goal-directed behaviour.</p>
<p>Goal-directed behaviour allows us to modify our actions to achieve certain goals or desires. For example, if you feel thirsty you will go to the fridge and get a drink. If you want a job promotion you will work hard and make sure you don’t offend your co-workers. If you enjoy skiing you might go on a trip to the snow.</p>
<p>When the brain’s goal-directed behaviour system goes awry, an individual may have difficulty choosing whether to continue eating despite feeling full, respond to another person’s distress, approach strangers or engage in their hobbies. As a result of losing goal-directed control, behaviour can become restricted and repetitive.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/six-things-you-can-do-to-reduce-your-risk-of-dementia-93061">Six things you can do to reduce your risk of dementia</a>
</strong>
</em>
</p>
<hr>
<h2>Where to from here?</h2>
<p>Limited awareness of frontotemporal dementia and the diversity of its symptoms often lead to misdiagnosis or delays in diagnosis. Behavioural changes tend to be mistaken for symptoms of depression or psychiatric disorders. </p>
<p>Educating the general public and health professionals about the different types of dementia and the variety of symptoms is an important step in reducing the time it takes to reach a diagnosis. </p>
<p>In the absence of a cure, a major challenge is to develop appropriate and effective management strategies for those living with dementia. We hope this <a href="https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awy123/4995212">new research</a> can help us find interventions for these often misunderstood symptoms.</p>
<hr>
<p><em>If you know someone with frontotemporal dementia or would like to get involved in our research, you can find more information <a href="https://sydney.edu.au/brain-mind/our-research/healthy-ageing-and-neurodegeneration/forefront-ageing-and-neurodegeneration-team/frontier-frontotemporal-dementia-research-group.html">here</a> or contact frontier@sydney.edu.au.</em></p><img src="https://counter.theconversation.com/content/95436/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Fiona Kumfor receives funding from the National Health and Medical Research Council (NHMRC). </span></em></p><p class="fine-print"><em><span>Rosalind Hutchings and Stephanie Wong do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Frontotemporal dementia typically affects people under 65 and is about more than memory loss – this is what to look out for.Stephanie Wong, Research officer, University of SydneyFiona Kumfor, Senior research fellow, University of SydneyRosalind Hutchings, PhD Candidate, University of SydneyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/206132013-12-11T03:37:55Z2013-12-11T03:37:55ZRobotic animals may help some people with dementia<figure><img src="https://images.theconversation.com/files/37314/original/y6yxtxv8-1386640420.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Animal-based therapies have a positive effect but having them visit nursing homes has a number of drawbacks.</span> <span class="attribution"><span class="source">Duane Keys</span></span></figcaption></figure><p>Late-stage dementia is characterised by increasing agitation that can be distressing for the person with the illness and their carers. So, researchers are investigating whether robots disguised as animals might be able to help reduce some of these difficult behaviours.</p>
<p>As their dementia progresses, people can become upset and pace or talk constantly, repeating meaningless words. Robotic animals may be able to help calm them by being engaging, giving them a sense of purpose and providing opportunities to communicate their feelings.</p>
<p>Animals have been used to help people with psychiatric problems or disabilities since the 1700s when people with mental disorders were encouraged to care for animals such as birds and rabbits as part of their therapy.</p>
<p>More recently, having dogs visit people in nursing homes has been shown to decrease levels of agitation and increase social behaviour. Indeed, a <a href="http://www.sciencedirect.com/science/article/pii/S0022395612003846">review</a> of the small number of research studies on the subject found animal-based therapies have a positive effect on communication and coping ability.</p>
<p>But having animals visit nursing homes has a number of drawbacks. Animals can be unpredictable, people may have allergies to them, they can be expensive and caring for them may be time-consuming.</p>
<h2>Using robots instead</h2>
<p>To address some of these problems, <a href="http://www.parorobots.com/">researchers in Japan</a> have designed a robotic baby seal, called Paro. This alternative to a real animal provides the benefits of animal therapy in places such as nursing homes and hospitals. </p>
<p>Paro has sensors that detect touch, light, sound and temperature, and is able to use this information to respond to people by fluttering its eyelashes or waving its tail and flippers. </p>
<p>The robots cost around A$5,000 each and can express emotions such as surprise, happiness, and anger. They can also learn to respond to their own name. </p>
<p><a href="http://www.healio.com/nursing/journals/jgn/%7B4148aa00-206b-4ba9-9e37-d730b6aecb90%7D/exploring-the-effect-of-companion-robots-on-emotional-expression-in-older-adults-with-dementia-a-pilot-randomized-controlled-trial">Early studies</a> have found that, just like animal therapy, the introduction of robotic animals can improve quality of life and mood in people with dementia.</p>
<p>But there are outstanding issues with using robots as therapy for dementia patients.</p>
<p>For starters, there’s still little <a href="http://www.sciencedirect.com/science/article/pii/S0022395612003846">evidence</a> supporting their use. Studies often include only a few people, and benefits are based on researcher observations rather than being measured systematically. </p>
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<iframe width="440" height="260" src="https://www.youtube.com/embed/Vx8mv87e6wE?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Japanese researchers have created this robotic seal called Paro.</span></figcaption>
</figure>
<p>And robot therapy may not be appropriate for all kinds of dementia.</p>
<h2>Emotional functioning and dementia</h2>
<p>Researchers have only been studying how social functioning and emotions are affected in people with dementia for a few years. </p>
<p>What has become clear in that time is the extent to which someone’s ability to understand and feel emotions is affected is dependent on the <a href="http://www.futuremedicine.com/doi/abs/10.2217/nmt.13.16">type of dementia</a> suffered, and the regions of the brain impacted. </p>
<p>The most common type of dementia is Alzheimer’s disease. In its early stages, people experience problems with their memories, with knowing what date it is and finding their way around.</p>
<p>But as brain shrinkage becomes more widespread, emotional functioning may be affected, and behavioural changes such as agitation become more common. </p>
<p>In contrast, in people with frontotemporal dementia, the earliest problems are changes in personality and behavioural functioning. </p>
<p><a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0067457">Research I have done with some colleagues</a> shows people with this kind of dementia have severe problems in understanding how other people feel. This can make social interaction particularly challenging, even in the very early stages of the disease. </p>
<h2>Who might benefit?</h2>
<p>Because the symptoms of these two types of dementia are so different, using robots as therapy might not be equally beneficial for everyone. </p>
<p>We know that people with frontotemporal dementia, for instance, have trouble distinguishing between emotions such as <a href="http://www.sciencedirect.com/science/article/pii/S0028393205000576">anger and sadness</a>. These people might find interactions with Paro confusing rather than comforting. </p>
<p>It’s also not clear whether robot-based therapy could improve cognition or thinking ability in people with dementia, and whether these types of interventions could change the way the brain functions. </p>
<p>Clearly, there’s still a long way to go in finding effective treatments for dementia. In the meantime, interventions that address some of the behavioural and social changes in people suffering dementia are of great importance.</p><img src="https://counter.theconversation.com/content/20613/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Fiona Kumfor 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>Late-stage dementia is characterised by increasing agitation that can be distressing for the person with the illness and their carers. So, researchers are investigating whether robots disguised as animals…Fiona Kumfor, Research Officer, Neuroscience Research AustraliaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/158722013-07-23T04:41:01Z2013-07-23T04:41:01ZMaking a mark on the brain - how emotion colours memories<figure><img src="https://images.theconversation.com/files/27884/original/g9x9b69p-1374553454.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Memories of emotionally-dense events are formed in great detail, allowing them to be remembered extremely vividly,</span> <span class="attribution"><span class="source">Julie Falk</span></span></figcaption></figure><p>All memories aren’t created equal. Whether you remember an event the next day, week or year, depends on a number of factors, the most important one of which is the emotion associated with it.</p>
<p>Emotional events capture attention faster that non-emotional ones. And people tend to reminisce more about them. So memories of emotionally-dense happenings are formed in great detail, allowing them to be remembered extremely vividly, even many years later.</p>
<h2>What you recall</h2>
<p>For instance, how well can you remember where you were when you heard the news of the September 11 terrorist attacks on the United States? Most people remember it in great detail – exactly where they were, who they were with, even the weather, or what was cooking in the kitchen. </p>
<p>Emotional memories such as these are known as “flashbulb memories”. These are special memories recalled in such great detail that it’s as if your brain took a photograph at the time.</p>
<p>The tendency for emotional events to be imprinted on the brain is not restricted to unexpected, public events. Events such as the birth of your child, your wedding day or arguments you’ve had, are also remembered more vividly and in greater detail than other routine events that occurred around the same time. </p>
<p>This remarkable phenomenon demonstrates how the brain adapts and colours our memory, depending on the circumstances.</p>
<h2>Where emotional memories are formed</h2>
<p>The idea that emotional memories are uniquely stored in the brain is not new. As early as 1890, the philosopher and psychologist William James suggested that emotional events leave “a scar upon the cerebral tissues”. </p>
<p>The brain regions underpinning this emotional boost, however, have not been well understood.</p>
<p>In 1994, neuroscientist Ralph Adolphs, described a woman he called S.M., who suffers from a rare genetic disease called Urbach-Wiethe disease. This illness causes a specific structure in the brain known as the amygdala to wither and shrink away.</p>
<p>Patient S.M. experiences no fear and has difficulty recognising fear in others. Most surprisingly, her emotional memories are severely affected, showing none of the emotional boost that is usually seen in healthy adults. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=572&fit=crop&dpr=1 600w, https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=572&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=572&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=719&fit=crop&dpr=1 754w, https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=719&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/27887/original/vhjv5yjk-1374554071.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=719&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"></span>
<span class="attribution"><span class="source">Zachary Veach</span></span>
</figcaption>
</figure>
<p>S.M. provided an important piece of information about where in the brain emotional memories may be formed. </p>
<h2>Memories and dementia</h2>
<p>In order to investigate emotional memories more closely, our research groups examined this fascinating phenomenon in patients with frontotemporal dementia. This is a rare form of dementia that affects people in their 50s and 60s. Unfortunately, no treatment or cure exists. </p>
<p>People with frontotemporal dementia struggle in social situations and have difficulty understanding how other people are feeling, suggesting that the parts of their brain important for emotion are affected. </p>
<p>We showed patients with frontotemporal dementia and healthy adults, pictures that normally evoke an emotional response (snakes, for instance, and car accidents). We then tested their memory for the emotional pictures and other non-emotional pictures (houses and cups). </p>
<p>Patients with frontotemporal dementia showed no emotional boost, whereas healthy adults remembered more of the pictures linked to strong feelings. This showed that emotional memories are disturbed in frontotemporal dementia. </p>
<p>When we related this loss of emotional memories to changes in the brain, we discovered that shrinkage in the orbitofrontal cortex was responsible. </p>
<p>Our findings provide new information about where emotional memories are formed. We showed that it’s not only the amygdala, but also the orbitofrontal cortex, that’s crucial for the formation of strong memories.</p>
<h2>A grey world</h2>
<p><a href="http://brain.oxfordjournals.org/cgi/content/full/awt185?%0Aijkey=W0toELuxV7zY9Wc&keytype=ref">Our results</a> provide crucial insight into how people with frontotemporal dementia experience the world. It appears that for these patients, emotional life events, such as attending their daughter’s wedding, are only as memorable as mundane events, such as refilling the car with petrol. </p>
<p>One can only imagine how isolating it must be for people to have their memories stripped of emotional content, as they cannot experience the rich detail of important life events that colours the memories of healthy people.</p>
<p>Continued understanding of the complex interplay between emotion and memory will not only help us identify <em>how</em> we remember things, but also <em>why</em> we remember some things better than others. </p>
<p>Improved understanding of these processes in the brain can offer important clues about how rich emotional experiences colour our memories and shape our experience of the world. </p><img src="https://counter.theconversation.com/content/15872/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Fiona Kumfor received funding from an Australian Postgraduate Award. This work was supported in part by an Australian Research Council Discovery Grant (DP1093279) and by the ARC Centre of Excellence in Cognition and its Disorders (CE110001021). </span></em></p>All memories aren’t created equal. Whether you remember an event the next day, week or year, depends on a number of factors, the most important one of which is the emotion associated with it. Emotional…Fiona Kumfor, Research Officer, Neuroscience Research AustraliaLicensed as Creative Commons – attribution, no derivatives.