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	<title>University of Bristol Archives - BRACE Alzheimer&#039;s Research</title>
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	<title>University of Bristol Archives - BRACE Alzheimer&#039;s Research</title>
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		<title>The South West Dementia Brain Bank</title>
		<link>https://www.alzheimers-brace.org/the-south-west-dementia-brain-bank/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Wed, 17 Feb 2021 16:21:07 +0000</pubDate>
				<category><![CDATA[South West Dementia Brain Bank]]></category>
		<category><![CDATA[University of Bristol]]></category>
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					<description><![CDATA[<p>The Brain Bank is based in the Learning and Research building at Southmead Hospital in Bristol, and contains brain tissue from more than 1300 donors.</p>
<p>The post <a href="https://www.alzheimers-brace.org/the-south-west-dementia-brain-bank/">The South West Dementia Brain Bank</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">The South West Dementia Brain Bank</span>
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	<p>BRACE has been a long-standing supporter of the South West Dementia Brain Bank (the Brain Bank), providing significant funding commitments since the charity’s creation in 1987.</p>
<p>It is one of the most influential dementia brain bank in the UK, with tissue samples from the bank underpinning dementia research projects across the country and globally.</p>
<p>The Brain Bank does not receive government funding and is reliant on charities like BRACE to keep their work going.</p>
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	<h3><strong>What is the Brain Bank?</strong></h3>
<p>The South West Dementia Brain Bank (SWDBB) is based in the Learning and Research building at Southmead Hospital in Bristol. It preserves and stores brain tissue from over 1,300 donors, including people who had various forms of dementia and older individuals without memory problems.</p>
<p class="whitespace-pre-wrap break-words">The donated tissue is frozen or fixed in formalin so it can be stored for a long time. Alongside each donation, comprehensive pathological information is collected. This preservation allows the tissue to remain viable for research for decades, supporting scientific studies across the UK and internationally.</p>
<p>It is a member of Brains for Dementia Research (BDR), a network of brain bank facilities across England and Wales. By coordinating work across brain banks, BDR aims to set a gold standard for brain donation, provide more information about the donors throughout their later life and increasing the number of brains donated. The Brain Bank is also a member of the UK Brain Bank Network, which was established to "provide high quality brain tissue to scientists and clinicians to carry out cutting edge neurosciences research" and to "support major initiatives on research into neurological disorders".</p>
<h3><strong>Why is the Brain Bank important?</strong></h3>
<p>The Brain Bank is a vital resource. New treatments cannot get to clinical trial stage without using human brain tissue first. Without it, we wouldn’t have drugs for Alzheimer’s disease.</p>
<p>Since 2011, the SWDBB has provided an extraordinary 81,577 tissue samples to researchers, enabling hundreds of peer-reviewed scientific publications and underpinning countless dementia research projects.</p>
<p>By comparing brain tissue from people who had dementia with tissue from those who did not, researchers can identify specific differences that reveal how dementia damages the brain. Post-mortem examination of brain tissue provides the only definitive diagnosis of dementia types, connecting specific symptoms with particular areas of brain damage.</p>
<p>BRACE has continuously supported the Brain Bank since 1987, providing over £2 million in funding during the past 20 years. With 761 potential donors currently registered and up to 50 new donations accepted annually, the Brain Bank continues to be a cornerstone of progress in dementia research.</p>
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	<p><a href="https://www.bristol.ac.uk/translational-health-sciences/research/neurosciences/research/south-west-dementia-brain-bank/" target="_blank" rel="noopener">For more information about the SWDBB, including how to become a brain donor, please click here</a></p>
<p><strong>The Medical Research Council produced this short video about the SWDBB:</strong></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/the-south-west-dementia-brain-bank/">The South West Dementia Brain Bank</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Research Snapshot: Dr Liz Coulthard &#8216;How does poor sleep relate to Alzheimer&#8217;s Disease?&#8217;</title>
		<link>https://www.alzheimers-brace.org/research-snapshot-dr-liz-coulthard-how-does-poor-sleep-relate-to-alzheimers-disease/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Wed, 17 Feb 2021 16:03:47 +0000</pubDate>
				<category><![CDATA[University of Bristol]]></category>
		<guid isPermaLink="false">https://www.alzheimers-brace.org/?p=1087</guid>

					<description><![CDATA[<p>'How does poor sleep relate to Alzheimer's Disease?'</p>
<p>The post <a href="https://www.alzheimers-brace.org/research-snapshot-dr-liz-coulthard-how-does-poor-sleep-relate-to-alzheimers-disease/">Research Snapshot: Dr Liz Coulthard &#8216;How does poor sleep relate to Alzheimer&#8217;s Disease?&#8217;</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">Research Snapshot: Dr Liz Coulthard 'How does poor sleep relate to Alzheimer's Disease?'</span>
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	<p>Dr Liz Coulthard is an Associate Professor in Dementia Neurology at University of Bristol. Dr Coulthard leads the ReMemBr group comprising of neurologists, psychologists and researchers based at Southmead Hospital.</p>
<p>In this talk, Dr Coulthard talks about the process of sleeping and how it may be important in preventing the onset of dementia. Sleep is a very active process, one that is complementary to being awake. During the slow-wave stage of sleep, natural brain oscillations may be responsible for the filtering of toxins from the brain. One such toxin is amyloid, a protein which researchers have proven accumulates during dementia. By improving our sleep, we may be able to reduce the amount of amyloid and therefore reduce our risk of dementia.</p>
<p>To learn more about this ground breaking research, please watch the short video below.</p>
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	<p>Dr Coulthard’s top tips for increasing the quality of your sleep</p>
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<li>Sleep in a dark, quiet room</li>
<li>Limit the amount of interruptions during your sleep</li>
<li>Go outside during the day - sunlight kick starts the hormones required for healthy sleep</li>
<li>Physical activity early in the day – this can help re-train biological rhythms in the brain leading to better sleep.</li>
<li>Don’t eat or drink too much just before going to bed – especially caffeinated or alcoholic drinks!</li>
<li>Don’t get stressed out before bed – don’t stress about lack of sleep. Resting in bed without sleep can be beneficial to the brain.</li>
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</div><p>The post <a href="https://www.alzheimers-brace.org/research-snapshot-dr-liz-coulthard-how-does-poor-sleep-relate-to-alzheimers-disease/">Research Snapshot: Dr Liz Coulthard &#8216;How does poor sleep relate to Alzheimer&#8217;s Disease?&#8217;</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Dr Liz Coulthard &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard-2/</link>
		
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		<pubDate>Sun, 17 Jan 2021 12:34:00 +0000</pubDate>
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					<description><![CDATA[<p>The ReMemBr Group (Research into Memory, the Brain and dementia) includes neurologists, psychologists and researchers.</p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard-2/">Dr Liz Coulthard &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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	<p>The ReMemBr Group</p>
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	<p><span style="color: #000080;"><em>See glossary at bottom of page for definition of underlined words.</em></span></p>
<p><strong>Summary</strong></p>
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<p>The ReMemBr Group (Research into Memory, the Brain and dementia) includes <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard#neurologist">neurologists</a>, psychologists and researchers from both the University of Bristol and the North Bristol NHS Trust. They diagnose and treat patients with dementia and also offer clinical research opportunities to people with and without dementia. Their research focuses on early diagnosis of dementia, understanding how memory is stored in the brain and how this can be enhanced, as well as <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard#clincal">clinical trials</a> for the treatment of dementia.</p>
<h6>Examples of current work involving BRACE</h6>
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<h6>Targeting the hippocampus</h6>
<p>The hippocampus is a part of the brain involved in memory and <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard#spatial">spatial navigation</a>. It is one of the first brain regions to show degeneration in Alzheimer’s disease, explaining some of the early symptoms including memory loss and disorientation.</p>
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<li>A project led by Professor Risto Kauppinen and Dr Liz Coulthard is using new technology to obtain high quality MRI scans of the hippocampus. They will compare the effects of normal ageing, mild cognitive impairment, Alzheimer's disease and frontotemporal dementia on the size of the hippocampus. Information from these scans will be combined with cognitive tests probing specific regions of the hippocampus to detect the earliest hippocampal changes in Alzheimer’s disease. This will help to spot the signs of Alzheimer’s disease as soon as possible, providing the best chance of preventing further degeneration.</li>
<li>There is evidence that exercise may enhance memory and cognition, and also increase the volume of the hippocampus. It may therefore act to reverse some of the effects of ageing. PhD student Netasha Shaikh, supervised by Dr Liz Coulthard and Dr Jack Mellor, aims to test the potential of exercise as a targeted therapy for Alzheimer’s disease, with a view to validating the need for a larger study into exercise and dementia.</li>
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<h6>Improving the accuracy of diagnosis</h6>
<p>Accurate diagnosis is important for those who have dementia, as well as those who do not. It allows the most appropriate treatment options to be established, and can prevent costly trips to <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard#memory">memory clinics</a> in situations where it is not necessary.</p>
<ul>
<li>A PhD project, supervised by Dr Liz Coulthard and Dr Margaret Newson, will improve the ability to differentiate between those diagnosed with MCI likely to develop dementia and those who perform poorly in cognitive tests for other reasons. Symptom validity tests help tell the difference, and could improve our ability to diagnose dementia accurately.</li>
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<h6>Could drugs currently used for other diseases help dementia?</h6>
<p>Drugs already approved for treating other diseases provide a great opportunity – they are often readily available and cheap, and do not require the lengthy testing procedures of new drugs.</p>
<ul>
<li>Previous work in Bristol has shown that manipulating the <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard#dopamine">dopamine system</a> with medications can improve <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard#consolidation">memory consolidation</a> in patients with Parkinson’s disease, meaning memories are stabilised and can be stored more easily. The team are looking to see if the same could be true for those with dementia.</li>
<li>Work funded by BRACE provided knowledge contributing to the start of the <a href="https://www.alzheimers-brace.org/radar">RADAR study</a>, which aims to investigate whether the commonly used blood pressure drug losartan can help slow down damage to brain tissue in Alzheimer’s disease. Previous research indicates that losartan could be helpful in this way but as yet no conclusive results, such as in a clinical trial, have been produced.</li>
<li>Caffeine is thought to enhance attention and they are also investigating whether or not caffeine might boost attention in people with dementia who have frequent lapses in attention.</li>
</ul>
<h6><strong>Glossary </strong></h6>
<p><u><a id="neurologist"></a>Neurologists</u> – Professionals who are well-versed in the treatment of conditions involving the central nervous system.<br />
<u><a id="clincal"></a>Clinical trials</u> – Trial to evaluate the effectiveness and safety of medications (or medical devices) by monitoring their effects on people.<br />
<u><a id="spatial"></a>Spatial navigation</u> – The ability to direct oneself to a desired location. This ability is controlled by the hippocampus of the brain.<br />
<u><a id="memory"></a>Memory clinics</u> – A session in which the person undergoes a memory assessment and is given information on how to effectively live with memory problems.<u><br />
<a id="dopamine"></a>Dopamine system</u> – The parts of the body responsible for the formation and circulation of the neurotransmitter dopamine. <u><br />
<a id="consolidation"></a>Memory consolidation</u> – A category of processes that stabilise a memory after its initial acquisition.</p>
<p>Further informationFor more information about The ReMemBr Group, and to see ways you can get involved with their research, please use the following links:</p>
<p><a href="https://www.nbt.nhs.uk/remembr-group" target="_blank" rel="noopener noreferrer">The ReMemBr Group website</a></p>
<p><a href="http://www.bristol.ac.uk/clinical-sciences/research/neurosciences/research/remembr/" target="_blank" rel="noopener noreferrer">The ReMemBr Group's University of Bristol page</a></p>
<p><a href="https://www.alzheimers-brace.org/research-snapshot-dr-liz-coulthard-how-does-poor-sleep-relate-to-alzheimers-disease" target="_self"><span class="post_link">Liz's talk on how sleep may affect dementia at Together4Dementia 2019</span></a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard-2/">Dr Liz Coulthard &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Dr Liz Coulthard &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Mon, 17 Feb 2020 10:58:00 +0000</pubDate>
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					<description><![CDATA[<p>Dr Liz Coulthard has received significant funding from BRACE since 2010 for a wide range of projects and research studies.</p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard/">Dr Liz Coulthard &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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	<p>Dr Liz Coulthard has received significant funding from BRACE since 2010 for a wide range of projects and research studies.</p>
<h3><span data-contrast="none">ReMemBr group</span></h3>
<p><span data-contrast="none">In 2010, Dr Liz set up </span><span data-contrast="none">the <a href="https://www.nbt.nhs.uk/our-services/a-z-services/dementia-remembr-group" target="_blank" rel="noopener">ReMemBr group</a>,</span><span data-contrast="none"> with</span><span data-contrast="none"> significant funding from BRACE.</span> The<span data-contrast="none"> dementia research group has </span><span data-contrast="none">neurologists, psychologists and researchers from the North Bristol Trust and the University of Bristol. The ReMemBr group diagnoses and treats people with dementia and also offers clinical research opportunities to people with or without dementia. </span><span data-ccp-props="{&quot;134233117&quot;:false,&quot;134233118&quot;:false,&quot;201341983&quot;:0,&quot;335551550&quot;:0,&quot;335551620&quot;:0,&quot;335559685&quot;:0,&quot;335559738&quot;:0,&quot;335559739&quot;:0,&quot;335559740&quot;:259}"> </span></p>
<h3><span data-ccp-props="{&quot;134233117&quot;:false,&quot;134233118&quot;:false,&quot;201341983&quot;:0,&quot;335551550&quot;:0,&quot;335551620&quot;:0,&quot;335559685&quot;:0,&quot;335559738&quot;:0,&quot;335559739&quot;:0,&quot;335559740&quot;:259}">Fastball - Early Alzheimer's Test</span></h3>
<p><span data-contrast="none">Dr </span><span data-contrast="none">Liz was a co-applicant with Dr George Stothart in the pilot study funded by BRACE to develop the Fast</span><span data-contrast="none">ball technique for earlier diagnosis of Alzheimer's. </span></p>
<p><span data-contrast="none">Currently diagnosis of dementia occurs too late, often up to 20 years after the disease's onset. There is a need for quicker diagnosis of dementia so patients can get earlier treatment or plan. This study tested electroencephalography (EEG) coupled with fast-periodic-visual stimulation</span><span data-contrast="none">, this </span><span data-contrast="none">technique</span><span data-contrast="none"> involved watching flashing images on a screen,</span><span data-contrast="none"> as a method of earlier diagnosis of A</span><span data-contrast="none">lzheimer’s</span><span data-contrast="none">. </span></p>
<p><span data-contrast="none">EEGs are noninvasive and affordable and </span><span data-contrast="none">provide</span><span data-contrast="none"> objective measures of cognitive functions.</span></p>
<p><span data-contrast="none">P</span><span data-contrast="none">articipants were shown streams of pictures at </span><span data-contrast="none">a very fast</span><span data-contrast="none"> rate</span><span data-contrast="none">, while wearing the Fastball device</span><span data-contrast="none"> EEG measures the brain waves, </span><span data-contrast="none">indicating</span><span data-contrast="none"> whether the patients can tell different pictures apart. </span></p>
<p><span data-contrast="none">The Fastball technique can detect changes in memory processing related to A</span><span data-contrast="none">lzheimer’s</span><span data-contrast="none">, even if these changes are not </span><span data-contrast="none">evident</span><span data-contrast="none"> in </span><span data-contrast="none">behavioural</span><span data-contrast="none"> or symptoms</span><span data-contrast="none"> observations. This study found that Fastball had a higher accuracy in classifying A</span><span data-contrast="none">lzheimer’s</span><span data-contrast="none"> compared to </span><span data-contrast="none">behavioural</span><span data-contrast="none"> measures </span><span data-contrast="none">of</span><span data-contrast="none"> memory recognition</span><span data-contrast="none">.  </span> <span data-ccp-props="{&quot;134233118&quot;:false,&quot;201341983&quot;:0,&quot;335551550&quot;:0,&quot;335551620&quot;:0,&quot;335559685&quot;:0,&quot;335559739&quot;:160,&quot;335559740&quot;:257}"> </span></p>
<p><span data-contrast="none">This pilot showed that a fastball can detect early-stage A</span><span data-contrast="none">lzheimer’s</span><span data-contrast="none">, and it works regardless of the language spoken by patients. </span></p>
<p>The findings from the initial study were published in the <a href="https://academic.oup.com/brain/article/144/9/2812/6372384?login=false" target="_blank" rel="noopener">BRAIN Journal in September, 2021. </a>and attracted i<a href="https://www.alzheimers-brace.org/eeg-test-early-alzheimers-diagnosis/" target="_blank" rel="noopener">nternational attention due to the revolutionary approach, on World Alzheimer's Day.</a></p>
<p><a href="https://www.alzheimers-brace.org/new-funding-awarded/" target="_blank" rel="noopener"><span data-contrast="none">In 2022 BRACE funded a follow-up PhD studentship into Fastball,</span></a><span data-contrast="none"> to investigate whether this</span><span data-contrast="none"> technique can </span><span data-contrast="none">be developed to diagnosis </span><span data-contrast="none">non-Alzheimer's dementia, such as vascular, Lewy body or frontotemporal dementia</span><span data-contrast="none">.  </span><span data-ccp-props="{&quot;134233118&quot;:false,&quot;201341983&quot;:0,&quot;335551550&quot;:0,&quot;335551620&quot;:0,&quot;335559685&quot;:0,&quot;335559739&quot;:160,&quot;335559740&quot;:257}"> </span></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-liz-coulthard/">Dr Liz Coulthard &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Dr Daniel Whitcomb &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Wed, 01 May 2019 11:01:00 +0000</pubDate>
				<category><![CDATA[PhDs]]></category>
		<category><![CDATA[University of Bristol]]></category>
		<guid isPermaLink="false">https://www.alzheimers-brace.org/?p=927</guid>

					<description><![CDATA[<p>Are neuronal catenins involved in the synaptopathology of Alzheimer’s disease? (2019 - 2022).</p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb/">Dr Daniel Whitcomb &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">PhD: University of Bristol, 2019</span>
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	<p>Are neuronal catenins involved in the synaptopathology of Alzheimer’s disease? (Pilot Grant)</p>
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	<p><span style="color: #000080;"><em>See glossary at bottom of page for definition of underlined words.</em></span></p>
<p><strong>Summary</strong></p>
<p>The loss of connection between neurones in the brain is believed to be one of the causes of Alzheimer’s disease. The role of a specific protein (catenin) in the breakdown of the connectivity between neurones is not known. This project seeks to utilise a series of molecular biology techniques to test the role of catenins in those suffering with dementia related diseases. In the future, catenins present themselves as a promising therapeutic target for dementia treatment.</p>
<p><strong>What do we already know?</strong></p>
<p>Dementia is believed to be caused by loss of connections between neurones in the brain. A specific class of molecules known as <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb#cam"><u>cell adhesion molecules</u></a> (CAM’s) have been found to be vital in maintaining neuronal connections in the brain. CAM’s themselves have been found to be regulated by a family of proteins known as <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb#catenins"><u>catenins</u></a>. <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb#amyloid"><u>Amyloid-β</u></a> (Aβ) is a key protein in Alzheimer’s disease (AD) and has been shown to break down catenins leading to a loss of neurone connectivity (summarised in Figure 1).</p>
<p><strong>What are we trying to find out?</strong></p>
<p>This project will look to find out whether catenin proteins are deficient in the brains of people who suffer from AD compared to those who do not. The effect of Aβ on catenins will also be investigated and the link between CAM’s and catenins will also be studied in further detail.</p>
<p><strong>How will this be done?</strong></p>
<p>Several molecular biology techniques will be used to identify the proteins found in brains of AD sufferers. Further techniques will allow the quantity of each protein to be measured. Comparison of catenin levels between AD sufferers and <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb#control"><u>control groups</u></a> will allow the links between catenin levels and onset of AD to be determined.</p>
<p><strong>Why is this important?</strong></p>
<p>This study will increase the understanding about the roles of different proteins within AD brains. The understanding of dementia on a general level will be increased and this could lead the way in highlighting catenins as important targets for potential dementia treating drugs.</p>
<p><strong>Glossary</strong></p>
<p><u><a id="catenins"></a>Catenins</u> – A class of proteins responsible for the production of cell adhesion molecues (CAM’s) among other things.<br />
<u><a id="cam"></a>Cell adhesion molecules (CAM)</u> - A class of small proteins which are essential for the normal functioning of neurones.<br />
<u><a id="amyloid"></a>Amyloid-β</u> - A peptide (small protein) which has been found to build up in brain cells of sufferers of Alzheimer’s disease. Amyloid-β will aggregate and form amyloid plaques which have been found to interfere with normal function of cells and tissues.<br />
<u><a id="control"></a>Control Group</u> – A group of test subjects which are left unexposed to compare with treated subjects. In this scenario the control group indicates a group of individuals who do not suffer from Alzheimer’s disease.</p>
<p><strong>Further Information </strong></p>
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	<p><strong>Figure 1:</strong> A figure showing how the interaction between cadherin (the cell adhesion molecule) and catenin maintains the link between neurons in the brain.</p>
<p><a href="https://research-information.bristol.ac.uk/en/persons/daniel-whitcomb(c7243b8a-5ee9-4325-a956-dc0e2c4b1d55).html">Please click here for more information about the work of Dr Daniel Whitcomb</a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-daniel-whitcomb/">Dr Daniel Whitcomb &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Dr Shelley Allen &#038; Dr Debbie Shoemark &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Tue, 01 May 2018 11:41:00 +0000</pubDate>
				<category><![CDATA[Pilot Projects]]></category>
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					<description><![CDATA[<p>Oral health and Alzheimer's disease (2018 - 2019). </p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark/">Dr Shelley Allen &#038; Dr Debbie Shoemark &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">Dr Shelley Allen & Dr Debbie Shoemark</span>
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			<span class="fl-heading-text">Pilot Project: University of Bristol, 2018</span>
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	<p>Oral health and Alzheimer’s disease</p>
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	<p><span style="color: #003366;"><em>See glossary at bottom of page for definition of underlined words.</em></span></p>
<p><strong>Summary</strong></p>
<p>Previous research has found that people who suffer from gum disease have a higher chance of developing Alzheimer's disease. One possible explanation for this incresed risk is the oral bacteria which are responsible for the gum disease. A previous BRACE-funded study (led by Dr Debbie Shoemark) has identified some types of oral bacteria associated with Alzheimer’s disease. This study looks to build on this work by conducting a feasibility study to see if sufferers of mild Alzhiemer’s disease are able to engage with good oral hygiene and whether this is economically feasible. This study may pave the way for an <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark#clinical"><u>NHS funded trial</u></a> into the effects of improved oral hygiene and the progression of Alzheimer’s disease.</p>
<p><strong>What do we know?</strong></p>
<p>It has been suggested that long-term bacterial infection results in an <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark#cascade">inflammatory cascade</a> in the brain, which triggers or contributes to the development of Alzheimer’s disease. The source of this infection could be oral bacteria – many are able to evade the <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark#immune">immune system</a>, and there is an increased risk of developing Alzheimer’s disease in those with gum disease and poor oral hygiene.</p>
<p><strong>What has been found out so far?</strong></p>
<p>A BRACE-funded study led by Dr Debbie Shoemark identified some types of oral bacteria associated with Alzheimer’s disease in post-mortem brain samples of dementia patients. It remains to be answered if these bacteria were present in the brain during life, and if reducing levels of such bacteria in the brain (and at the source in the mouth) can benefit those with Alzheimer’s disease.</p>
<p>This study also established a saliva test which was able to identify whether or not a subject had gum disease. This was done by looking at the DNA content of a mouthwash swill. Those with gum disease had around 25 times more DNA in the swill than those without, due to the presence of a lot of bacterial DNA. This test can now be used as an indicator for how well oral hygiene treatments are reducing levels of bacteria.</p>
<p><strong>The following publication provides a comprehensive background to the subject:</strong></p>
<p>Shoemark, DK &amp; Allen, SJ 2014, ‘The Microbiome and Disease: Reviewing the Links between the Oral Microbiome, Aging, and Alzheimer's Disease’. J Alzheimers Dis.</p>
<p><strong>What next? - Feasibility study</strong></p>
<p>The next step is to establish if patients with mild Alzheimer’s disease can engage and cope with the treatments, self-help and good oral hygiene protocol required to reduce oral bacteria - an obvious necessity if such treatments are to be effective. This study will be led by Dr Shelley Allen with Dr Debbie Shoemark, Professor Nicola West and her team from the Bristol Dental Hospital and Dr Liz Coulthard and team from the Memory Disorders Clinic. This will hopefully lead to an <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark#clinical">NHS funded trial</a> to see if improved oral hygiene can slow down the progression of Alzheimer’s disease.</p>
<p><strong>How will they do this?</strong></p>
<p>In this first pilot study, up to 20 people with mild Alzheimer’s or vascular dementia or Mild Cognitive Impairment and with gum disease, will be treated at the Bristol Dental Hospital over a period of two years to improve the health of their gums and we will determine how easy it is for participants to achieve and maintain good oral hygiene. The participants will need to be accompanied by a project partner (for instance a friend or adult relation). Those interested should ring 0117 342 9637 at the Dental Hospital or email <a href="mailto:dental-clinical-trials@bristol.ac.uk">dental-clinical-trials@bristol.ac.uk</a> and a member of the study team will provide more information and answer any questions.</p>
<p><strong>Why is this important?</strong></p>
<p>Compared to many other <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark#therapeutic">therapeutic approaches</a>, improving oral hygiene could be a relatively simple and non-invasive task which does not require excessive contact time with clinical staff. It could therefore be used widely to prevent the onset or to slow the progression of Alzheimer's disease symptoms.</p>
<p><strong>Glossary</strong></p>
<p><u><a id="cascade"></a>Inflammatory cascade</u> – The series of biological processes (known collectively as a cascade) responsible for inflammation.<br />
<u><a id="immune"></a>Immune system</u> – The human body’s natural defence mechanism against pathogens (things that may harm the body).<br />
<u><a id="clinical"></a>Clinical trial</u> – Trial to evaluate the effectiveness and safety of medications (or medical devices) by monitoring their effects on people.<br />
<u><a id="therapeutic"></a>Therapeutic treatment (therapeutic approach)</u> – A treatment which is designed to reduce or reverse the symptoms of a disease.</p>
<p><strong>Further information </strong></p>
<p><a href="/wp-content/uploads/2021/02/A5_flyer_v2_02Aug17.pdf" target="_blank" rel="noopener">Poster of study</a></p>
<p><a href="http://www.bris.ac.uk/biochemistry/people/deborah-k-shoemark/overview.html" target="_blank" rel="noopener noreferrer">Please click here for more information about the work of Dr Debbie Shoemark.</a></p>
<p><a href="http://www.bris.ac.uk/clinical-sciences/people/shelley-j-allen-birt/index.html" target="_blank" rel="noopener noreferrer">Please click here for more information about the work of Dr Shelley Allen.</a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-shelley-allen-dr-debbie-shoemark/">Dr Shelley Allen &#038; Dr Debbie Shoemark &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Dr Lindsey Sinclair &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-dr-lindsey-sinclair/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Tue, 05 Sep 2017 11:05:00 +0000</pubDate>
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		<category><![CDATA[University of Bristol]]></category>
		<guid isPermaLink="false">https://www.alzheimers-brace.org/?p=933</guid>

					<description><![CDATA[<p>The relationship between later life depression and Alzheimer’s disease: bystander or participant? (2017 - 2018).</p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-lindsey-sinclair/">Dr Lindsey Sinclair &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">Pilot Project: University of Bristol, 2017</span>
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	<p>The relationship between later life depression and Alzheimer’s disease: bystander or participant?</p>
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	<p><span style="color: #000080;"><em>See glossary at bottom of page for definition of underlined words.</em></span></p>
<p><strong>Summary</strong></p>
<p>Later-life depression and dementia are thought to be linked through similar changes to the blood vessels in the brain. This research seeks to assess this link by looking at brain tissue from groups of people who suffer with dementia, those who suffer from later-life depression and those who do not suffer from either.</p>
<p><strong>What do we already know?</strong></p>
<p>Depression and dementia are common diseases but the link between them has not been fully characterised. It has been estimated that late life depression leads to a doubling of the risk of dementia, but it is not clear whether later life depression is an early sign of dementia, or a risk factor for dementia developing.</p>
<p><strong>What are we trying to find out?</strong></p>
<p>It has been hypothesised that changes in blood circulation in the brain (<a href="https://www.alzheimers-brace.org/university-of-bristol-dr-lindsey-sinclair#vascular"><u>vascular changes</u></a>) are associated with <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-lindsey-sinclair#depression"><u>depression in later life</u></a>. These vascular changes are also thought to play a large part in the onset of Alzheimer’s disease (AD). This project seeks to characterise the link between later-life depression and dementia – and to characterise the link of both disorders to vascular changes in the brain.</p>
<p><strong>How will this be done?</strong></p>
<p>The main hypothesis of this work is to understand whether a link between dementia and depression exists. Tissues of different groups of patients will be analysed. The levels of specific proteins of the tissue will be measured and compared. By comparing the brain tissue of sufferers of dementia and sufferers of later-life depression we hope to find out whether later life depression is an early sign of Alzheimer’s Disease (AD), or if it seems to be a risk factor for AD.</p>
<p><strong>Why is this important?</strong></p>
<p>By understanding some of the biggest contributors to Alzheimer’s disease (AD) this research has the potential to delay the onset of AD. A delay of 5 years would lead to a reduction in the number of sufferers of this disease by 36%. This research has the potential to understand the <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-lindsey-sinclair#neurological"><u>neurological changes</u></a> that occur in the brains of patients who suffer from AD and later-life depression – something which is not yet fully understood.</p>
<p><strong>Glossary</strong></p>
<p><u><a id="depression"></a>Later-life depression</u> – A bout of depression that typically occurs for the first time in older patients.<br />
<u><a id="vascular"></a>Vascular Changes</u> – Changes to the blood vessels which are responsible for providing blood supply to the brain.<br />
<u><a id="neurological"></a>Neurological Changes</u> – Changes to the neurones (brain cells) that make up the neurological system of the brain.</p>
<p><strong>Further Information</strong></p>
<p><a href="https://research-information.bristol.ac.uk/en/persons/lindsey-i-sinclair(01865b8c-fcdb-4070-b096-5e52b96896ec).html">Please click here to learn more about Dr Lindsey Sinclair's research</a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-lindsey-sinclair/">Dr Lindsey Sinclair &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Dr Alastair Wilkins, Prof Seth Love &#038; Dr Kelly Hares &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares/</link>
		
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		<pubDate>Thu, 25 May 2017 11:10:00 +0000</pubDate>
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					<description><![CDATA[<p>Neuronal railways: identifying the mechanism behind dysfunctional protein transport in dementia (2017 - 2018).</p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares/">Dr Alastair Wilkins, Prof Seth Love &#038; Dr Kelly Hares &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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	<p>Neuronal railways: identifying the mechanism behind dysfunctional protein transport in dementia (Pilot Project)</p>
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	<p><span style="color: #000080;"><em>See glossary at bottom of page for definition of underlined words.</em></span></p>
<p><strong>Summary</strong></p>
<p>The degradation of neurons is thought to play a very important role in the onset of the symptoms of dementia. In order for neurons to function properly, proteins and other structures need to be transported from the nucleus (where they are made) to the synapse (where they are needed) by <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#motor"><u>motor proteins</u></a>. KIF5A is a motor protein that binds to KLC1 (kinase light chain) to transport proteins involved in Alzheimer’s disease. In this project, the effect of turning on production of KLC1 (with respect to KIF5A and KLC1) will be tested using brain tissue from BRACE funded South West Dementia Brain Bank. Understanding how this cellular railway system works may lead to effective treatments that can slow neuron degradation and the subsequent symptoms of dementia.</p>
<p><strong>What do we already know?</strong></p>
<p>In order for neurons to work properly, proteins and other structures are transported to where they are needed within the cell.  For instance, proteins involved in the function of synapses (chemical junctions between neurons) are made in the cell nucleus and are transported (often long distances) to the synapse.  These transport mechanisms are complex and rely on “motor proteins”.  Motor proteins bind to specific protein cargoes and carry them on microtubules (essentially railway track-like structures) to where they are needed.</p>
<p>KIF5A is a motor protein that binds to KLC1 (kinase light chain) to transport proteins involved in Alzheimer’s disease.  It is known that a gene variation in KLC1 gene is linked to Alzheimer’s disease, and can predict conversion from mild cognitive impairment (MCI) to Alzheimer’s disease.  Reduced or <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#dysregulated">dysregulated</a> function of KLC1 may cause an increase in KIF5A expression, to improve the clearing of <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#aggregates">protein aggregates</a> involved in Alzheimer’s disease.</p>
<p><strong>What is this group trying to find out?</strong></p>
<p>The interactions between KIF5A (the motor proteins), microtubules (the “rails”) and KLC1 (the link that binds the motor proteins to the microtubules) are still unclear.  This study aims to determine how the KLC1 gene variation affects the expression of KIF5A and KLC1, as well as the transport of Alzheimer’s disease-related proteins such as APP and amyloid-β.  This may help determine why some Alzheimer’s disease sufferers have a much more severe disease course than others.</p>
<p><strong>How do they do this?</strong></p>
<p>Genetic analysis of human brain tissue from Alzheimer’s disease sufferers and healthy age-matched controls (without any cognitive impairment) will be used from the South West Dementia Brain Bank.  <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#rna">RNA</a> and protein will be extracted from human tissue, KLC1  and  KIF5A  expression  will  be  analysed  based  on  <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#genotype">genotype</a>  and  correlated  with  common markers of AD <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#neuropathology">neuropathology</a>, such as <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#amyloid">amyloid-β</a> and <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#tau">tau</a> levels.</p>
<p><strong>Why is it important?</strong></p>
<p>Defective protein transport appears to precede protein aggregation, and therefore may represent a “window of opportunity” for preventing pathological aggregates.  Improving our understanding of the interactions between KIF5A, KLC1 and microtubules – and how these are affected by genetic variations linked to Alzheimer’s disease – may help us discover new <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares#neuroprotective">neuroprotective</a> mechanisms and develop potential drug treatments.</p>
<p><strong>Glossary</strong></p>
<p><u><a id="motor"></a>Motor proteins</u> – Specific proteins responsible for the transport of other proteins around the cell utilising cell ‘railway tracks’ known as microtubles. <u><br />
<a id="dysregulated"></a>Dysregulated (proteins)</u> – Regulation of DNA is one of the ways the production proteins is switched on or off. Dysregulation is when production of proteins is turned off (due to regulatory factors).<br />
<u><a id="aggregates"></a>Protein aggregates</u> – Protein aggregates are formed when proteins clump together. The clumping together of proteins to form toxic lumps and tangles is a common feature of dementia related diseases.<br />
<u><a id="rna"></a>RNA </u>– Stands for ribonucleic acid, this biomolecule is closely related to DNA and is involved in the formation of proteins from DNA.<br />
<u><a id="genotype"></a>Genotype</u> – The genetic makeup of an organism. Our genetic makeup is responsible for many of the characteristics we possess (including hair colour, eye colour etc.)<br />
<u><a id="neuropathology"></a>Neuropathology</u> – The scientific study of diseases that affect the central nervous system.<br />
<u><a id="amyloid"></a>Amyloid-β</u> – Small peptides which aggregate to form amyloid plaques in Alzheimer’s disease. These plaques will eventually lead to the death of cells in the brain.<u><br />
<a id="tau"></a>Tau</u> – Proteins that stabilise a cell component known as microtubules. In Alzheimer’s and Parkinson’s disease these tau proteins are defective and no longer functional.<br />
<u><a id="neuroprotective"></a>Neuroprotective</u> – Something that aids the formation of new brain cells (neurons)</p>
<p><strong>Further information</strong></p>
<p><a href="http://www.bristol.ac.uk/clinical-sciences/people/alastair-wilkins/index.html">Please click here for more information about the work of Dr Alastair Wilkins.</a></p>
<p><a href="http://www.bristol.ac.uk/clinical-sciences/people/seth-love/index.html">Please click here for more information about the work of Prof Seth Love.</a></p>
<p><a href="http://www.bristol.ac.uk/clinical-sciences/people/kelly-m-hares/index.html">Please click here for more information about the work of Dr Kelly Hares.</a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-dr-alastair-wilkins-prof-seth-love-dr-kelly-hares/">Dr Alastair Wilkins, Prof Seth Love &#038; Dr Kelly Hares &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Prof Jeremy Henley &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Mon, 21 Nov 2016 11:38:00 +0000</pubDate>
				<category><![CDATA[PhDs]]></category>
		<category><![CDATA[University of Bristol]]></category>
		<guid isPermaLink="false">https://www.alzheimers-brace.org/?p=974</guid>

					<description><![CDATA[<p>Processes controlling the communication between brain cells in Alzheimer’s disease and Down’s syndrome (2016 - 2019).</p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley/">Prof Jeremy Henley &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">PhD: University of Bristol, 2016</span>
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	<p>Processes controlling the communication between brain cells in Alzheimer’s disease and Down’s syndrome (PhD Studentship)</p>
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	<p><span style="color: #000080;"><em>See glossary at bottom of page for definition of underlined words.</em></span></p>
<p><strong>Summary</strong></p>
<p>The <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#neurodegenerative"><u>neurodegenerative</u></a> effects of dementia may be caused by incorrect positioning and lack of replacement of AMPA <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#receptor"><u>receptors</u></a> within nerve cells. Nerve cells are responsible for the transmission of signals across the body (AMPA receptors are vital for this process), when this stops functioning cell death occurs. This project aims to characterise the effect of <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#sumoylation"><u>SUMOylation</u></a> on the positioning of AMPA receptors in the brains of dementia sufferers. If this research successfully implicates the SUMOylation of proteins in neurodegeneration caused by dementia, then this may provide a new <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#therapeutic"><u>therapeutic targets</u></a> for treating the disease.</p>
<p><strong>What do we already know?</strong></p>
<p>The brain is composed of billions of nerve cells which communicate by sending out chemical signals called <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#neurotranmitter">neurotransmitters</a>. Neurotransmitters travel across the gaps between cells and interact with <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#receptor">receptor proteins</a> on other nerve cells to send them a signal – this junction is called a synapse. AMPA receptors are found at synapses and are involved in receiving fast communication signals in the brain. In the early stages of dementia this signalling between cells goes wrong because AMPA receptors are not correctly positioned to receive neurotransmitter signals.</p>
<p>In normal brain cells, AMPA receptor numbers can be increased and decreased depending on the incoming signals, but in Alzheimer's disease and Down's syndrome too many receptors are removed and not replaced, leading to degeneration of synapses and eventually death of cells in the brain. Those with Down’s syndrome have a tendency to develop dementia at a younger age than the general population.</p>
<p><strong>What is this project trying to find out?</strong></p>
<p>This project aims to investigate what goes wrong with the processes controlling AMPA receptors in dementia, particularly looking at <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#sumoylation">SUMOylation</a>. SUMOylation is the process by which the small protein SUMO is attached to target proteins to change their characteristics. It has a role in controlling the location of AMPA receptors at synapses, and has been implicated in many diseases including cancer, <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#stroke">stroke</a> and Parkinson's disease.</p>
<p><strong>How is this being done?</strong></p>
<p>Post-mortem brain samples will be used from Alzheimer's disease and Down's syndrome patients, together with healthy brain samples from subjects of a similar age. The changes in SUMOylated proteins will be profiled using a technique called monoclonal <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#antibody">antibody</a>-based affinity <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley#chromatography">chromatography</a>, where proteins that have SUMO attached can be isolated from other proteins. The proteins isolated can then be analysed to see how the level of SUMOylation changes, and if there are any changes in which proteins are SUMOylated in diseased brains.</p>
<p><strong>Why is it important?</strong></p>
<p>If we know some of the signalling proteins or pathways which are disrupted in dementia, this will allow them to be specifically targeted by therapies which may help to prevent synapse degeneration and cell loss in the brain.</p>
<p><strong>Glossary</strong></p>
<p><u><a id="neurodegenerative"></a>Neurodegeneration</u> – The death of cells in the brain (neurons). Neurodegeneration is a characteristic sign of dementia related diseases.<u><br />
<a id="sumoylation"></a>SUMOylation</u> – Small protein SUMO is attached to other proteins to change their characteristics<br />
<u><a id="therapeutic"></a>Therapeutic targets</u> – A therapeutic target is the protein / receptor that a pharmaceutical drug will bind to in order to elicit its effect.<br />
<u><a id="neurotranmitter"></a>Neurotransmitters</u> – Any substance, such as acetylcholine or dopamine, responsible for sending nerve signals across a synapse between two neurons.<br />
<u><a id="receptor"></a>Receptor proteins</u> – A protein which binds a specific molecule strongly.<br />
<u><a id="stroke"></a>Stroke </u>– A blood clot in the brain leading to inadequate blood supply and cell death in a localised region of the brain.<br />
<u><a id="antibody"></a>Antibody</u> – A large protein which is able to specifically bind a certain molecule (known as an antigen).<br />
<u><a id="chromatography"></a>Chromatography</u> – A technique for the separation of complex mixtures based on the different properties of the constituent parts.</p>
<p><a href="http://www.bris.ac.uk/biochemistry/people/jeremy-m-henley/research.html" target="_blank" rel="noopener noreferrer">Please click here for more information about the work of Professor Jeremy Henley.</a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-jeremy-henley/">Prof Jeremy Henley &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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		<title>Prof Yoav Ben-Shlomo &#8211; University of Bristol</title>
		<link>https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo/</link>
		
		<dc:creator><![CDATA[admin]]></dc:creator>
		<pubDate>Thu, 11 Aug 2016 11:13:00 +0000</pubDate>
				<category><![CDATA[PhDs]]></category>
		<category><![CDATA[University of Bristol]]></category>
		<guid isPermaLink="false">https://www.alzheimers-brace.org/?p=944</guid>

					<description><![CDATA[<p>Using in-home sensors to predict Alzheimer’s disease and monitor treatment (2016 - 2019). </p>
<p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo/">Prof Yoav Ben-Shlomo &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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			<span class="fl-heading-text">PhD: University of Bristol, 2016</span>
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	<p>Using in-home sensors to predict Alzheimer’s disease and monitor treatment (Pilot Study)</p>
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<p><b>Summary</b></p>
<p>One of the main challenges of dementia research is the lack of a diagnostic tool for the early detection of the disease. Most of the current diagnostic tests are not 100% reliable and are only able to detect the disease once permanent cellular damage has taken place. This project seeks to combat this using new SPHERE (Sensor Platform for HEalthcare in a Residential Environment) technology. Participants with cognitive decline will be monitored at home using SPHERE sensors and undergo tests to probe the areas of the brain known to be affected in Alzheimer’s disease. This coupled with state-of-the-art structural imaging techniques (<a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#mri"><u>MRI</u></a> and <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#pet"><u>PET</u></a>) may provide preliminary data for a new diagnostic test for the treatment of dementia.</p>
<p><strong>What do we already know?</strong></p>
<p>Alzheimer’s disease (AD), Vascular Dementia and mixed dementia account for 89% of cases of dementia, and annual UK dementia healthcare costs are £4.3 billion.  Although there are several treatments available, these have marginal benefit and only slow disease progression, not curing the underlying <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#disorder">neurological disorder</a>.  This is because treatment is often started too late in the disease progress, and so the development of effective <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#biomarker">biomarkers</a> to detect and monitor Alzheimer’s disease in its early stages is a heavy focus of dementia research.  Therefore the focus of this project is to use unique new SPHERE technology to develop non-invasive, accurate, early diagnosis of the commonest type of dementia (AD) and sensitive disease monitoring that is meaningful in terms of day-to-day function.</p>
<p><strong>What is this group trying to find out?</strong></p>
<p>The Bristol-based SPHERE (Sensor Platform for HEalthcare in a Residential Environment) is an engineering project using both wearable and home-based sensors to detect and prevent a wide range of medical conditions through monitoring activity in the home (e.g. predicting falls and detecting strokes so that help may be summoned).  The SPHERE project is an untapped opportunity to enhance dementia research with the potential to improve early diagnosis through in-home monitoring of natural behaviour to distinguish presence and subtype of dementia.  In particular, Prof. Ben-Shlomo’s group aim to identify behavioural signatures that can distinguish between early stage dementia and other disorders such as vascular dementia and Functional Cognitive Disorder (FCD – a mistaken belief that you are developing Alzheimer’s disease).  Moreover, the group wants to find out whether these signatures of early stage Alzheimer’s disease are sensitive to <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#drugtherapy">drug therapy</a>.</p>
<p><strong>How do they do this?</strong></p>
<p>Prof. Ben-Shlomo’s group will recruit participants with cognitive decline but no dementia to the SPHERE project, as well as the partners/carers as controls. The houses of participants would have SPHERE sensors installed and the group will monitor naturalistic behaviour plus add in some “real world” <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#cognitive">cognitive</a> tasks to probe cognitive domains known to be affected early in Alzheimer’s disease (e.g. long term memory).  Participants would all also undergo state-of-the-art structural and molecular imaging (<a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#mri">MRI</a> and amyloid <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#pet">PET</a>) to define their disease subtype as precisely as possible using the current gold standard.</p>
<p>To test whether the signatures are sensitive to treatment, individuals newly diagnosed with AD would be recruited and would be recorded for one month prior to starting standard Alzheimer’s disease medication and then for another month when they were on the drug.  Changes in behavioural SPHERE signatures would be compared to changes detected in standard <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo#tests">neuropsychological tests</a>.</p>
<p><strong>Why is it important?</strong></p>
<p>The initial results would form the preliminary data for a much larger trial. The eventual outcome would be a new, non-invasive diagnostic tool for early dementia and a sensitive technique for disease monitoring.</p>
<p><strong>Glossary</strong></p>
<p><u><a id="disorder"></a>Neurological Disorder</u> – A disorder that effects the central nervous system (brain and spinal cord).<br />
<u><a id="biomarker"></a>Biomarker</u> – Biological molecule that can be detected and measured in parts of the body, such as the blood.<br />
<u><a id="drugtherapy"></a>Drug Therapy</u> – The treatment of diseases using a pharmaceutical drug.<br />
<u><a id="cognitive"></a>Cognitive </u>– Relating to cognition - the mental process of knowing, including aspects such as awareness, perception, reasoning, and judgement.<br />
<u><a id="mri"></a>MRI (Magnetic Resonance Imaging)</u> – A scanning technique which provides an image of the soft tissue in the body using magnet and radio waves.<br />
<u><a id="pet"></a>PET (Positron Emission Tomography)</u> – A scanning technique which can be used to produce a three-dimensional image that reflects the chemical activity of the brain.<br />
<u><a id="tests"></a>Neuropsychological tests</u> – A test designed to quantify behavioural changes caused by a brain disorder.</p>
<p><strong>Further information</strong></p>
<p><a href="http://www.bristol.ac.uk/social-community-medicine/people/yoav-ben-shlomo/index.html">Please click here for more information about the work of Prof Yoav Ben-Shlomo.</a></p>
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</div><p>The post <a href="https://www.alzheimers-brace.org/university-of-bristol-prof-yoav-ben-shlomo/">Prof Yoav Ben-Shlomo &#8211; University of Bristol</a> appeared first on <a href="https://www.alzheimers-brace.org">BRACE Alzheimer&#039;s Research</a>.</p>
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