Tag Archives: Alzheimer

Diet High in Vitamins and Fish May Protect Cognition and Brain Size

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US scientists have found people with high levels of certain vitamins and omega 3 fatty acids in their blood do better in cognitive tests, and are less likely to have brain shrinkage associated with Alzheimer’s disease.

The study, which is published online in the journal Neurology on 28 December, is one of the first to investigate a range of nutrients in people’s blood, instead of using questionnaires to assess people’s diets. The researchers believe this method gives a more accurate picture of a person’s food intake, because it does not rely on people’s memory or honesty when answering questions about their diet.

Researchers at the Oregon Health & Science University, in Portland, studied blood samples from 104 healthy older people with an average age of 87, who had few known risk factors for Alzheimer’s. They categorised the participants into eight groups according to the profile of nutrients contained in their blood, and analysed how people in each group performed in a series of cognitive tests.

They found those whose blood contained more vitamin B, C, D and E were the best performers in cognitive tests, while people with higher levels of omega 3 fatty acids also had high scores in these tests. Vitamins B, C and E are mainly found in fruits and vegetables, while vitamin D and omega 3 fatty acids are mainly contained in fish.

Conversely, people whose blood had higher levels of trans fats – found mainly in cakes and fried foods – had the worst cognitive scores.

The researchers also analysed MRI scans from 42 of the participants, and found that those whose blood had higher levels of vitamins and omega 3 were also more likely to have bigger total brain volume. In comparison, those with more trans fats in their blood had less brain volume.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:

“One strength of this research is that it looked at nutrients in people’s blood, rather than relying on answers to a questionnaire. It’s important to note that this study looked at a small group of people with few risk factors for Alzheimer’s disease, and did not investigate whether they went on to develop Alzheimer’s at a later stage. There is a clear need for conclusive evidence about the effect of diet on our risk of Alzheimer’s, which can only come from large-scale, long-term studies.

“Although there is no sure-fire way of preventing Alzheimer’s yet, we know that risk factors for heart disease and stroke can also increase the risk of dementia. The best advice at the moment is to eat a balanced diet with plenty of fruit and vegetables, and keep healthy by not smoking, taking regular exercise and keeping blood pressure and cholesterol in check.

“Currently 820,000 people are affected by dementia in the UK and with a rapidly ageing population, those numbers are expected to soar. We urgently need to find ways to prevent dementia if we are to head off a future crisis, and that means it’s vital to invest in research.”

For further information, or to speak with Dr Simon Ridley, please contact Kirsty Marais, Media Officer at Alzheimer’s Research UK on 01223 843304, 07826 559233 or email press@alzheimersresearchuk.org 

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Brain Size May Predict Alzheimer’s Risk Years Before Symptoms Appear

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US scientists have found brain scans measuring the thickness of certain regions of the brain may help identify people who have a higher risk of developing Alzheimer’s disease.

Researchers at Massachusetts General Hospital, in Boston, and the University of Pennsylvania, in Philadelphia, studied MRI scans from 159 cognitively normal older people. The scientists looked at measurements of the brain’s cortex in nine regions that, in earlier studies, have been shown to shrink in Alzheimer’s disease. They theorised that those with a thinner than average cortex would have a higher risk of Alzheimer’s, and those with a thicker than average cortex would have lower risk.

The scientists analysed cognitive test results for 125 participants, and found that 21% of those with a thinner cortex showed signs of cognitive decline over three years. In comparison, just 7% of those with a cortex of average thickness showed decline, and among participants with a thicker cortex, none showed a decline.

The researchers also looked at cerebrospinal fluid (CSF) samples taken from 84 of the participants after three years, checking for levels of amyloid – a hallmark protein found in the brains of Alzheimer’s patients. They found 60% of those with a thinner cortex had abnormal amyloid levels in their CSF, similar to those seen in Alzheimer’s, compared to 36% of those with a cortex of average thickness and 19% of those with a thicker cortex.

The findings, which are published online today (21 December) in the journal Neurology, add to previous evidence suggesting that brain shrinkage may start years before the symptoms of Alzheimer’s, such as memory loss, begin to show. The researchers believe that MRI scans measuring cortical thickness may be useful for helping to identify people at greater risk of developing the disease. However, they stress that studies with a longer follow-up period are now needed.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:

“The ability to predict who will develop Alzheimer’s disease is a key target for dementia research, as it would allow new treatments to be trialled early, when they are more likely to be effective. These findings add weight to existing evidence that Alzheimer’s begins long before symptoms appear, although it’s important to note that the study did not assess who went on to develop the disease. This research provides a potential new avenue to follow, but we need to see larger and longer-term studies before we can know whether this type of brain scan could accurately predict Alzheimer’s.

“There are currently 820,000 people in the UK affected by dementia, yet research into the condition is desperately underfunded compared to other serious diseases. We urgently need to invest in research if we are to find new ways to diagnose, treat and prevent dementia.”

For further information, or to speak with Dr Simon Ridley, please contact Kirsty Marais, Media Officer at Alzheimer’s Research UK on 01223 843304, 07826 559233 or email press@alzheimersresearchuk.org 

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Cambridgeshire Big Walk Huge Success for Alzheimer’s Research UK

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Alzheimer’s Research UK’s Big Walk on Sunday 13 May was a huge success, and on target to raise thousands of pounds for pioneering dementia research. Shirley Cramer CBE, Chief Executive of the UK’s leading dementia research charity, cut the ribbon to mark the start of the nine mile circular walk in and around Comberton, in South West Cambridgeshire.

The event was sponsored by Greens health and fitness club in Cambridge and some 300 people stepped up to the challenge from all over the county and beyond to take part in Alzheimer’s Research UK’s Big Walk. Everyone joined in a warm-up session before they set off in the long awaited sunshine. Walkers enjoyed exploring Comberton’s peaceful country lanes and an off-road ramble, following tracks through fields and country paths, alongside beautiful woodland areas. The youngest walker was 8 years old and many people bought their four-legged friends along too.

Several walkers talked about the day and their inspiration for supporting Alzheimer’s Research UK’s Big Walk:

David Pitches from Haverhill was one of the first walkers across the finishing line and said:

“It was a really pretty route and I was pleased to be one of the first to finish – it took me just under two hours. I lost my mum Jean to Alzheimer’s last year so supporting Alzheimer’s Research UK is very important to me.”

Elaine King from Sutton, near Ely, said:

“My father-in-law George had Alzheimer’s and my husband and I joined in the Big Walk to raise much needed money for Alzheimer’s Research UK. The route was really lovely and it was a very well organised event.” 

Lisa Dimaline from Cambourne walked with her husband Simon and their two children Thomas, 15, and Amy, 10, and said:

“My mum Jean has Alzheimer’s so we’re doing the Big Walk for her. It’s a horrible disease and this is our way of raising money for new treatments to give hope to other people and future generations.”

Shirley Cramer, Chief Executive of Alzheimer’s Research UK, added:

“It was a fantastic day and a brilliant sight as a sea of purple t-shirts set off down the country lanes in Comberton for our Big Walk. Everyone had the same aim in mind – to help us achieve our vision at Alzheimer’s Research UK of a world free from dementia.

“Thanks to the generosity of the hundreds of people who took part or made a donation, the Big Walk is set to make a fantastic contribution to our world-class research – it’s just amazing! The money is still coming in and it will pay for a pilot research project to help defeat Alzheimer’s disease and other forms of dementia and fund vital equipment for our scientists.

“We’d like to say a huge thank you to Greens health and fitness centre who sponsored our Big Walk and to the hundreds of people who took part or volunteered to help on the day. A team from St John Ambulance were on standby too and a number of companies kindly contributed water and food to keep everyone’s stamina up and some super raffle prizes to add to the fun of the day. 

“There are over 6,000 people in Cambridgeshire living with dementia today and over 820,000 across the UK, with numbers forecast to rise substantially in the next generation. We rely entirely on our wonderful supporters to fund our vital research. Every penny raised through our Big Walk will bring us closer to finding ways to diagnose, prevent, treat and cure dementia. Research is the only answer.”  

To help Alzheimer’s Research UK defeat dementia, donate online at www.alzheimersresearchuk.org or call 01223 843899.

For further information, photos or to speak with Shirley Cramer, please contact Sue Armstrong, Media Officer at Alzheimer’s Research UK on 01223 843304, 07500 119514 or email press@alzheimersresearchuk.org

Retinal Damage Linked to Cognitive Decline

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US scientists have found that women with retinal damage are more likely to show signs of cognitive decline and vascular damage in the brain. The study is published in the journal Neurology.

Research led at the University of California studied 511 women with an average age of 69, who were enrolled in the Women’s Health Initiative Memory Study. The women all took cognitive tests to measure their thinking and memory skills once a year, for up to ten years. About four years into the study, the participants were given an eye exam to check for damage to the retina – damage to the tiny blood vessels in the eyes – and about four years later, the women underwent MRI scans to check for brain size and signs of vascular damage to the brain.

They found that 39 of the women showed signs of retinal damage, which was not severe enough to cause significant symptoms. Those with retinal damage had lower cognitive scores across the ten-year period, and had more areas of vascular damage in their brains.

Retinal damage is a known complication of type 2 diabetes and high blood pressure. The researchers believe retinal damage could be an early marker for declining brain health, and suggest that in the future, eye exams to check for this damage could be a useful tool for detecting potential problems.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“Accurate early detection of the cognitive decline that can be associated with dementia could unlock our ability to treat it. This small study offers clues for another possible route doctors could consider when monitoring for the signs of cognitive decline. Further, larger studies will need to determine how reliable it could be. As part of an approach to detection, a non-invasive eye test could be beneficial as a means for spotting signs of early cognitive decline.

“The study adds to mounting evidence linking vascular health to cognitive decline, and underlines the importance of looking after our hearts. It will be useful to see whether the people in this study went on to develop dementia.

“Numbers of people living with dementia are increasing rapidly and research offers our only hope of detection, treatment or prevention. In the face of this generation’s greatest health challenge, we must increase research funding now or we risk failing countless families who will be affected by dementia.”

This material has been published with the kind permission of Alzheimer Research UK.

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Common Alzheimer’s Drug May Benefit Patients in Later Stages of Disease

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UK scientists have found that the drug donepezil, which is approved for use only in the mild to moderate stages of Alzheimer’s disease, could benefit patients in the later stages of the disease. The study is published in the New England Journal of Medicine.

The study, led by researchers at King’s College London, set out to assess the effects of two Alzheimer’s drugs – donepezil (often known as Aricept) and memantine (known as Ebixa or Axura). Donepezil is currently licensed in the UK for use in people with mild to moderate Alzheimer’s, while memantine is used in people in the moderate and severe stages of the disease. Both drugs can help with some of the symptoms of Alzheimer’s.

The study followed 295 people with moderate or severe Alzheimer’s disease over the course of a year. All the participants were living at home and had been prescribed donepezil, but not memantine, for at least three months before the study began, and were being assessed by their doctors for a possible change in their medication. They were randomly assigned to one of four treatment options: continuing donepezil, replacing donepezil with a placebo, stopping donepezil and switching to memantine, or taking both donepezil and memantine.

The researchers tested the participants’ cognition and their functional ability (the ability to carry out everyday tasks) several times over the course of the trial, and at the end of the study. They found those who continued taking donepezil showed less decline than those who stopped taking the drug. Meanwhile, those who took memantine also showed some benefit compared to those on a placebo, although the effect was smaller than those on donepezil.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“We know that people can have different responses to donepezil, but these findings suggest that some people with Alzheimer’s may benefit for longer than previously thought. Trials such as this are extremely important for informing decisions about the way medication is prescribed, potentially helping even more people. It would be helpful to see longer-term trials to determine exactly how long the benefits seen in this study might last.

“While donepezil and memantine can help with the symptoms of Alzheimer’s, and are an enormous boost for many people, sadly we still lack a treatment that can stop the disease in its tracks. With 500,000 people affected by Alzheimer’s in the UK, we desperately need effective new treatments that can halt the disease if we are to offer them hope – that means we must invest in research.”

This material has been published with the kind permission of Alzheimer Research UK.

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Scientists Discover How Sugars Control Hallmark Alzheimer’s Protein

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A study by scientists in Canada and the US has shown that a chemical change to a hallmark Alzheimer’s protein, tau, can stop it from forming toxic tangles – a characteristic of the disease. The findings, published online on 26 February in the journal Nature Chemical Biology, open up new avenues for research into treatments to slow the progression of the disease.

A defining feature of Alzheimer’s is the over activation of a protein called tau – causing it to form toxic tangles inside nerve cells. The researchers found that adding a sugar molecule called O-GlcNAc to tau could prevent it from sticking together.

The scientists tested the approach using mice which have high levels of a sticky form of tau. In these mice, tau builds up over time – killing nerve cells and causing movement and behaviour problems. These mice were treated for 36 weeks with a drug which increases the amount of O-GlcNAc on tau and researchers found that the mice had fewer tau tangles in the brain, including the parts of the brain involved in thinking and memory. While tau in these mice was still over activated, O-GlcNAc appeared to block the next step of tangle formation.

Problems with sugar metabolism have been seen in brain cells in the early stages of Alzheimer’s and the researchers suggest this may limit the amount of O-GlcNAc available to protect tau – driving the formation of toxic tangles.

Dr Marie Janson of Alzheimer’s Research UK, said:
“We know that the toxic build up of tau is a key feature in Alzheimer’s and other dementias, but what is still unclear is exactly what causes it and how it can be stopped. This study provides some answers and encouragingly shows that small changes to tau can have a real effect on how it behaves inside cells.

“Understanding more about how hallmark proteins involved in Alzheimer’s are controlled at a molecular level will provide clues for disease prevention and help us develop ways of tackling this devastating disease. Over 820,000 people in the UK live with dementia, so the need for more research has never been greater.”

This material has been published with the kind permission of Alzheimer Research UK.

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Edinburgh Study Could Bring Early Alzheimer’s Diagnosis a Step Closer

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Scientists in Edinburgh have found particles in cerebrospinal fluid (CSF) that could be harnessed to identify changes in the brain that occur during Alzheimer’s disease. The study, which was part-funded by Alzheimer’s Research UK, could pave the way for a new test to diagnose the disease in its earliest stages.

Researchers at the University of Edinburgh hope to be able to detect Alzheimer’s by measuring changes in exosomes – tiny particles that are released by cells into different bodily fluids. Because exosomes contain proteins and other materials from the cells that release them, they could offer a wealth of information about what is happening to those cells.

Although exosomes have already been shown to be present in fluids such as blood and saliva, the scientists set out to discover whether they could also be found in people’s cerebrospinal fluid (CSF). It’s hoped that changes in CSF will give a more accurate picture of any changes occurring in the brain.

The researchers used state-of-the-art techniques to study samples of CSF from five people who were undergoing surgery for aortic aneurism. They found not only that exosomes were present in CSF, but that these exosomes also contained a variety of different proteins. The results are published this month in the Journal of Translational Medicine, and the researchers now plan to develop new techniques to isolate the different proteins contained in these exosomes. It’s hoped this approach could ultimately be used to detect changes in people with Alzheimer’s.

Alzheimer’s disease is the most common cause of dementia, which currently affects 5,000 people in Edinburgh alone and 820,000 people across the UK.

Dr James Dear, who co-authored the study, said:
“This is an exciting development for us, but in order for these findings to help people with Alzheimer’s it’s vital that we now follow up this work. If we can refine our methods and get a detailed look at the proteins these particles contain, we hope this approach could help detect Alzheimer’s disease at an early stage. If this method proves successful, it could also help clinical trials by allowing researchers to monitor how patients are responding to potential new treatments.”

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “We’re delighted to have supported this study, which has demonstrated that in principle, this method may be useful for detecting Alzheimer’s disease. We now need to see whether this approach will be able to pick up some of the early changes associated with Alzheimer’s.

“The ability to detect Alzheimer’s disease early is a key goal for research – such a test would allow new drugs to be trialled in the right people, as early as possible, when they are more likely to have a beneficial effect. These are promising results, and if they are to be translated into a test that could be used in the clinic, we must continue to invest in research.”

The study was funded by Alzheimer’s Research UK and the British Heart Foundation.

This material has been published with the kind permission of Alzheimer Research UK.

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Low Omega-3 Fatty Acid Levels Linked to Markers of Brain Ageing

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Scientists in the US have linked low levels of the omega-3 fatty acid, docosahexaenoic acid (DHA), to lower scores on cognitive tests and lower brain volume. The study is published in the journal Neurology.

Researchers at the University of California in Los Angeles studied blood samples from 1,575 cognitively healthy people, with an average age of 67. Participants were also given MRI scans to assess their total brain volume, and a series of cognitive tests were carried out.

The results showed that those with the lowest levels of DHA in their red blood cells tended to have lower brain volume compared to those with the highest levels of DHA. Those with less DHA also scored lower on some cognitive tests.

The researchers suggest that the lower brain volumes seen in their study were equivalent to approximately two years of ‘brain ageing’. They argue that further study is needed to confirm whether people with diets low in omega-3 fatty acids – which are mainly found in oily fish – are more likely to develop dementia.

Dr Marie Janson, Director of Development at Alzheimer’s Research UK, said:
“There has been much research into the effects of omega-3, and this study will add to that debate. One strength of this study is that it used blood samples to measure people’s dietary intake of omega-3, rather than relying on answers to questionnaires to assess the link between omega-3 and cognition. However this research does not tell us whether the people studied got worse or better over time.

“We would need to see large-scale, long-term studies before we can know whether a diet high in omega-3 can protect against dementia, and people shouldn’t fill their freezers with oily fish just yet. The best evidence for reducing your risk of dementia is to eat a healthy, balanced diet, take regular exercise and keep your blood pressure and cholesterol in check.

“With 820,000 people affected by dementia in the UK, and a rapidly ageing population, we urgently need to find ways to prevent and treat the condition – that means we must invest in research.”

This material has been published with the kind permission of Alzheimer Research UK.

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Councillor Tony Orgee Backs Alzheimer’s Research UK’s Big Walk

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The Chairman of South Cambridgeshire District Council, Cllr Tony Orgee, is urging everyone to take part in Alzheimer’s Research UK’s Big Walk in the county on Sunday 13 May. The UK’s leading dementia research charity, based in Great Shelford, aims to raise £50,000 for pioneering dementia research.

Hundreds of people are expected to join in the nine mile circular Big Walk, which starts in the picturesque village of Comberton. Walkers will enjoy exploring peaceful country lanes and an off-road ramble, following tracks through fields and country paths, alongside beautiful woodland areas.

Cllr Orgee talked about his motivation for supporting Alzheimer’s Research UK’s Big Walk:
“This is a Big Walk with a very important focus – to raise desperately needed funds for research into Alzheimer’s disease and other forms of dementia. Dementia is a devastating condition affecting not just the individual but their families and a far wider network of people.

“We are fortunate to have the UK’s leading dementia research charity based here in Cambridgeshire. It is essential that new treatments are found and Alzheimer’s Research UK is working hard to achieve that goal.

“The route for the Big Walk passes through beautiful countryside in South Cambridgeshire. I would encourage everyone to join in to help Alzheimer’s Research UK raise money to progress its crucial research.”

Miranda Mays, Community Fundraising Manager for Alzheimer’s Research UK, added:
“It’s brilliant to have Cllr Orgee’s backing for our Big Walk, helping us achieve our aim of raising £50,000. This amount will pay for an entire pilot research project, bringing us closer to finding ways to diagnose, prevent, treat and cure dementia.

“We’re delighted with the support we’ve received so far and there’s still time for people to sign up to take part or come along as a volunteer. We rely entirely on our wonderful supporters to fund our vital research and we hope everyone in Cambridgeshire and beyond will join us to help defeat dementia.

“There are 820,000 people across the UK living with dementia today, including over 6,000 people in Cambridgeshire alone. Numbers are forecast to rise substantially in the next generation and research is the only answer.”

Alzheimer’s Research UK’s Big Walk starts at 10am on Sunday 13 May, at Comberton Village College, West Street, Comberton CB23 7DU. To take up the challenge telephone 01223 843899 or email bigwalk@alzheimersresearchuk.org. Registration is £15 for adults and £7.50 for under 18s. More information is also available online at www.alzheimersresearchuk.org/big-walk

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Specific Antipsychotic Drugs Increase Risk of Death in Elderly

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US scientists have found certain antipsychotic drugs increase the risk of death in elderly nursing home patients, when compared with other antipsychotics. The study is published in the BMJ online.

Researchers at Harvard Medical School studied medical records from 75,445 people over 65 who were living in nursing homes. They assessed the risk of death in people taking different forms of antipsychotics over six months, using one particular drug – risperidone – as a comparison.

They found that one of the drugs, haloperidol, increased the risk of death when compared with risperidone. Three other treatments – aripiprazole, olanzapine and ziprasidone – showed no significant difference, while the risk of death was reduced in people taking a sixth drug, called quetiapine. The effect for haloperidol was strongest during the first 40 days of treatment, and higher doses increased the risks for all of the drugs except quetiapine.

Previous research has already shown that long-term use of antipsychotics can double the risk of death in patients with Alzhiemer’s disease, but the differences between different antipsychotic drugs have been less well studied. The researchers believe that where doctors feel they need to prescribe antipsychotics to people with dementia, these latest results could help inform their decisions about which drug to give, and what dose.

Rebecca Wood, Chief Executive of Alzheimer’s Research UK, said: “The risks associated with antipsychotics are well-established, and these findings underline the importance of ensuring that where these drugs are prescribed, their use must be carefully monitored. Antipsychotics should only be used for people with dementia where there is no alternative for dealing with challenging behaviour. Alzheimer’s Research UK has called for action to reduce the use of antipsychotics and develop alternatives, yet progress has been frustratingly slow.

“While we welcome research that can inform doctors’ decisions about prescribing existing medication, we urgently need to find safer, more effective treatments for people with dementia. These can only come through research, but funding for dementia research still lags far behind that of other serious diseases. If we are to improve the lives of people with dementia, we must invest in research.”

This material has been published with the kind permission of Alzheimer Research UK.

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Sleep Disruption Linked to Early Alzheimer’s Markers

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Scientists in the US have found cognitively healthy people with disrupted sleep patterns may be more likely to have markers associated with early Alzheimer’s disease. The study is due to be presented at the American Academy of Neurology’s 64th Annual Meeting in April.

Researchers at Washington University School of Medicine, in St Louis, studied 100 people with no cognitive problems between the ages of 45 and 80. They used a monitoring device called an actigraph to measure the participants’ sleeping patterns for two weeks, and analysed sleep diaries and questionnaires.

The researchers took samples of cerebrospinal fluid (CSF) to check for levels of amyloid, a protein that builds in the brain in Alzheimer’s. The participants also underwent PET scans to track the amount of amyloid in their brains.

A quarter of the group had increased amounts of amyloid in the brain or abnormal levels of the protein in their CSF – changes that are believed to be linked to the earliest stages of Alzheimer’s disease. The markers were more likely to be seen in people with disrupted sleep patterns, who woke more than five times an hour during the night.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“These results are yet to be published in full, but the study does raise new questions about the possible relationship between sleep patterns and the likelihood of developing Alzheimer’s disease. It’s not clear whether any of the people in this study went on to develop Alzheimer’s, and we cannot conclude from this research that disrupted sleep causes the disease – but larger, long-term studies could help us to better understand how the two may be linked.

“Experts believe that Alzheimer’s begins to develop in mid-life, years before symptoms appear, but we still need to know much more about the changes that occur in the earliest stages of the disease. The better we can understand how Alzheimer’s develops, the greater our chance of finding an effective treatment for the disease – but that means it’s vital to invest in research.”

This material has been published with the kind permission of Alzheimer Research UK.

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Specific Antibodies Halt Alzheimer’s in Mice

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Antibodies that block the process of synapse disintegration in Alzheimer’s disease have been identified, raising hopes for the development of a treatment to combat early cognitive decline in the disease.

During Alzheimer’s, a protein called amyloid-beta builds in the brain and causes the loss of synapses – the connections between brain cells.

Scientists at UCL, part-funded by Alzheimer’s Research UK, studied a second protein called Dkk1. They discovered that specific antibodies that block the function of Dkk1 completely suppressed amyloid-beta’s toxic effect on synapses. The findings are published in the Journal of Neuroscience.

Dr Patricia Salinas, from the UCL Department of Cell & Developmental Biology, who led the study, said:
“These novel findings raise the possibility that targeting this secreted Dkk1 protein could offer an effective treatment to protect synapses against the toxic effect of amyloid-beta.

“Importantly, these results raise the hope for a treatment and perhaps the prevention of cognitive decline early in Alzheimer’s disease.”

Research has shown high levels of Dkk1 in brain samples from people with Alzheimer’s disease, but the significance of these findings was previously unknown. Scientists at UCL have found that amyloid-beta causes the production of Dkk1, which in turn leads to the loss of synapses in the hippocampus, an area of the brain responsible for learning and memory.

The scientists studied the progression of synapse disintegration in the hippocampus after exposure to amyloid-beta, using brain slices from mice. They were able to monitor how many synapses survived in the presence of a specific antibody that targets Dkk1, compared to how many synapses survived without the antibody.

The results showed that brain cells that were exposed to the antibody remained healthy, and the synapses remained intact.

Dr Salinas said:
“Despite significant advances in understanding the molecular mechanisms involved in Alzheimer’s disease, no effective treatment is currently available to stop the progression of this devastating disease.”

She added:
“This research identifies Dkk1 as a potential therapeutic target for the treatment of Alzheimer’s disease.”

Alzheimer’s is the most common cause of dementia, accounting for about two-thirds of cases. Currently, dementia costs the UK economy £23 billion a year – more than cancer and heart disease combined – and the number of people with the condition is expected to double within a generation.

The research was funded by Alzheimer’s Research UK and the Biotechnology and Biological Sciences Research Council, UK.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“We’re delighted to have supported this study, which sheds new light on the processes that occur as Alzheimer’s develops. By understanding what happens in the brain during Alzheimer’s, we stand a better chance of developing new treatments that could make a real difference to people with the disease.

“Studies like this are an essential part of that process, but more work is needed if we are to take these results from the lab bench to the clinic. Dementia can only be defeated through research, and with the numbers of people affected by the condition soaring, we urgently need to invest in research now.”

This material has been published with the kind permission of Alzheimer Research UK.

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Cancer Drug Clears Alzheimer’s Protein and Improves Cognition in Mice

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US scientists have found that a skin cancer drug is able to clear a known Alzheimer’s protein, amyloid, from the brains of mice. The study, which also showed the mice had cognitive improvements, is published in the journal Science.

Researchers at Case Western University studied the effects of a drug called bexarotene, which is currently used as a cancer treatment, in mice generated to develop amyloid, a protein that builds in the brain in Alzheimer’s.

Bexarotene is known to increase the production of a protein called apoE, which is controlled by the APOE gene. One variant of the gene, APOE4, is a known risk factor for Alzheimer’s disease, and the scientists wanted to find out whether increasing the amount of apoE could help clear amyloid from the brain.

They found that a single dose of the drug was able to reduce the amount of amyloid after six hours, although after 84 hours, the protein had returned to its initial levels. Daily doses of the drug led to a progressive reduction in amyloid levels over time, while the mice also showed improvements in a range of behavioural and cognitive tests.

The scientists believe their results suggest that bexarotene could be a useful treatment for Alzheimer’s disease.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“While this early study may look promising, success in mice unfortunately does not always guarantee success in people. We would need to see the results of clinical trials before we could know whether bexarotene could prove beneficial for people with Alzheimer’s – and it would also be important to weigh up the risks of any potential side effects.

“There are a number of drugs in development that aim to clear amyloid from the brain, and the jury is still out on whether this approach will be successful as a treatment for Alzheimer’s. It may be that these treatments could be more effective if given early, meaning early detection of the disease will be crucial. If we can fully understand the causes of the disease, we stand a better chance of finding a treatment that could benefit people.

“With 820,000 people affected by dementia, we urgently need new, effective treatments for the condition – that means it’s vital that we invest in research.”

This material has been published with the kind permission of Alzheimer Research UK.

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Councillor Tony Orgee Backs Alzheimer’s Research UK’s Big Walk

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The Chairman of South Cambridgeshire District Council, Cllr Tony Orgee, is urging everyone to take part in Alzheimer’s Research UK’s Big Walk in the county on Sunday 13 May. The UK’s leading dementia research charity, based in Great Shelford, aims to raise £50,000 for pioneering dementia research.

Hundreds of people are expected to join in the nine mile circular Big Walk, which starts in the picturesque village of Comberton. Walkers will enjoy exploring peaceful country lanes and an off-road ramble, following tracks through fields and country paths, alongside beautiful woodland areas.

Cllr Orgee talked about his motivation for supporting Alzheimer’s Research UK’s Big Walk:

“This is a Big Walk with a very important focus – to raise desperately needed funds for research into Alzheimer’s disease and other forms of dementia. Dementia is a devastating condition affecting not just the individual but their families and a far wider network of people.

“We are fortunate to have the UK’s leading dementia research charity based here in Cambridgeshire. It is essential that new treatments are found and Alzheimer’s Research UK is working hard to achieve that goal.

“The route for the Big Walk passes through beautiful countryside in South Cambridgeshire. I would encourage everyone to join in to help Alzheimer’s Research UK raise money to progress its crucial research.”

Miranda Mays, Community Fundraising Manager for Alzheimer’s Research UK, added:

“It’s brilliant to have Cllr Orgee’s backing for our Big Walk, helping us achieve our aim of raising £50,000. This amount will pay for an entire pilot research project, bringing us closer to finding ways to diagnose, prevent, treat and cure dementia.

“We’re delighted with the support we’ve received so far and there’s still time for people to sign up to take part or come along as a volunteer. We rely entirely on our wonderful supporters to fund our vital research and we hope everyone in Cambridgeshire and beyond will join us to help defeat dementia.

“There are 820,000 people across the UK living with dementia today, including over 6,000 people in Cambridgeshire alone. Numbers are forecast to rise substantially in the next generation and research is the only answer.”

Alzheimer’s Research UK’s Big Walk starts at 10am on Sunday 13 May, at Comberton Village College, West Street, Comberton CB23 7DU. To take up the challenge telephone 01223 843899 or email bigwalk@alzheimersresearchuk.org. Registration is £15 for adults and £7.50 for under 18s. More information is also available online at www.alzheimersresearchuk.org/big-walk

Cambs Charity Receives Grant From Million Dollar Round Table Foundation

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Great Shelford-based charity, Alzheimer’s Research UK, has received a boost of $10,000 (equivalent to £6,100) from the Million Dollar Round Table Foundation (MDRT) in America. This grant is thanks to Simon Gibson, a Cambridgeshire supporter of the UK’s leading dementia research charity. He attended the cheque presentation, which took place at MDRT’s conference in London on 21 February at Kensington Town Hall.

Simon Gibson, who lives in Burwell, is a director of financial planning specialists Atkinson Bolton Consulting. For the past thirteenyears he has been a member of the MDRT, an international association which represents the top 40,000 financial advisors worldwide.

Simon talked about the MDRT Foundation’s generous grant and his inspiration for supporting Alzheimer’s Research UK:

“The MDRT Foundation invites its members to submit applications for charitable grants. As I am acutely aware that dementia research is desperately underfunded, and have been personally touched by this devastating disease,I nominated Alzheimer’s Research UK. This proactive charity is working hard to defeat Alzheimer’s disease and other forms of dementia and relies entirely on donations to fund its pioneering research.

“Dementia poses one of the greatest threats to public health now and in the future and so many people I speak to these days know someone affected by it. New treatments and a cure are desperately needed and research is the only answer. Not only do I have clients and personal friends who have or are suffering, my father was diagnosed over two years ago. He was a professional man for 51 years, famed among other things for his memory. It is so encouraging to see the progress that research is making and, while it may not be in time for his generation, it offers hope for mine.”

Presenting the cheque, Jennifer Borislow, President of the MDRT Foundation, said:

“The MDRT Foundation was created in 1959 and provides it members with a means to give back to their communities. We provide grants to organisations around the world and we are pleased to be able to make a contribution to Alzheimer’s Research UK. This charity’s innovative research offers new hope to those people living with the daily reality of dementia.”

Dr Marie Janson, Director of Development for Alzheimer’s Research UK, attended the cheque presentation and added:

“We are very grateful to the MDRT Foundation and Simon Gibson for this generous grant and their much valued support of our work. This money will pay for hundreds of hours of world-class dementia research and fund vital equipment for our scientists, bringing us closer to finding ways to diagnose, prevent, treat and cure dementia.

“There are 820,000 people in the UK living with dementia today, including 6,000 in Cambridgeshire. Numbers are forecast to rise substantially in the next generation and we need to fund more research urgently in order to beat this dreadful condition.”

UK’s Largest Dementia Research Conference Comes to Birmingham in 2012

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Over 250 leading dementia scientists from across the globe will gather in Birmingham this week for Alzheimer’s Research UK Conference 2012, the country’s largest dedicated dementia research conference. The event, which takes place on 27 and 28 March, will share the latest evidence on a wide range of research topics, including talks from UK-based scientists on midlife risk reduction, and the importance of early life cognition in understanding cognitive ageing.

Alzheimer’s Research UK is the UK’s leading dementia research charity and one of the top three charity funders of dementia research in the world. It holds its annual conference in a different city each year and the 2012 Birmingham event will cover a range of topics, including:

· Prof Eef Hogervorst, of Loughborough University, who will describe how people could reduce their risk of developing dementia from midlife through simple lifestyle choices;
· Prof John Starr of University of Edinburgh on the importance of early life cognition in understanding cognitive ageing.
· Dr Ottavio Arancio, of Columbia University in New York, who will talk about new approaches to developing treatments for Alzheimer’s disease, the most common cause of dementia;
· Prof Patrizia Mecocci, of the University of Perugia in Italy, who will describe the role of antioxidants in brain ageing;

Dr Eric Karran, Research Director at Alzheimer’s Research UK, said:
“UK dementia researchers punch above their weight in the global battle to defeat Alzheimer’s disease and other causes of dementia, and this conference is a crucial way for the field to collaborate. Dementia is complex, and requires scientists from many different disciplines to defeat it, so it’s important to keep this multifaceted field talking.

“Dementia is now the greatest health challenge our society faces – with 820,000 people in the UK affected, including 9,000 people in Birmingham alone, and the condition already costs our economy £23bn a year. The need for effective treatments for dementia has never been more urgent, but if we are to achieve this, it will take a huge research effort.”

Jamie and Vicki Graham, of Dauntsey near Chippenham, know only too well the devastating effects of dementia, as Jamie was diagnosed with early-onset Alzheimer’s disease in 2007 when he was just 59. The pair have since raised thousands for dementia research, and have been made Champions of Alzheimer’s Research UK in recognition of their support for the charity.

Vicki said:
“When Jamie was diagnosed with Alzheimer’s our whole world changed. Jamie has enormous courage and still has his sense of humour, but seeing him slowly deteriorate is incredibly difficult.

“We chose to raise money for Alzheimer’s Research UK because we believe that research is the only way to beat this devastating disease, yet dementia research is desperately underfunded. It’s great to see this important event bringing researchers together, and to know that scientists are making such good progress.”

Dr Sarah Aldred, of the University of Birmingham, co-ordinates Alzheimer’s Research UK’s Midlands Research Network, which will host this year’s conference. She said:
“We’re thrilled to be hosting this conference, which is a great way of bringing together scientists from a range of research backgrounds who all have a common mission – defeating dementia. We urgently need better ways to diagnose, treat and prevent dementia, and scientists must work together if we are to achieve those goals. This annual event is a fantastic chance for researchers to share their knowledge, and helps foster a collaborative spirit that can be a real boost to research.”

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Virtual Reality Exercise Games May Improve Cognition in Older Adults

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Scientists in the US today revealed the finding of a clinical trial investigating the effects of “exergaming”, or virtual reality-enhanced exercise, on cognition in a group of older adults. The study, one of the first trials of its kind, showed greater cognitive benefit for those who played exergames than those who took part in traditional exercise.

Of those participants who were enrolled, 63 completed the three month study, published in the American Journal of Preventive Medicine. All of the volunteers, aged between 58 and 99 years, rode exercise bikes an average of three times a week. Half of the volunteers rode a traditional exercise bike, whereas half rode a bike equipped with a virtual reality display. This ‘cybercycle’ provided users with 3D tours and allowed them to compete against an avatar of their last performance.

The volunteers were given cognitive assessments at the start of the study and after one and three months. Although there was no difference in exercise frequency, duration and intensity between the two groups, the cybercyclists performed better on a number of cognitive tests. In addition, fewer of the cybercyclists went on to develop mild cognitive impairment, a state of early cognitive impairment not quite severe enough to be diagnosed as dementia.

The scientists also analysed blood samples from 30 of the volunteers for a protective protein called brain-derived neurotrophic growth factor (BDNF). They found higher levels of the BDNF protein in the blood of the cybercyclists than those taking traditional exercise, suggesting that virtual reality-enhanced exercise may stimulate a greater physiological effect in the brain.

Dr Marie Janson of Alzheimer’s Research UK, said:
“We already know that exercise is an important way to keep body and mind healthy. The results from this small study suggest that combining physical and mental exercise through exergaming could have even more beneficial effects on cognition in older adults than normal exercise alone. Larger and more detailed studies will be needed to get to the bottom of exactly what aspect of exergaming could be giving the benefit, but the early results are very interesting.

“Although it may be unrealistic to expect people to invest in exergaming technology, the findings show that both mental and physical exercise are important in keeping our minds active in old age. With 820,000 people in the UK already living with dementia, and an increasingly ageing population, it is important that we invest in research into preventative strategies that could help to maintain our cognition for that little bit longer.”

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Coleraine Researchers Find New Drugs Boost Brain Cell Growth

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Scientists in Northern Ireland have found drugs that mimic some of the actions of insulin may encourage the growth of new brain cells. It’s hoped the study, funded by Alzheimer’s Research UK, could pave the way for the design of new treatments for Alzheimer’s disease.

Researchers at the University of Ulster’s Coleraine Campus studied the effects of two compounds in mice. These compounds were designed to imitate the effects of a hormone called glucose-dependent insulinotropic polypeptide (GIP), which helps cells to release insulin.

It’s known that people with diabetes, who are unable to produce enough insulin or are unable to use insulin properly, have a higher risk of developing Alzheimer’s disease. Previous research has suggested that GIP may also help protect the brain, and the team in Coleraine set out to discover what effect compounds that mimic GIP could have on the brain.

Led by Dr Emilie Faivre – who was supported by a PhD Scholarship award from Alzheimer’s Research UK – the scientists used healthy mice to test two compounds called (Pro3)GIP and D-Ala2GIP. One group of mice was given a single injection of one of the two compounds, or a saline solution, while a second group received daily injections for 30 days. They discovered that for both compounds, daily injections improved communication between brain cells and triggered the growth of new cells in part of the hippocampus – the part of the brain responsible for memory. The mice also showed a small improvement in some learning and memory tasks.

The results are published in the European Journal of Pharmacology. The scientists now want to further investigate the compounds to find out whether they may be useful as a treatment for Alzheimer’s disease, the most common cause of dementia.

Dr Faivre said:
“We were excited to see that the compounds we studied appear to have beneficial effects for the brain, but we now need to find out what effect they might have in Alzheimer’s disease. We know that diabetes is a risk factor for Alzheimer’s, and if we can understand exactly how these compounds work in the brain, we could also uncover new clues about the links between these two diseases. We still desperately need an effective treatment for Alzheimer’s, and I hope our results could take us a step closer to that goal.”

Prof Christian Hölscher, who co-authored the study, said:
“Finding ways to protect brain cells and keep them communicating could be an important step forward for fighting Alzheimer’s. More research is needed before these compounds could be tested in people, and the next step will be to investigate what causes them to affect the brain in this way. Dementia can only be defeated through research, and we hope these findings could eventually open the door to new treatments.”

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“These findings could be an important first step towards the development of new treatments for Alzheimer’s, and we now need to see whether drugs like this are able to help people with the disease. There are 16,000 people with dementia in Northern Ireland alone, yet research into the condition is desperately underfunded. It’s vital that we invest in research so that we can build on results like these, giving us a better chance of taking new treatments from the lab to the clinic.”

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Nicotine Patches May Slow Progression to Alzheimer’s

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Scientists in the US today announced clinical trial results showing that nicotine patches may improve cognitive performance in elderly people with early memory problems. The findings could take scientists a step closer to the development of new treatments to tackle dementia.

The study, published in the journal Neurology, was completed by 67 volunteers. All of the volunteers were non-smokers and had mild cognitive impairment (MCI), thinking and memory problems not yet severe enough to be diagnosed as dementia. Half of the volunteers wore a transdermal nicotine patch for the six month trial, while half wore a placebo patch which did not contain nicotine.

Nicotine, a chemical found in tobacco, is known to stimulate nerve cells in the brain – one reason why cigarettes are so addictive. Some of the nerve cells which are stimulated by nicotine in the brain play a role in preserving cognitive function and these cells can have trouble firing in people with Alzheimer’s. This had led some scientists to believe that nicotine may hold a clue to how to get these cells firing again.

Over the course of the trial, the volunteers took several different types of memory and performance test and the researchers followed their performance. The results showed that, although there was no significant difference in overall improvement between those with nicotine patches and placebo, volunteers with the nicotine patch performed better on specific tests of long term memory and attention.

Although a nicotine-based therapy is unlikely to prevent or cure the disease, the scientists hope it could in future present a way of slowing the progression from MCI to Alzheimer’s and treating some of the symptoms of the disease.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“This small study looks promising as people with MCI treated with nicotine patches showed improvements in several cognitive tests. Larger and longer term studies will be needed to get a bigger picture of the potential of nicotine-based treatments in Alzheimer’s. As we know, nicotine is highly addictive and smoking can increase our risk of Alzheimer’s as well as other serious diseases, and so we must interpret the results sensibly.

“We hope that the findings can push scientists towards developing safe and effective therapies to tackle dementia, and with 820,000 people in the UK living with dementia, this need has never been greater.”

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Stacey Solomon Gets It Right for Cambs Charity in Who Wants to Be a Millionaire

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Stacey Solomon, who shot to fame in The X Factor in 2009, has won £12,500 for Great Shelford-based Alzheimer’s Research UK, on ITV’s Who Wants To Be A Millionaire. Stacey sat in the hot seat for the Celebrity New Year Special, broadcast on Tuesday 3 January, and teamed up with comedian Lee Mack.

Stacey and Lee faced show host, Chris Tarrant as they attempted to reach the million. Between them they won £50,000 with 50% going to a lucky phone-in caller at home and the remaining 50% split between each celebrity’s chosen charity.

Recently-engaged Stacey, 22, has become a national sweetheart since rising to fame. As an ambassador for Iceland Foods, she decided to raise money for the frozen food giant’s Charity of the Year for 2011, Alzheimer’s Research UK.

Stacey said:
“I’ve watched the show on telly loads and shout out the answers. But it’s scary when you’re actually in the hot seat. Winning thousands of pounds for an amazing charity like Alzheimer’s Research UK is just fantastic.”

Rebecca Wood, Chief Executive of Alzheimer’s Research UK, the UK’s leading dementia research charity, added:
“This makes a brilliant start to the New Year and we can’t thank Stacey enough for this marvellous windfall. This huge contribution will pay for hundreds of hours of pioneering research and vital equipment for our scientists, bringing us closer to finding ways to diagnose, prevent, treat and cure dementia.

“It’s wonderful to have Stacey’s continued support as an ambassador for Iceland Foods. In December we were thrilled to learn she was releasing a Christmas single to boost our funds – a cover of Driving Home for Christmas – now this, it’s incredible!

“Over 6,000 people in Cambridgeshire are living with dementia today and 820,000 across the UK, with numbers forecast to increase significantly in the next generation. Research is the only answer but funding lags far behind that of other serious diseases. We rely entirely on our wonderful supporters to fund our vital dementia research, including people like Stacey, staff at Iceland Foods and our many fundraising volunteers in Cambridgeshire.”

To help Alzheimer’s Research UK defeat Alzheimer’s and other forms of dementia, donate online at www.alzheimersresearchuk.org or call 01223 843899.

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Stem Cell Technology Reveals Clues to Alzheimer’s

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Scientists in the US have used stem cells from patients to overcome the challenge of obtaining live brain cells, allowing them to learn more about the causes of Alzheimer’s. The study, published online today in the journal Nature, provides new opportunities for scientists to model the complex disease.

Induced pluripotent stem cells, or iPSCs, are cells which have been taken from one part of the body and can be reprogrammed into other cell types. They allow scientists to overcome the challenge of obtaining live cells from the brain – as they can take skin cells from people and transform them into brain cells.

The scientists used iPSCs to investigate what goes wrong in brain cells of people with both late-onset Alzheimer’s, and those with familial Alzheimer’s – an inherited form which tends to affect people at a younger age. Skin cells (or fibroblasts) were obtained from two people with familial Alzheimer’s, two people with late-onset Alzheimer’s disease, and two people without dementia to act as controls. The fibroblast cells were transformed into brain nerve cells in the lab and the scientists looked for features of Alzheimer’s in these cells.

The study showed that nerve cells derived from the two volunteers with familial Alzheimer’s and one of those with late-onset Alzheimer’s produced high levels of amyloid and tau, two characteristic proteins involved in Alzheimer’s. They also produced high levels of a protein called active GSK-3β which can be responsible for turning tau into its more toxic form. They also found that one particular inhibitor of amyloid production could reduce the levels of all three proteins in these cells.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“Induced pluripotent stem cells have the potential to provide a great resource for scientists to study diseases such as Alzheimer’s – where getting access to human brain cells to study is a huge challenge. The authors have shown that these cells can reveal vital clues about the biological changes taking place during Alzheimer’s and we hope further studies can expand on these early findings.

“In light of the recent European ban on patents using human embryonic stem cells, it may prove important to increase our use of technology using these non-embryonic stem cells. We hope that studies like this one will drive scientific research forward and help us to understand the biology behind different forms of Alzheimer’s and test new treatments. With 820,000 in the UK living with dementia, the need for such research has never been greater.”

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Bath Scientists Secure £220k Funding Boost for Dementia Research

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A major research project into the role of iron in dementia with Lewy bodies is getting underway in Bath, thanks to grants worth £220,500 from two charities dedicated to funding dementia research. Alzheimer’s Research UK and Alzheimer’s research charity BRACE have teamed up to fund a unique three-year project that could bring new understanding of the disease.

Led by Prof David Brown, the scientists at the University of Bath will study a protein called alpha-synuclein, which accumulates in the brain in dementia with Lewy bodies, as well as other diseases such as Parkinson’s.

Dementia with Lewy bodies is the third most common cause of dementia, affecting about 100,000 people in the UK. People with the disease experience distressing symptoms such as hallucinations, problems with movement similar to Parkinson’s disease and ‘cognitive fluctuations’ – variations in alertness, attention and thinking skills.

Until recently, the normal role of alpha-synuclein has been poorly understood, but Prof Brown and his team have discovered that the protein helps convert iron into a form that can be used by cells. Cells need a certain amount of iron to function properly, and the scientists believe that alpha-synuclein’s normal activity may help protect brain cells. They now want to find out what happens to this activity when the protein begins to accumulate.

One theory suggests that as the protein builds in the brain, it may stop working properly, leading to a lack of iron that can be used by cells. Alternatively, as the amount of alpha-synuclein increases, its activity may also increase, leading to a surplus of iron in the brain. By finding the answers to these important questions, the scientists hope to gain new insight into the chain of events that causes cell death in dementia with Lewy bodies.

Prof Brown said:
“We’re extremely pleased to have secured this funding, which will allow us to gain a much better understanding of some of the processes that occur as alpha-synuclein builds in the brain. Discovering this protein’s normal role was a crucial step forward, but this funding will enable us to investigate what goes wrong in this process. If we can understand what goes wrong in cells as diseases like dementia with Lewy bodies take hold, we stand a much better chance of finding ways to stop those diseases in their tracks.”

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“We’re delighted to be supporting this important project, which could bring us vital new information about a disease that has so far been under-researched. This study could greatly enhance our understanding of the causes of dementia with Lewy bodies, potentially giving us new clues for the development of treatments that could really benefit people.

“It’s especially pleasing to be able to work with such a well-regarded local charity to fund this project, and we hope this partnership could help us make real progress towards our common goal of defeating dementia. With more than 2,000 people affected by dementia in Bath and North East Somerset alone, there is an urgent need for research projects like this one.”

Mark Poarch, chief executive of BRACE, said:
“It’s wonderful to be able to partner Alzheimer’s Research UK and to fund this vital work at Bath University. Some of the most ground breaking research into dementia is being undertaken here in the South West. BRACE is proud to be helping some of the brightest minds in medical research beat this terrible disease.”

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Cambridge Scientists Use Down’s Syndrome Stem Cells to Model Alzheimer’s

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Scientists at the University of Cambridge have developed a new and innovative way to study Alzheimer’s disease in the lab. The stem cell technique, which allows researchers to track the disease over a matter of weeks, could provide a valuable tool for scientists to unravel the complexity of Alzheimer’s and test potential new treatments. The findings, funded by Alzheimer’s Research UK and the Wellcome Trust, will be published today in the journal Science Translational Medicine.

The scientists used skin cells donated from healthy volunteers and those with Down’s syndrome and turned them into stem cells. These stem cells were then used to generate networks of functioning nerve cells in the lab, which resemble the complex wiring of cells in the human cerebral cortex. The cortex, which makes up over three quarters of the brain, houses many of the nerve cells involved in memory and thinking and suffers particular damage during Alzheimer’s.

People with Down’s syndrome have an extra copy of chromosome 21, a segment of DNA that carries a gene responsible for producing the Alzheimer’s protein amyloid. Due to this extra version of the gene, people with Down’s syndrome have a much higher incidence of Alzheimer’s than the rest of the population. By generating nerve cells from skin cells of people with Down’s syndrome, the scientists could observe the disease process over a period of weeks and compare this to those cells derived from healthy volunteers.

Dr Rick Livesey, who led the study at the Wellcome Trust and Cancer Research UK Gurdon Institute at the University of Cambridge, said:

“One of the biggest challenges facing dementia researchers at the moment is a lack of good ways to track the disease over time. By using stem cells donated from people with Down’s syndrome – who are much more likely to develop Alzheimer’s – we have been able to track how the disease develops over a shorter time period than has been possible in the past.”

Within 28 days, the nerve cells made from people with Down’s syndrome showed more than double the amount of the Alzheimer’s protein amyloid than those from healthy volunteers and this built up into amyloid plaques within two months. The scientists also observed that a protein called tau became abnormally altered and distributed in the cells- one of the common later-stage characteristics of the disease.

Dr Livesey added:

“What is promising about this stem cell technique is that we can create functioning human cortex cells in a dish, allowing us to more closely model what is happening in our brains. Not only this, but our new model shows many of the characteristic features of human Alzheimer’s disease and will allow us to test new treatments more easily.”

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, welcomed the findings. He said:

“We are pleased to have contributed funding towards this study and we hope it can be used to unravel some of the remaining questions about how Alzheimer’s progresses. Modelling a complex disease like Alzheimer’s is a big challenge, but innovative approaches like this can improve our understanding. As the stem cells in this study were donated by people with Down’s syndrome, they differ genetically to the rest of the population, but could still offer valuable insight into the disease processes in Alzheimer’s.

“Increasing our understanding of dementia is essential not only for people with Down’s syndrome, but for the 820,000 people across the UK living with the condition. It is essential that we improve the models that we have for understanding dementia, but this can only be done through research. As dementia research is so desperately underfunded, we must invest now if we are to find the answers that are so urgently needed.”

For further information, or to speak with Dr Rick Livesey or Dr Simon Ridley, please contact Laura Phipps, Science Communications Officer at Alzheimer’s Research UK on 01223 843304, mobile 07500 803936 or email press@alzheimersresearchuk.org  

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Uk Scientists Uncover New Clues for Early Diagnosis of Alzheimer’s

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Scientists in Nottingham have found abnormal levels of seven different proteins in spinal fluid could act as markers for detecting Alzheimer’s disease. The study, which was part-funded by Alzheimer’s Research UK, the UK’s leading dementia research charity, could lead to the development of a new test to detect the disease in its early stages.

Researchers at the University of Nottingham’s Human Genetics department and Nottingham Trent University’s John van Geest Cancer Research Centre studied samples of cerebrospinal fluid (CSF) to look for potential markers of Alzheimer’s. They compared CSF samples from 33 people with Alzheimer’s disease, 20 healthy older people and ten people with mild cognitive impairment (MCI) – a condition that causes problems with memory and thinking, but not to an extent that interferes with daily life.

Dr Baharak Vafadar-Isfahani and her colleagues first analysed each CSF sample to build a profile of the proteins it contained, and looked for patterns that could distinguish between people with Alzheimer’s and healthy people. They found people with the disease tended to have higher levels of four specific proteins, and lower levels of three other proteins, suggesting that together they could act as markers for the disease.

One protein in particular, called SPARCL1, was the strongest predictor for the disease. When the CSF samples were tested for changes in SPARCL1 alone, the researchers were able to detect whether a person had Alzheimer’s disease with 65% accuracy. When they checked for abnormal levels of all seven proteins, accuracy improved to 95%. The discovery of SPARCL1, amongst other proteins, resulted from the application of technologies developed at the John van Geest Cancer Research Centre.

The scientists then tested their findings on a new set of CSF samples, taken from 32 healthy people and 30 Alzheimer’s patients. All seven markers taken together were able to detect Alzheimer’s within this new cohort with 85% accuracy.

The researchers now plan to use their results, which are due to be published online in the Journal of Alzheimer’s Disease on 7 February, to help develop a blood test that could diagnose Alzheimer’s in its earliest stages.

Prof Kevin Morgan of the University of Nottingham, who co-authored the study, said: “Our results have given us a new lead for improving early diagnosis of Alzheimer’s disease. An early diagnosis would not only help people prepare for the future, but would also enable people to be involved in clinical trials at a much earlier stage, when new treatments are more likely to have a positive effect.

“It will also be important to investigate what causes these specific proteins to change as Alzheimer’s develops. If we can understand the biochemical changes that occur during Alzheimer’s, we stand a better chance of developing new treatments that can tackle the disease. Dementia can only be defeated through research, and I hope these findings could take us a step closer to that goal.”

Professor Robert Rees, the Director of the John van Geest Cancer Research Centre at Nottingham Trent University, said:“The results of this study were obtained using analytical techniques to generate complex protein profiles from patient and control samples, coupled with advanced data analysis. We believe these findings will prove extremely important in allowing us to gain further insight into this disease.”

Dr Marie Janson, Director of Development at Alzheimer’s Research UK, said: “Improving diagnosis of Alzheimer’s disease is a key target for scientists, and these important findings have opened up a new avenue for research. Alzheimer’s can be difficult to diagnose in the clinic, as memory problems on their own can be due to a variety of reasons. This study has the potential to help create a vital tool for doctors to identify patients that need further investigation – but these results must now be followed up in order to achieve that goal.

“Currently 820,000 people are affected by dementia, yet for many people a diagnosis comes too late. If we are to improve diagnosis for future generations, we must invest in research now.”

For further information, or to speak with Prof Kevin Morgan or Dr Marie Janson, please contact Kirsty Marais, Media Officer at Alzheimer’s Research UK on 01223 843304, 07826 559233 or email press@alzheimersresearchuk.org

To speak with Prof Robert Rees or Prof Graham Ball, co-authors of the study, please contact Dave Rogers, Senior Press Officer at Nottingham Trent University on 0115 848 8782 or email dave.rogers@ntu.ac.uk 

The study was supported by Alzheimer’s Research UK, the Big Lottery Fund and the EU FP6 Program through BIOPATTERN.

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Virtual Reality Exercise Games May Improve Cognition in Older Adults

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Scientists in the US revealed the finding of a clinical trial investigating the effects of “exergaming”, or virtual reality-enhanced exercise, on cognition in a group of older adults. The study, one of the first trials of its kind, showed greater cognitive benefit for those who played exergames than those who took part in traditional exercise.

Of those participants who were enrolled, 63 completed the three month study, published in the American Journal of Preventive Medicine. All of the volunteers, aged between 58 and 99 years, rode exercise bikes an average of three times a week. Half of the volunteers rode a traditional exercise bike, whereas half rode a bike equipped with a virtual reality display. This ‘cybercycle’ provided users with 3D tours and allowed them to compete against an avatar of their last performance.

The volunteers were given cognitive assessments at the start of the study and after one and three months. Although there was no difference in exercise frequency, duration and intensity between the two groups, the cybercyclists performed better on a number of cognitive tests. In addition, fewer of the cybercyclists went on to develop mild cognitive impairment, a state of early cognitive impairment not quite severe enough to be diagnosed as dementia.

The scientists also analysed blood samples from 30 of the volunteers for a protective protein called brain-derived neurotrophic growth factor (BDNF). They found higher levels of the BDNF protein in the blood of the cybercyclists than those taking traditional exercise, suggesting that virtual reality-enhanced exercise may stimulate a greater physiological effect in the brain.

Dr Marie Janson of Alzheimer’s Research UK, the UK’s leading dementia research charity, said:

“We already know that exercise is an important way to keep body and mind healthy. The results from this small study suggest that combining physical and mental exercise through exergaming could have even more beneficial effects on cognition in older adults than normal exercise alone. Larger and more detailed studies will be needed to get to the bottom of exactly what aspect of exergaming could be giving the benefit, but the early results are very interesting.

“Although it may be unrealistic to expect people to invest in exergaming technology, the findings show that both mental and physical exercise are important in keeping our minds active in old age. With 820,000 people in the UK already living with dementia, and an increasingly ageing population, it is important that we invest in research into preventative strategies that could help to maintain our cognition for that little bit longer.”

Image reproduced from http://www.poly.edu

Men at Higher Risk of Mild Memory Loss in Old Age

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US scientists have found that men may be at higher risk than women of mild cognitive impairment – a stage that often precedes dementia. The study is published online in the journal Neurology.

Researchers from the Mayo Clinic in Rochester, Minnesota, studied 1,450 people between the ages of 70 and 89, for an average of three years. Participants took part in evaluations every 15 months to assess whether or not they had mild cognitive impairment (MCI). MCI causes problems with memory and other thinking skills, but not to an extent that interferes with everyday life. Roughly half of all people who are diagnosed with MCI go on to develop dementia, usually Alzheimer’s disease, within five years.

Over the course of the study, 296 people were diagnosed with MCI, but the researchers found that men were more likely to develop the condition than women. The results were surprising because previous research has shown women are more likely to develop dementia than men.

Further analysis showed that MCI with memory loss – known as amnestic MCI – was more common than non-amnestic MCI, where memory loss is not a major symptom. People who had less education or were not married were also more likely to develop MCI. The scientists suggest that further research could reveal whether different risk factors affect separate groups of people in different ways.

Dr Marie Janson, Director of Development at Alzheimer’s Research UK, said:
“These surprising results suggest that men may be at greater risk for MCI despite having a lower risk for dementia, and it will be important to see whether further studies can replicate these findings. A key goal for research is to identify why some people with MCI develop dementia while others don’t. If we can understand why some people have a greater risk for cognitive decline and dementia, we stand a better chance of being able to prevent the condition.

“With 820,000 people affected by dementia, and a rapidly ageing population, the need for research to find new ways to treat and prevent the condition has never been more urgent.”

Image reproduced from http://www.pediatrics.med.ubc.ca