Are You A Man or A Mouse?

How the Mus musculus is furthering our understanding of human inherited diseases

In 1907 Cuenot mated two yellow mice giving an unexpected, unmendelian 2:1 offspring ratio.
5 years later Castle and Little repeated the experiment, determining that 1 in every fourth offspring had died during embryonic development.
Nearly a century ago, mice where already paving the way to crucial discoveries, such as that of lethal genes, imagine what they have taught us to this day.

Are you a man or a mouse?

The film set of a laboratory is never truly complete without several cages of our rodent acquaintances, the Mus musculus. However, it may come as a shock to know that these creatures are lifting the lid on a number of human inherited diseases such as Marfan’s Syndrome, which affects 1 in 4,000 people and Huntington’s disease affecting 1 in 15,000. The concept of man and mouse being essentially constructed by nearly identical genetic instructions seems ludicrous; nevertheless scientifically unravelling our genetic code has brought up numerous startling findings.

The human genome consists of approximately 20,000-25,000 genes, hereditary units of coded information determining specific characteristics displayed by living organisms and unnervingly more than 3,700 are known to have 100,000 germline mutations associated with human inherited diseases. Research is crucial to understand these diseases, though the use of human subjects springs up an endless list of complications, from timescale needed to gather results and observations to unethical risk to life. As a result, scientists use a whole host of creatures to further our understanding of human genetics from the roundworm Caenorhabditis elegans, to the humble fly, Drosophila melongaster. The questions ‘What exactly do I have in common with these creatures?’ and ‘Surely the research could never be directly applicable to humans?’ may come to mind and are more than fair to ask. The correct term for these creatures is model organisms; organisms such as the Mus musculus with their mammalian origin and 99% genes in common with human beings. In addition, the Haldane report has fully sequences the mouse genome, another advantage to having a much smaller genome than ours. On a practical level, mice are easy to care for, quick to breed and provide results within a feasible timescale. The key is that mice can be afflicted with the same diseases as humans; therefore duplicating a gene such as exon 3 on the cftr allele swiftly creates a mouse model for cystic fibrosis. Experimentation further allows us to understand the nature of the disease, as 40% of the mice died within 7 days due to intestinal obstruction.

The importance of maternal diet during pregnancy is relatively well acknowledged, however a study using mice coat colours, may have mothers-to-be everywhere thinking twice about what they consume. Mutation of the agouti gene by unmethylation led to mice with yellow coat colour, it was discovered that these mice where more likely to be obese as well as prone to diabetes and cancer. Mice with brown coats have methylated agouti genes and these where found to be of healthy weight and at a lower risk of disease. Pregnant yellow mice with a methyl-rich diet birthed brown coat colour mice, indicating that nutrition does genetically affect a foetus during pregnancy also highlighting that human disease such as obesity can be inherited as a result of maternal diet during pregnancy. In another study researchers drew a similar conclusion that nutrition influences gene expression during embryonic development, which was passed down through generations because of epigenetic inheritance; intracisternal A-particle (repeated transposable elements e.g. there are one thousand copied in the mouse genome) (IAP) reterotransposon was inserted in front of the agouti gene to produce patchy mouse coat colour down the female germ line but not the male germ line.

Most recently gene targeting in embryonic stem cells produces mice with alterations to specific endogenous genes, knock-out mice are providing great insight into human inherited disorders as individual genes can be targeted and more advanced techniques are being developed. With over 300 new inherited disease genes being found every year, and one hundred year’s on since their first (if accidental) use, the role of mus musculus in broadening our knowledge of human inherited disorders is unarguably spectacular. So next time a mouse scuttles into the kitchen, perhaps it would be more fitting for it to find a piece of cheese on a plate rather than a mouse trap.

Cognitive Activity Throughout Life Linked to Lower Levels of Alzheimer’s Protein

Scientists in the US have found that healthy older people who have engaged in cognitive stimulation activities throughout their life have lower levels of the protein amyloid in their brains, a hallmark of Alzheimer’s. The study is published online today in the journal Archives of Neurology.

The researchers recruited 65 cognitively normal older people, alongside ten people with Alzheimer’s disease and 11 young people to act as controls. The healthy older volunteers were asked to report how often they took part in common cognitive activities such as writing emails or letters, reading books and newspapers, and playing games. They were also asked to report how often they took part in physical activity such as cycling or walking. The volunteers were then asked to take memory tests and brain scans to look at the amount of amyloid in their brains.

The study showed an association between the amount of cognitive activity reported in early to middle life and the amount of amyloid in the brains of the healthy elderly volunteers. Although large amounts of amyloid in the brain is a characteristic feature of Alzheimer’s disease, lower levels of amyloid can also be seen in the brains of older people with no reported cognitive problems. The study found that the more cognitive activity that the volunteers took part in throughout life, the less amyloid could be seen on their brain scans.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“The authors of this small study suggest that there may be benefits to keeping an active mind throughout life, not just in old age. Whilst the study found an association between cognitive activity and the levels of amyloid protein in the brain of healthy elderly volunteers, we cannot conclude that one directly causes the other.

“It would be important to follow these healthy participants and see whether those that reported higher cognitive activity were less likely to develop Alzheimer’s in the long run. With 820,000 people in the UK living with dementia, it is essential that we understand the factors that can lower our risk, so we must invest in more research.”

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Genetic Factors May Influence Intelligence Change Throughout Life

An international team of scientists has discovered that genetic factors are likely to influence how much a person’s intelligence changes, in comparison to their peers, throughout their lifetime. The study of nearly 2,000 people, which was part-funded by Alzheimer’s Research UK, is the first of its kind to look at a large sample of people tested on two occasions more than half a century apart.

Scientists from the University of Edinburgh and the University of Aberdeen collaborated with researchers in Queensland, Australia to study unique cohorts of people, known as the Lothian and Aberdeen Birth Cohorts. The participants had all taken an IQ-type test at the age of 11, as part of the Scottish Mental Surveys of 1932 and 1947. Decades later, the researchers tracked down surviving members and asked them to re-take the same and other cognitive tests at age 65, 70 or 79. This allowed them to see how people’s intelligence test scores had changed from childhood to old age. By collecting a wealth of extra information on the participants – such as their medical history and social and environmental factors – the scientists aim to uncover different things that influence mental ageing.

In the current study, the DNA of 1,940 people was analysed using a genetic chip that tested more than half a million genetic markers. The researchers set out to discover whether changes – and stability – in intelligence over a lifetime could be down to genetic factors.

Using a new, complex statistical method, the team was able to estimate how far genetic variations were likely to contribute to intelligence over a lifetime. Their results, which are published online in the journal Nature, suggest that genetic factors contribute to intelligence in childhood and old age, and to about a quarter of the changes in between. The scientists explain that further study is needed to identify the exact genetic causes of changes in intelligence.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“Cognitive decline in old age is a known risk factor for Alzheimer’s disease, and understanding what may cause or protect against this decline is crucial for dementia research. This study has identified a possible genetic cause for changes in cognitive ability over time, and it will now be important to discover exactly how our genes may contribute to cognitive decline. If we can understand how our genes influence cognitive decline, this may provide new clues for developing effective treatments for Alzheimer’s.

“We’re delighted that funding from Alzheimer’s Research UK has helped make this study possible, and it’s now essential that these results are followed up. With 820,000 people affected by dementia in the UK, we urgently need to find new ways to treat and prevent the condition, and that means we must invest in research.”

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Virtual Reality Exercise Games May Improve Cognition in Older Adults

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

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

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

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 or call 01223 843899.

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Stem Cell Technology Reveals Clues to Alzheimer’s

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

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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The Optimum Health Clinic Research Paper published

We are very proud to be able to share with you the first published paper for the OHC Research Department. It was published in the Journal of Integral Theory and Practice in the USA in December 2011, and has received excellent feedback. It outlines the OHC approach to ME, CFS and Fibromyalgia in academic terms, and is a great introduction to the already published research that supports the OHC model. You can watch a video about the paper with Alex and Dr Arroll below, along with downloading the paper in full. Please do take the time to take a look, we believe this is one of the most important documents we have released in the eight years we have been running. Please also do post your comments!

   Click here to download the paper in full.

Practitioner Course

We still have just a few places left for the practitioner training starting in February, so if you are interested in having more support for your healing path, whilst also opening up exciting future career prospects, please visit and if you are interested in applying.

Conscious Transformation

Finally, after a number of requests over the past year, Alex’s groundbreaking seminar “Conscious Transformation” is making a return later this month. It is in a brand new web-based format and broken down into weekly training sessions, meaning you can take part from the comfort of your own home. Alex has also added some very exciting new material! Keep an eye on your e-mail for the official announcement and details sometime hopefully next week!

Content reproduced with the kind permission of the Optimum Health Clinic.

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

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  

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Men at Higher Risk of Mild Memory Loss in Old Age

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.”

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Government Announces New Plans to Boost Medical Research

Alzheimer’s Research UK has broadly welcomed the government’s announcement to boost research and innovation in life sciences in the UK. The Prime Minister’s speech, which coincides with the release of the government’s Strategy for UK Life Sciences, has pushed for greater collaboration between the health service and private medical companies to promote medical advances in the UK.

As part of the package of new measures proposed, David Cameron has laid out plans to allow private health care companies access to anonymised patient records from the NHS. Other schemes set out in the life science strategy include a £180m ‘catalyst fund’ to drive the development of new treatments and technologies, and an ‘early access scheme’ to allow some seriously ill patients to have access to new drugs which have shown promise in clinical trials but not yet been fully licensed.

The government hopes that the strategy will boost the life sciences industry in the UK, seen as a great potential area for economic growth. By making it easier for medical advances to reach the clinic, it hopes to provide greater benefit to patients and maintain the UK’s position as a global leader in research and innovation despite the tough economic climate.

Rebecca Wood, Chief Executive of Alzheimer’s Research UK, said:
“The Prime Minister’s announcement has the potential to give patients more effective treatments sooner.

“A scheme to make greater use of public data will need to be subject to tight regulation, but if it could drive the development of new treatments and advance our knowledge of global health problems such as dementia, we should allow it to be fully considered.

“The prime minister has highlighted the achievements being made by UK dementia scientists. It is essential that the advances being made are translated into patient benefits as quickly as possible. With dementia research so hugely underfunded, effective collaborations between charity funders, pharmaceutical companies and the NHS could lead to the breakthroughs we so desperately need.

“With 820,000 people in the UK living with dementia, we must invest in research now if we are to beat this devastating disease.”

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Brain Changes Could Predict Alzheimer’s Earlier

Scientists in Finland have discovered changes in the brain that may signify the transition between early memory problems and Alzheimer’s. The study, published in the journal Translational Psychiatry, opens up new avenues for improving early diagnosis of the disease and identifying people at risk.

The researchers from the VTT Technical Research Centre examined factors which could predict whether someone with early memory problems, called mild cognitive impairment (MCI), would go on to develop Alzheimer’s disease. The scientists performed a prospective study, taking blood samples from 143 people diagnosed with MCI, 37 people with Alzheimer’s disease and 46 healthy controls and followed the participants for up to 31 months.

Blood samples were analysed for their content of ‘metabolites’- small molecules found in body tissue and fluid involved in chemical reactions. There are a number of factors which can shift the balance of metabolites in the body, including age, diet, and disease. By looking at the profile of different metabolites in the blood of the volunteers, the scientists could identify signatures of particular molecules which were most associated with each state of health.

At follow up, 52 out of the 143 people who started the study with MCI had progressed to Alzheimer’s. Analysis of their biochemical signature showed changes in a metabolic pathway – called the pentose phosphate pathway – was associated with this transition. The study highlights the role metabolites could play in developing new techniques for earlier diagnosis of Alzheimer’s, or predictions of who may go on to develop the disease.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“With many billions of chemical reactions happening in our body all the time, metabolites present a gold mine of potentially useful information for scientists. This study presents promising early results that biochemical signatures in blood could aid in the identification of people at a higher risk of developing Alzheimer’s. The study has highlighted important biological pathways which should be investigated further.

“Alzheimer’s Research UK is funding similar studies to understand more about the profiles of metabolites and how they could help us develop new ways to defeat dementia. With 820,000 people in the UK living with dementia, there is a desperate need to learn more about the changes taking place in the body and we must invest in research now if we are to make the strides which are urgently needed.”

For further information, or to speak with Dr Simon Ridley, please contact Laura Phipps, Science Communications Officer at Alzheimer’s Research UK on 01223 843304, mobile 07500803936 or email

  • Alzheimer’s Research UK is the UK’s leading charity specialising in finding preventions, treatments and a cure for dementia.
  • To help us defeat dementia, donate today by visiting or calling 01223 843899.
  • We are currently supporting dementia research projects worth over £18 million in leading Universities across the UK.
  • Research discussed is ‘Metabolome in progression to Alzheimer’s disease’ M OreÅ¡ič et al., Translational Psychiatry (2011)

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Olympian Backs Big Walk for Alzheimer’s Research UK

Britain’s number one female javelin thrower Goldie Sayers is putting her weight behind Alzheimer’s Research UK’s Big Walk in Cambridgeshire on Sunday 22 May. Goldie is urging everyone to step up to the challenge and help the UK’s leading dementia research charity raise £10,000 to pay for 500 hours of pioneering dementia research.

Hundreds of people are expected to take part in the ten mile Big Walk, which starts and finishes in Great Shelford, home to Alzheimer’s Research UK. The route heads towards the centre of Cambridge, via footpaths and countryside, passing the Botanical Gardens and on through Grantchester Meadows.

Cambridge-based Goldie, 28, who represented Britain at the Beijing and Athens Olympics, said:
“This is a Big Walk with a fantastic focus – to raise desperately needed funds for dementia research. It’s a marvellous opportunity to keep fit, have fun and see some beautiful areas of Cambridgeshire that can only be fully appreciated on foot. And keeping fit can help reduce the risk of many serious diseases, including dementia, so everyone’s a winner!

“It’s great to know Alzheimer’s Research UK is there for us all, dedicated to finding new treatments for dementia so that future generations can reap the benefits.

“Representing Britain and competing in the Olympics takes real dedication too and my training for the London 2012 trials takes up all my time. My thoughts will be with everyone on the day of the Big Walk and I hope as many people as possible will join in to help Alzheimer’s Research UK defeat dementia.”

Miranda Mays, Community Fundraising Manager for Alzheimer’s Research UK, added:
“Our Big Walk is a first for Alzheimer’s Research UK and we plan to make it a regular date on the Cambridgeshire calendar. It’s just brilliant to have Goldie’s backing for this event and we look forward to following her progress with the London 2012 Olympics.

“We’ve been amazed by 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, and help us achieve our goal of raising £10,000. Every step taken and every penny raised will bring us closer to finding ways to diagnose, prevent, treat and cure dementia.

“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. Dementia can only be defeated through research but funding lags far behind other serious diseases and we rely entirely on our wonderful supporters.”

To take up the challenge or volunteer to help on the day, contact Alzheimer’s Research UK’s Big Walk team on 01223 843899 or email To register, adults £15, under 18s £7.50. More information is also available online at

About Alzheimer’s Research UK: Alzheimer’s Research UK is the UK’s leading dementia research charity specialising in finding preventions, treatments and a cure for dementia. Based in Cambridge, they believe that science and innovation hold the key to defeating dementia. Alzheimer’s Research UK conducts world-class research to prevent, treat and cure dementia. They help people to understand dementia and the progress they are making. Alzheimer’s Research UK forges partnerships with Government and other key organisations to make dementia research a national priority. For further details, check out the Alzheimer’s Research UK website.

Image courtesy of Alzheimer’s Research UK