Tag Archives: Alzheimer’s disease

UK researchers have suggested existing drugs for conditions such as high blood pressure and diabetes could have potential benefits for people with Alzheimer’s. The review paper is published on Wednesday 31 October 2012 in the journal Nature Reviews Drug Discovery.

The researchers carried out a review of existing evidence for a range of different drugs used to treat a number of different conditions. Based on the available evidence, the team identified several drugs for conditions including hypertension, diabetes and skin conditions, which they believe may have potential to fight Alzheimer’s disease.

Lab experiments from previous studies have suggested that some of these drugs may be capable of reducing a protein called amyloid, which accumulates in the brain during Alzheimer’s, while other studies have shown some of the treatments had a positive effect on cognition in mice. The researchers suggested a number of steps that could be taken to investigate these drugs further – such as carrying out early clinical trials to investigate their benefits in patients with Alzheimer’s.

Rebecca Wood, Chief Executive of Alzheimer’s Research UK, said:
“The idea that drugs for other conditions could also fight Alzheimer’s is appealing, as drugs already licensed for use in people could potentially be made available far sooner – but it’s not yet clear that such a drug exists. Alzheimer’s is a complex disease with many risk factors and it may prove difficult to unpick how existing drugs for other conditions could affect the disease. Large clinical trials would be needed to discover whether any of the drugs highlighted in this review could have benefits for people with Alzheimer’s.

“While Alzheimer’s Research UK is funding a number of studies investigating the potential of existing drugs, efforts to develop treatments specifically designed to alter the course of the disease must also continue. Research to understand the causes of Alzheimer’s, which currently affects half a million people in the UK, is vital if we are to find a way to stop the disease in its tracks.”

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

Scientists in the Netherlands have found that people who feel lonely – distinct from their actual social situation – are more likely to develop dementia later in life. The research, which is part of the Amsterdam Study of the Elderly, is published online on 10 December in the Journal of Neurology Neurosurgery and Psychiatry.

The researchers from VU University in Amsterdam followed 2,173 people over the age of 65 who did not have dementia and were living at home. The participants were asked to complete questionnaires covering a range of characteristics including health, cognition, daily functioning, depression, anxiety and feelings of loneliness. Social isolation was also assessed as whether participants lived alone, were unmarried or receiving no social support. Memory and thinking tests were used to test the cognitive performance of participants at the start of the study and after three years of follow-up.

The research found that, after adjusting for other risk factors, those participants who rated themselves as feeling lonely were 1.64 times more likely to develop dementia than those who did not express such feelings. However, this was distinct from social isolation factors such as living alone or being unmarried, which did not show a link to dementia risk.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“Research is showing us that there are a wide range of risk factors for dementia, including age, lifestyle and genetics. Age still remains the biggest risk factor for dementia, but this study links feelings of loneliness to a slightly higher risk of the condition. While such a finding could have important consequences for society, it is hard to determine cause and effect at this stage – feelings of loneliness could be a consequence of the early stages of dementia rather than a contributing factor.”

“With an increasingly ageing population in the UK, social isolation of the elderly is already a growing problem and it will be important to understand more about its effects on our health and wellbeing. There are 820,000 people in the UK already living with dementia, so unravelling the risk factors for the condition is of vital importance.”

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

Three studies have been presented at the Annual Meeting of the Radiological Society of North America, shedding more light on the factors that might influence brain health in ageing.

The first study was led by scientists from the University of California in Los Angeles, who studied data from a group of 876 over-65s. Participants filled out a questionnaire on their leisure-time activities, including sports, gardening, cycling and dancing. They were also given memory and thinking tests and had an MRI scan to look for changes in the volume of grey matter – the part of the brain that holds the bodies of nerve cells. The scientists report that physical activity is associated with higher grey matter volume on brain scans, indicating better brain health.

Rebecca Wood, Chief Executive of Alzheimer’s Research UK, said:
“These results suggest that physical activity may help preserve grey matter, adding to existing evidence that what’s good for your heart is also good for your head. Although it’s not clear from this study whether an active lifestyle was also linked to better thinking skills, we do know that exercise can help lower the risk of dementia.

A second study, presented by Chicago scientists, used brain scans to look at the movement of water molecules through the brain. They used this technique as an indicator of the structural integrity of the brain, something that breaks down during Alzheimer’s. A group of 152 elderly volunteers were assessed using the brain scan, and asked to rate how often they engaged in mentally stimulating activities, like puzzles, playing games and reading the newspaper. The team found that those participants who reported taking part in more mentally engaging activities had better signs of brain integrity on the brain scan.

Rebecca Wood, said:
“This research suggests that keeping mentally active later in life could help maintain the brain’s integrity, but it is not clear from the research what this may mean for someone’s health in the long run. It would be interesting to see whether these structural changes were also linked to a risk of cognitive decline and dementia in this group of volunteers.

“The idea that keeping the brain active in old age could help stave off cognitive decline is not a new one, but scientists are still piecing together exactly why this may be. With 820,000 people in the UK living with dementia and this number rising, research into healthy brain ageing is becoming increasingly important.”

The third study presented at the conference compared the rate and pattern of brain shrinkage in a group of 109 volunteers. The participants had brain scans when they were first diagnosed with Alzheimer’s and these were compared to scans taken a year before and after the diagnosis. The team mapped the patterns of brain cell loss in each volunteer, building up a picture of how the brain changed with the progression of the disease. They found that the female participants initially showed a greater rate of brain shrinkage, with men matching that at a later stage with a more aggressive period of decline.

Dr Laura Phipps of Alzheimer’s Research UK, said:
“It is interesting to see differences between men and women in the rate of brain shrinkage during Alzheimer’s, but the potential reasons for this variation aren’t yet clear. The findings highlight the need to delve a little further into gender differences in Alzheimer’s, as it could have implications for the design of new treatments or research studies.

“We know that diseases like Alzheimer’s are incredibly complex, and understanding gender differences in the disease could help point to potential risk factors. With more and more people being affected by the disease, funding for research into Alzheimer’s and other dementias has never been more important.”

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

Scientists have identified a molecular chain of events thought to drive inflammation during Alzheimer’s, and shown that blocking this cascade could reduce signs of the disease in mice. The findings are published in the journal Nature.

The study, a collaborative effort between scientists in Germany, Spain and the US, focused on the growing evidence for the role of inflammation in Alzheimer’s disease. The team studied a group of proteins known to trigger inflammation, some of which have already been linked to rheumatoid arthritis.

One of the proteins, called caspase-1, was found to be more active in the brains of people with Alzheimer’s, suggesting it could play a role in the development of the disease. The researchers set out to study this protein in more detail, along with a second inflammatory protein called NLRP3. To do this, the team bred mice to show features of Alzheimer’s, including the build-up of the hallmark Alzheimer’s protein, amyloid. The scientists also bred mice to lack either caspase-1 or NLRP3, to help them understand what role both proteins may play in the development of the disease.

The researchers compared the performance of the mice on memory tasks and found that those that lacked either caspase-1 or NLRP3 appeared protected from the memory problems normally associated with features of Alzheimer’s. Blocking the action of the two proteins also led to lower levels of amyloid in the brains of the mice.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“Recent research has highlighted inflammation as a key process in the development of Alzheimer’s disease and this study adds further support to this. The findings are still at an early stage, but it is only by unravelling these molecular details that will we will understand how inflammation could contribute to Alzheimer’s and how this damage may be stopped.

“More research is needed to build on these findings, but with a growing body of support, research into inflammation in Alzheimer’s is an important area for the future. We need to see long-term commitment to dementia research to ensure that new areas of research get the investment they need, to take us closer to finding answers for the hundreds of thousands affected by these devastating diseases.”

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

Research published this week has identified a gene called Hes1, which appears to protect nerve cells from the toxic effects of the hallmark Alzheimer’s protein, amyloid. The study is published in the journal Alzheimer’s Research and Therapy.

One of the characteristic features of Alzheimer’s disease is the build-up of a protein called amyloid into plaques in the brain. These plaques can cause nerve cells to die, but the exact way this happens still remains to be understood.

The scientists, from the Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) in Spain, had previously discovered that amyloid can block the action of a protein called nerve growth factor, important for keeping nerve cells healthy. Their work showed that amyloid blocked a chain of events normally triggered by nerve growth factor, causing a reduction in the activity of a gene called Hes1. This appeared to prevent nerve cells from communicating effectively with each other, causing them to die.

In this study, the scientists took this research a step further, using their findings to develop new ways to protect nerve cells from amyloid. To do this, the team used mouse nerve cells, taken from an area of the brain called the hippocampus, known to be important for memory.

The researchers boosted Hes1 activity, either directly or by altering proteins known to control it, and found it could protect these nerve cells from the toxic effects of amyloid. The cells appeared healthier, had more connections and were more likely to survive when treated with amyloid. The laboratory findings suggest potential new strategies for blocking the effects of amyloid in human nerve cells.

Shirley Cramer CBE, Chief Executive of Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“Understanding what causes the loss of brain cells in Alzheimer’s is a key goal for the development of new treatments for this devastating disease. This study highlights an important molecular chain of events blocked by the hallmark Alzheimer’s protein amyloid. The results show that restoring the activity of this cascade could protect nerve cells in the lab against the toxic effects of amyloid.

“While there may be a long way to go before these findings could be turned into a potential new treatments in people, this kind of early stage research is vital for helping us piece together the puzzle. There are more than half a million people in the UK living with Alzheimer’s disease and that number is expected to rise. There must be a concerted effort to make research into dementia a national priority and secure long-term investment for research.”

Image reproduced from http://static.ddmcdn.com/

Two research studies published today suggest that physical activity may not only protect against signs of brain ageing in people in their 70’s, but it is also associated with lower rates of dementia in people over the age of 90.

Signs of brain ageing

Scientists from the University of Edinburgh have revealed that exercise may be more beneficial for protecting against signs of brain ageing than mental activity. The research, published on 23 October in the journal Neurology, followed 691 volunteers from a research group called the Lothian Birth Cohort 1936. All the participants were born in 1936, and the team has been studying the factors affecting their memory and thinking ability as they age.

When they were 70, the volunteers completed questionnaires rating their physical activity and how often they participated in social and intellectual leisure activities. Three years later, they had an MRI brain scan to look for structural features in the brain associated with cognitive decline.

The researchers found that volunteers who reported higher levels of physical activity had less brain shrinkage three years later when their scan was compared to an estimate of their brain size from youth. They also had fewer structural features in the brain normally associated with a decline in memory and thinking skills. In contrast, the amount of mental activity reported by volunteers was not associated with signs of ageing on brain scans.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“This study links physical exercise to fewer signs of ageing in the brain, suggesting that it may be a way of protecting our cognitive health. While we can’t say that exercise is the causal factor in this study, we do know that exercise in middle age can lower the risk of dementia later in life. It will be important to follow the volunteers to see whether these structural features are associated with greater cognitive decline over the coming years. More research is also needed to tease out how physical activity might be having a beneficial effect.

“We need to understand more about the risk factors of cognitive decline, but this knowledge can only come through research. We must continue to support dementia scientists to provide the answers.”

Physical activity in the oldest old

Researchers from the University of California have followed 629 people over the age of 90, revealing that better physical performance is linked to lower rates of dementia in the oldest old. The study is published online on 22 October in the journal Archives of Neurology.

The volunteers, including 31 centenarians, completed a range of physical activities including a four metre walk, five timed chair-stands and a 10-second standing balance task. They were scored based on their ability to complete each task and also underwent memory and thinking tests.

The scientists found that participants who were unable to walk were more than 30 times more likely to have dementia. Those who had better physical performance were less likely to have the condition.

Dr Ridley said: “Age is the biggest risk factor for dementia, and with more people living into their 90s and beyond, understanding the factors affecting brain health in the oldest old will be increasingly important. This study reports higher rates of dementia in people over 90 who are unable to complete light physical tasks, but it is hard to draw firm conclusions on cause and effect at this stage.

“While the findings highlight the profound effect that dementia can have on our whole body, more research will be needed to find out whether the lack of movement may have contributed to the condition. With research into dementia so desperately underfunded, we must ensure that research into Alzheimer’s and other dementias remains a national priority.”

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

A major five-year trial of gingko biloba extract in elderly people has shown the supplement does not prevent the onset of Alzheimer’s disease. The study is published on Thursday 6 September in the journal Lancet Neurology.

Researchers in France, led by a team at the University of Toulouse III, studied 2,854 people over the age of 70 who had mild memory problems, but not Alzheimer’s disease, at the start of the study. The participants were randomised into two groups, with 1,406 people receiving 120mg of gingko biloba extract twice a day over a five-year period, and 1,414 people receiving a placebo.

Gingko biloba extract, derived from the leaves of the gingko biloba tree, had previously been suggested by some as a potential method of preventing Alzheimer’s disease, but there has been a lack of good evidence to show that the supplement has any beneficial effect. This latest study aimed to comprehensively test whether gingko biloba was able to stave off the disease.

The participants’ thinking skills and functional abilities were assessed at the start of the study and on an annual basis throughout the trial. By the end of the study, 61 people taking ginkgo biloba had developed Alzheimer’s disease (4%), compared to 73 people in the placebo group (5%).

The researchers concluded that gingko biloba had no protective effect against Alzheimer’s.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“While negative results are always disappointing, large-scale trials like this one are vital for people to make informed decisions about whether to take supplements such as gingko biloba. These results, backed up by previous research, give us the clear evidence that gingko biloba is not the ‘magic pill’ people desperately hope for.

“While we can’t yet prevent Alzheimer’s, the best evidence for reducing the risk of the disease is to eat a healthy diet, exercise regularly, and keep blood pressure and cholesterol in check. This trial underlines the urgent need for effective ways to prevent Alzheimer’s disease, and research has the potential to uncover these.

“Currently half a million people in the UK are living with Alzheimer’s disease, the most common cause of dementia, and as our population ages that number is expected to soar. To head off a future crisis and find ways of preventing the disease, we must invest in research now.”

Image reproduced from http://static.ddmcdn.com/

A study has shed light on successful cognitive aging by revealing that high levels of a protein in people over the age of 75 are associated with a lower risk of dementia in close family members. The findings are reported online on 15 August in the journalNeurology.

Researchers set out to investigate the factors that influence healthy cognitive aging in people over the age of 75. They looked at a protein called C-reactive protein (CRP), known to play a role in inflammation. High levels of CRP have been linked to cognitive decline in midlife but appeared to have the reverse effect in late-old age.

To investigate whether CRP could be linked with healthy cognitive ageing, the scientists studied a group of 277 male veterans from New York who were all over the age of 75 and cognitively healthy. As well as providing scientists with details about their life and health, the volunteers provided a blood sample that scientists used to measure levels of the protein in their blood.

The team collected information about 1329 parents and siblings of the volunteers, to see how many first-degree relatives had dementia. They found that close relatives of volunteers with the highest levels of CRP had a lower risk of dementia. The link was further confirmed in a second independent group of 51 volunteers over the age of 85.

The results suggest that high levels of CRP in cognitively healthy older people could be a marker for dementia resistance, and this resistance may pass through families.

Shirley Cramer CBE, Chief Executive of Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“Understanding the factors that drive healthy ageing is important for determining why some people are more likely to develop dementia. The findings suggest that high C-reactive protein levels in older people may be an indicator of healthy ageing in that their near relatives appear more resistant to dementia. The next step will be for researchers to learn more about why these family members appear to be more protected, and whether there are specific genes involved.

“It is incredibly important to understand the risk factors for dementia. Delaying the onset or progression of the diseases that cause dementia by even a year could have a huge impact on the families and society. With over 820,000 people in the UK living with dementia, we must invest in research to move us towards a world free from dementia.”

Image reproduced from http://static.ddmcdn.com/

Research from Australia has revealed that the presence of the hallmark Alzheimer’s protein amyloid in the brain is a greater predictor of memory decline than carrying the Alzheimer’s risk gene APOE4. The research is published on 16 October in the journal Neurology.

The protein amyloid occurs naturally in the brain, but can start to clump together to form amyloid ‘plaques’ in the brain during Alzheimer’s disease. In this study, the scientists used advanced brain scanning techniques to measure the build-up of amyloid in 141 healthy older adults over an 18month period.

The volunteers, who had an average age of 76, also underwent cognitive testing and provided blood samples for the researchers. The blood samples were used to detect whether or not the volunteers had the Alzheimer’s risk gene APOE4. While having this risk gene does not cause someone to get the disease, it can increase a person’s risk.

The study showed that participants with high levels of amyloid in their brain showed a faster rate of memory decline over the study than those with low levels. Volunteers with the APOE4 gene also showed faster decline in visual memory over the 18 month period than those without the risk gene, but this was not as marked as volunteers with high amyloid levels.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“We know that people with the APOE4 gene can be at higher risk of Alzheimer’s, but it doesn’t mean they will definitely develop the disease. This study shows that the amount of the hallmark Alzheimer’s protein amyloid in the brain is a stronger indicator of memory decline than whether someone has the APOE4 gene.

“There is a lot of research currently underway to develop ways of stopping amyloid from building up in the brain. These findings suggest that drugs which prevent amyloid build-up could have real potential for slowing the disease. We know that amyloid can start to appear years before symptoms, so testing potential new drugs at an early stage of the disease will be vital. With over half a million people in the UK living with Alzheimer’s, we must invest in research to defeat this devastating disease.”

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

Scientists in the US have tracked some of the earliest Alzheimer’s changes in a group of people with high risk of a rare early-onset form of the disease. The findings will help scientists to understand what happens in the brain during Alzheimer’s and could aid early detection of disease. The two research papers are published online on 6 November in the journal Lancet Neurology.

The studies focused on a group of individuals from Columbia who are all members of an extended family group that carries a rare genetic mutation that causes Alzheimer’s disease. Family members who have the mutation will develop Alzheimer’s at an average age of 45, and their children will have a 1 in 2 chance of developing the disease too.

To look for the earliest signs of the disease in family members at risk of developing this form of Alzheimer’s, scientists followed 44 members of the group. All of the volunteers were aged between 18 and 26 and none had any memory or thinking problems, but 20 out of the 44 had the genetic mutation which destined them to develop the disease. Participants underwent brain scans to look for brain activity and had blood and cerebrospinal fluid samples taken for analysis.

The study found characteristic changes in the activity of particular brain regions in volunteers who had the mutation compared to those who did not. They also found that volunteers with the mutation showed higher levels of the Alzheimer’s protein amyloid in their blood and cerebrospinal fluid around 20 years before symptoms were expected to show.

The second study followed 50 volunteers from the same Colombian group, using brain scans to detect amyloid build-up in the brain. The team could detect amyloid as early as age 28 in those with the mutation, about 21 years before dementia appeared. Amyloid levels continued to rise over time, before reaching a plateau at around 38 years of age.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:

“By generously agreeing to take part in research, these affected families are helping scientists get a unique insight into how this devastating disease develops. Although early-onset inherited Alzheimer’s is rare and may not entirely represent the more common late-onset form, the findings highlight changes can take place in the brain decades before symptoms show. Mapping what changes happen early in the brain will help scientists to improve detection of the disease and allow potential new treatments to be tested at the right time.
“New drugs are being developed and tested to stop amyloid from taking hold, but studies like these show that timing could be crucial for whether these drugs are successful. With no treatments currently available to slow or stop the progression of Alzheimer’s, and diagnosis rates low, there is an urgent need for more research to understand how the disease develops and take us one step closer to a cure.”

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

A study by US researchers has linked hormone replacement therapy (HRT) in women to both an increased and a decreased risk of Alzheimer’s disease, depending on the type of hormones used and the timing of the therapy. The study, which suggests there could be a ‘critical window’ in which HRT may have a protective effect, is published on Wednesday 24 October in the journal Neurology online.

Previous research into the possible effects of HRT has shown mixed results, with observational studies linking it to a reduced risk of Alzheimer’s, but clinical trials showing the therapy can increase the risk of the disease. The researchers set out to investigate whether the risk of Alzheimer’s varied depending on the timing of hormone therapy.

The team looked at data on 1,768 women who took part in the Cache County Study, a long-term study investigating potential risk factors for dementia. Of these women, 1,105 (62.5%) had used HRT.

Analysis of the data showed that women who began HRT within five years of menopause were 30% less likely to develop Alzheimer’s than those who had no HRT. However, the results also showed that after the age of 65, women who began a combined therapy of oestrogen and progestin were slightly more likely to develop the disease than those on oestrogen alone.

The researchers suggest there may be a critical window of time in which HRT may offer some protection against Alzheimer’s, and argue that further research is needed to investigate this theory.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“Previous research into HRT has shown mixed results, but this useful study suggests the timing of hormone use may be critical for either raising or reducing the risk of Alzheimer’s. More work is needed to understand this link and help women make informed decisions about whether to start HRT, and these findings could be important for guiding future research in this area. Any medication may carry a number of potential benefits and drawbacks, and anyone who is concerned about hormone replacement therapy should speak to their GP.

“Half a million people in the UK are affected by Alzheimer’s disease, the most common cause of dementia, and with a rapidly ageing population that number is expected to rise dramatically. If we could delay the onset of Alzheimer’s by five years we could halve the number of people who die with the disease, but for that to happen, research is crucial.”

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

Researchers in Italy have found consuming flavanol-rich cocoa once a day may help improve brain function in people with mild cognitive impairment. The study is published in the journal Hypertension.

The study at the University of L’Aquila followed 90 older people with mild cognitive impairment (MCI) for eight weeks. MCI is a condition that causes problems with memory and thinking skills, although not to an extent that interferes with everyday life. Roughly half of people with MCI will go on to develop dementia within five years of diagnosis.

Over the course of the study, the participants were given a dairy-based drink rich in cocoa flavanols – naturally occurring antioxidants – once a day. Members of the group were given either a ‘low dose’ drink containing 45mg of flavanols, an intermediate dose of 520mg or a high dose of 990mg each day.

The researchers also carried out a series of tests to assess the participants’ memory and thinking skills, and found those taking the highest dose of flavanols had significantly better scores than those drinking the lowest level. Those in the high and intermediate groups also performed better on some tests than those in the ‘low dose’ group, and had decreased insulin resistance, lower blood pressure and a reduction in free radicals – molecules that can be harmful to cells in excessive amounts.

The researchers believe their findings may suggest high levels of cocoa flavanols, as part of a healthy diet, may be helpful for brain function. They argue that further research is needed to discover whether cocoa flavanols may help prevent or slow the onset of dementia.

Dr Laura Phipps at Alzheimer’s Research UK, said:
“Cocoa-based treatments for brain function would likely have patients queuing out the door, but this small study of flavanols is not yet conclusive. It’s not clear from the research whether other factors may have been responsible for the improvements seen in the group of people who took part. This early-stage trial took place over a very short period, and it would be useful to see more long-term studies to investigate the lasting effects. Ultimately we would need to see the results of large-scale trials to know whether cocoa flavanols could help prevent or delay dementia.

“While we do not yet have a sure-fire way to prevent dementia, the best evidence for lowering your risk is to eat a healthy, balanced diet with plenty of fruit and vegetables. Regular exercise, keeping your blood pressure and cholesterol in check and not smoking have also been shown to reduce the risk of dementia.

“Currently 820,000 people are affected by dementia in the UK and with that number rising, we urgently need to find a way to prevent the condition – but this can only come through research.”

Image reproduced from http://static.ddmcdn.com/

A study of 6401 Whitehall civil servants has revealed that obesity and metabolic abnormalities, including high blood sugar, abnormal lipid levels and high blood pressure, can increase the risk of cognitive decline. The research, by scientists at the INSERM research institute in Paris and University College London, are published on 21 August in the journal Neurology.

Research groups have been following Whitehall civil servants for a number of decades, gaining valuable insight into risk factors for ill health. This research, part of the Whitehall II study, followed 4556 male and 1845 female civil servants over a ten year period to look for factors influencing cognitive decline. The average age of the volunteers was 50 at the start of the study.

Over the course of the study, each civil servant was assessed for body mass index (BMI), metabolic status and cognitive function. Metabolic status took into account blood pressure, blood lipid levels and blood sugar levels. Volunteers were classed as having a ‘metabolic abnormality’ if two of the measures were out of the normal range, including high blood pressure, high blood glucose or diabetes, low levels of ‘protective’ HDL cholesterol, or high levels of triglycerides in blood. Cognitive status was tested three times over the ten year period using memory and thinking tests.

The team found that cognitive performance at the start of the study was poorer in those with a higher BMI in the metabolically normal group, suggesting obesity to be a standalone risk factor for cognitive decline. For volunteers of a normal weight, metabolic abnormality was also associated with poorer performance on memory and thinking tests.

When looking over the ten year period, the scientists observed a trend towards faster cognitive decline with increasing BMI in volunteers with metabolic abnormalities, suggesting both may contribute to memory and thinking problems later in life.

Shirley Cramer CBE, Chief Executive of Alzheimer’s Research UK, said:
“This large study of Whitehall civil servants may not be representative of the population as a whole, but it does provide valuable insight into the potential risk factors for cognitive decline. We do not yet know why obesity and metabolic abnormality are linked to poorer brain performance, but with obesity levels on the rise, it will be important to delve a little deeper into this association.

“While the study itself focuses on cognitive decline, previous research suggests that a healthy diet, regular exercise, not smoking and controlling blood pressure and cholesterol in midlife can also help stave off dementia. With dementia figures spiralling towards a million, the findings suggest we should be conscious of our general health throughout life.”

Image reproduced from http://static.ddmcdn.com/

Research suggests that despite the risk of Alzheimer’s increasing with age, those in their 60s and 70s show faster rates of decline than people who develop the disease at an older age. The study is published online on 2 August in the journal PLoS ONE.

While developing the disease is not an inevitability, age is the biggest known risk factor for late-onset Alzheimer’s, and almost half of people over the age of 85 developing the disease. Scientists believe that as our bodies change with age, we may become more susceptible to the triggers of the disease. While this would suggest that those who developed the disease at a very old age would be hardest hit, researchers from the US have presented findings suggesting that the ‘youngest old’ may decline the fastest.

The team from the University of California followed 723 people between the ages of 65 to 90 years for up to three years. The volunteers were either cognitively healthy, had Alzheimer’s disease, or had mild cognitive impairment – a state of memory and thinking problems not severe enough to be classed as dementia. The scientists used MRI brain scans to look for changes in the volunteers’ brains over time, and used a spinal tap to measure levels of markers of the Alzheimer’s in their cerebrospinal fluid (CSF). Memory and thinking skills were also measured using cognitive tests.

The team found that older people with Alzheimer’s showed a slower rate of decline than younger people with the disease. The study showed that those with Alzheimer’s disease over the age of 80 had less change on their brain scans over time, slower decline in performance on cognitive tests, and less evidence of disease in their CSF compared to those of a younger age.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“These findings challenge the misconception that Alzheimer’s and dementia is only a problem for much older people, suggesting it may be more aggressive in people in their 60s and 70s. The results highlight the importance of helping younger people with Alzheimer’s to access clinical trials, as new drugs could have a big impact on their lives.

“With more people reaching retirement age, it is important to understand how Alzheimer’s affects people of different ages. Understanding why very elderly people with Alzheimer’s are less likely to feel its full force could provide new clues for preventing or slowing the disease. To answer these questions, we must invest in research.”

Image reproduced from http://static.ddmcdn.com/

TauRx Therapeutics Ltd has today announced that it will begin two phase III clinical trials using a drug intended to slow or stop the progression of Alzheimer’s. The drug, called LMTX™, aims to prevent the build-up of a protein called tau in the brain and will be tested in people with mild to moderate Alzheimer’s.

Tau is a protein found normally in cells, but during Alzheimer’s and other dementias it can behave abnormally and clump together to form ‘tangles’. The company state that LMTX, also called TRx0237, can help to dissolve these clumps of tau and may help to slow or stop the progression of Alzheimer’s and other dementias.

The first of the two trials will treat 833 people with mild to moderate Alzheimer’s for a year, and the second will treat 500 people with mild Alzheimer’s with LMTX for 18 months. The company has also recently announced a phase III trial using LMTX in people with frontotemporal dementia, where the build-up of tau in the brain is also a key feature.

Rebecca Wood, Chief Executive of Alzheimer’s Research UK, said:

“It is promising to see another potential new Alzheimer’s treatment moving into late stage clinical trials. While a number of other drugs in development are targeting the hallmark Alzheimer’s protein amyloid, this drug is intended to prevent the build-up of a different protein, tau. We won’t know whether the treatment has real benefits until the trials are complete, but we look forward to the results. With current Alzheimer’s drugs acting to relieve symptoms, there is a desperate need for new treatments which can slow or stop the disease.

“It takes many decades of research to get a new treatment through to the final stages of clinical testing, but with dementia research so underfunded, we risk losing the chance to capitalise on our research findings. Support for research must be maintained if we are to keep building on our knowledge and developing potential new ways to beats this devastating disease.”

These trials are not yet recruiting in the UK, but to learn more about how to get involved in research studies, you can contact DeNDRoN (Dementias & Neurodegenerative Diseases Research Network) on 0203 2064960 or visit their website.

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

The BBC recently reported on new figures from the Office for National Statistics showing that the number of people dying with Alzheimer’s and dementia has risen by 6% over the last decade. Alzheimer’s and dementia was the second most common cause of death in women in 2011, accounting for over 10% of all female deaths.

Dr Marie Janson of Alzheimer’s Research UK, said:
“These figures provide a stark reminder of the growing burden of dementia and we must take them seriously. Technical changes to how the figures were calculated this year may have contributed to some of the rise seen over the last decade, with more accurate classification of vascular dementia. With a rapidly aging population in the UK, and more people living beyond 80, dementia is a condition that society cannot afford to ignore.

“It is heartening to see that mortality from other serious diseases is falling, but we must provide the same answers for people with dementia. Funding for research into dementia lags far behind that of other diseases – for every dementia scientist, six work on cancer. We must ensure that research into dementia remains a national priority if we are to head off this looming health crisis.”

Read the full report from the Office of National Statistics here.

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

Research has shown that antibodies designed to block two proteins involved in inflammation, can reduce features of Alzheimer’s in mice. The study, which uses similar antibodies to ones approved for treatment of psoriasis, is published online on 25 November in the journal Nature Medicine.

There is increasing evidence that inflammation in the brain can play a role in Alzheimer’s disease. Specialist immune cells in the brain called microglia are thought to be involved in the inflammatory response in the brain that may contribute to the disease.

To study this further, the scientists from Universities in Germany and Switzerland studied mice bred to develop features of Alzheimer’s. The team discovered that the mice had high levels of two messengers called IL-12 and IL-23 in the brain. Both are made up of protein building blocks, and a protein called p40 is a common component of both. The researchers stopped the p40 protein from being produced in the mice and observed a marked decrease in brain levels of the hallmark Alzheimer’s protein amyloid.

The team then used antibodies designed to stick to p40 and stop it from working. The antibodies were given to the mice for 60 days and the team saw both a reduction in amyloid levels and an improvement in the cognitive problems normally seen in these mice.

When the researchers looked for p40 in cerebrospinal fluid of people, they found higher p40 levels in people with Alzheimer’s compared to those without the disease.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“There is increasing evidence that inflammation is a key player in Alzheimer’s and it is an exciting area for researchers working to defeat this devastating disease. This promising research adds further support for the role of the immune system in Alzheimer’s, linking two inflammatory proteins to the disease in mice. Early studies like these are crucial to help highlight new targets for drug development, but we need to be careful not to assume that what is true for mice is true for men. Before any new Alzheimer’s drug can reach patients, first it must be rigorously tested in clinical trials.

“Alzheimer’s Research UK is funding many research studies delving deeper into the link between inflammation and Alzheimer’s, but without continued support the potential of studies like these is at risk. Research into dementia remains hugely underfunded compared to other diseases, and with a growing number of people affected by Alzheimer’s, we must rally together to tackle this disease before it is too late.”

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

A phase II safety trial to investigate a potential new treatment for Alzheimer’s has begun. MSD, known as Merck & Co Inc, will trial a drug called MK-8931 in people with mild to moderate stage Alzheimer’s disease.

MK-8931 aims to block an enzyme called BACE, which is known to play a role in the production of amyloid – a protein that builds in the brain during Alzheimer’s disease. Experts believe this build-up of amyloid may act as a trigger for the disease, and it’s hoped the drug will be able to tackle the disease by blocking BACE and stopping the build-up of amyloid.

The initial phase II trial will assess whether the drug is safe for use in a group of 200 people with mild and moderate stage Alzheimer’s. The firm then hopes to begin a phase III trial with up to 1,700 patients, to see whether MK-8931 is able to improve their thinking skills and ability to carry out everyday tasks. This phase III trial is expected to be completed in December 2016.

Dr Eric Karran, Director of Research at Alzheimer’s Research UK, said:
“It takes many years of research in the lab before a clinical trial can begin, and it’s great to see research into potential new treatments for Alzheimer’s disease progressing in this way. This drug is designed to target the first step in the chain of events that produces the amyloid protein, which is a hallmark of Alzheimer’s disease. The challenge for these trials will be to determine whether the drug is safe for use in people with Alzheimer’s and, crucially, whether it has benefits for these people. We look forward to seeing the results of these trials in four years’ time.

“Half a million people are affected by Alzheimer’s in the UK yet there is still no way to stop the disease in its tracks. We desperately need new treatments for Alzheimer’s, but for these to become a reality we need to see many more drugs being trialled and much more invested in research.”

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

Scientists in Belfast are embarking on a project that could bring a simple blood test for Alzheimer’s disease a step closer, thanks to a £99,754 grant from Alzheimer’s Research UK, the UK’s leading dementia research charity. Researchers at Queen’s University Belfast will use a state-of-the-art-technique to find ways of identifying people with Alzheimer’s and those who are at greater risk of developing the disease.

The two-year project will see Dr Brian Green and his team investigate how metabolites – tiny molecules that are involved in biochemical reactions in the body – may be used to detect Alzheimer’s disease. These molecules act as ‘chemical fingerprints’, offering clues about what is happening inside our cells. The researchers hope to be able to identify different patterns of metabolites that are most associated with Alzheimer’s, as the first step to developing a new test to diagnose the disease in its earliest stages.

The team has already tested several different ways of profiling metabolites, using brain samples from people who died with Alzheimer’s and people without the disease. One specific method, which rapidly analyses thousands of metabolites, was able to detect a pattern of metabolites that were linked to late-stage Alzheimer’s disease. The researchers now want to see whether this method can detect the disease at a much earlier stage.

As part of the project, the researchers will team up with clinical collaborators at Belfast City Hospital’s memory clinic to recruit volunteers to take part in the study. Using blood samples from healthy volunteers and people with Alzheimer’s, the researchers will search for different patterns of metabolites that can distinguish between the two. The study will also include people with mild memory problems, who are at a higher risk of Alzheimer’s, to see whether metabolites can be used to predict which of them will develop the disease. The funding will also allow the team to collaborate with researchers in Galway, Bristol and Coleraine and will permit them to test their method on generously donated brain tissue.

Dr Green said:
“A simple, reliable blood test for Alzheimer’s is a ‘Holy Grail’ for clinical diagnosis, and we hope our study could form the foundation for such a test to predict and diagnose the disease. By understanding what changes in metabolites are associated with Alzheimer’s, we should also gain more understanding about what happens as the disease develops – potentially aiding the development of new treatments. We’re extremely grateful for this funding, which will allow us to build on our results and take us closer to a new way of diagnosing Alzheimer’s.”

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“We’re delighted to be supporting this study, which has real potential for improving the way Alzheimer’s is diagnosed. This project is a good example of collaborative research, with scientists from different centres coming together to pool their expertise and tackle this problem. Alzheimer’s can be notoriously difficult to diagnose in the early stages, and an accurate test for the disease could make a real difference to people’s lives, allowing them to access care and existing treatments far sooner. The ability to predict Alzheimer’s would also be a huge boost for research, allowing people to be recruited to clinical trials in the earliest stages of the disease, when treatments are more likely to be successful.

“Alzheimer’s is the most common cause of dementia, which affects more than 15,000 people in Northern Ireland alone, yet currently there are no treatments to stop the disease in its tracks. If we are to find treatments for the future, we must invest in research today.”

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

US researchers have found older African Americans who report going without food as children may have a slower rate of cognitive decline in later life. The study is published in the journal Neurology.

Researchers at Rush University Medical Center, in Chicago, studied 6,158 people with an average age of 75, and followed them for up to 16 years. They asked the participants a number of questions about their childhood environment, such as asking them to rate their health and body size compared with other children their own age, and asking how often they went without enough food to eat as a child.

The participants were given a series of tests to assess their thinking and memory skills at the start of the study, and again every three years. The researchers analysed the results for African Americans and white participants separately, to account for each group’s different socioeconomic conditions in the early 1900s, when they were children.

The results showed that among African American participants, those who reported sometimes, often or always going without enough food as a child had a slower rate of cognitive decline in later life. In contrast, for white participants the results showed no link between the amount of food eaten in childhood and the rate of cognitive decline in old age.

Dr Marie Janson, of Alzheimer’s Research UK, said:
“Cognitive decline in older people can be a warning signal for dementia, and unpicking the factors involved could help understanding into preventing the condition. These surprising findings suggest that diet in early life may affect different groups of people in different ways, but it’s unclear whether other factors may have influenced the results. The information about childhood diets in this study was recorded through a questionnaire decades later, so may not have been reliable. It’s not possible to draw firm conclusions about the causes of cognitive decline from this study, and we don’t recommend restricting children’s food intake.

“The best evidence shows that eating a healthy, balanced diet can help reduce the risk of Alzheimer’s and other diseases that cause dementia. With 820,000 people affected by dementia in the UK, and a rapidly ageing population, finding ways to prevent the condition is crucial – that means we must invest in research.”

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

Two talented dementia scientists will benefit from a total of £380,000 in a US/UK exchange programme aimed at improving the understanding of Alzheimer’s disease. The initiative teams the world’s two leading dementia research charities, Alzheimer’s Research UK and the Alzheimer’s Association (US), for a cross-Atlantic partnership to improve collaboration among scientists. Each organisation will fund one researcher to spend time in a lab in the other country, learning new skills and sharing resources to help move their research forward.

Dr Rita Guerreiro, of UCL (University College London), will collaborate with a number of research groups in the US, Canada, Spain and Turkey to investigate the genetics of early-onset Alzheimer’s disease, which strikes people under the age of 65. Although three genetic mutations that cause Alzheimer’s in younger people have been identified, there are some families affected by early-onset Alzheimer’s who do not appear to carry any of these known mutations. Dr Guerreiro plans to work with a number of these families, collecting DNA samples from volunteers with and without the disease to analyse their genetic make-up in detail.

As part of her three-year project, Dr Guerreiro will work alongside Dr Andrew Singleton at the Laboratory of Neurogenetics, NIA, NIH, looking for genetic variations in these families that may cause early-onset Alzheimer’s.

Dr Guerreiro said:
“I’m delighted to receive this funding, which will enable me to work with a unique set of samples with a wealth of potential information to be unlocked. By identifying additional genes that are involved in early-onset Alzheimer’s disease, we can gain a clearer picture of some of the causes of the disease – the first step towards developing effective treatments. I’m looking forward to this exciting collaboration and hope that our study can help boost the search for new treatments.”

Meanwhile, Lindsay Reese, PhD, of the University of Vermont, will work with Dr Karen Horsburgh at the University of Edinburgh as part of a three-year project to investigate changes in the blood-brain barrier, a shield of tightly connected cells that regulates which proteins can pass in and out of the brain that may be connected with Alzheimer’s disease progression. Previous research has shown that about 80% of people with Alzheimer’s disease have beta amyloid protein accumulation in the brain and the brain’s extensive blood vessel walls, which may be involved in disease progression. Dr Reese and colleagues will examine the role of impaired blood flow and amyloid deposition in blood-brain barrier damage. By studying human brains and several different models of Alzheimer’s disease, Dr Reese hopes to understand how these disease features are linked.

“I’m genuinely grateful for and inspired by this grant, and I look forward to the intellectual exchange and advancement that can occur as a result,” Dr Reese said. “My vision is that more clearly understanding the linkage between Alzheimer’s, amyloid and the blood-brain barrier will lead to new ideas about possible treatment strategies.”

Dr Eric Karran, Director of Research at Alzheimer’s Research UK, said:
“We are delighted to be working with the Alzheimer’s Association to fund this work, and we hope this partnership could help us make real progress towards our common goal of defeating dementia. Collaboration is vital for research to move forward – the more people working on a problem, the faster we can achieve results, but we also need to keep researchers talking if they are to make the most of those results. The more we can encourage people to share resources, skills and ideas, the better our chances of developing effective treatments for Alzheimer’s and other diseases that cause dementia.”

“Alzheimer’s disease and other dementias are a global problem, a growing epidemic, and international research collaboration is an important component in spurring new knowledge and new discoveries,” said Heather Snyder, PhD, Alzheimer’s Association senior associate director of Medical and Scientific Relations. “We’re very pleased to join with Alzheimer’s Research UK to provide an opportunity for these two scientists to advance their studies.”

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

A new study from UK researchers suggests more people with dementia may be receiving antipsychotic prescriptions than previously thought. The study is published in the journal BMC Psychiatry.

Antipsychotics can be used for people with dementia to help combat challenging behavioural symptoms such as severe agitation. Moves to reduce their use came after a study funded by Alzheimer’s Research UK showed they doubled the risk of death in people with dementia when taken over a prolonged period. Since then the charity has called for a reduction in their use, and last year backed a Dementia Action Alliance campaign calling for patients with dementia to have their prescriptions reviewed.

Researchers at Aston University and the University of East Anglia worked with NHS Kent and Medway to determine how many people with dementia were being prescribed antipsychotics, and to implement medication reviews aimed at reducing the number of people receiving these drugs.

As part of the study, they collected data from 59 GP practices – 98.3% of practices in the area – and found that over 15% of people who had been diagnosed with dementia were receiving low-dose antipsychotics at the start of the study. When they compared this to data from the government’s National Dementia and Antipsychotic Prescribing Audit, they found that figures from this audit were much lower, with just under half of GP practices taking part in the audit, and 6.8% of people with dementia being prescribed antipsychotics. The researchers concluded that the numbers of people being prescribed the drugs may have been under-estimated.

Dr Marie Janson of Alzheimer’s Research UK, the UK’s leading dementia research charity, said: “Findings from Alzheimer’s Research UK highlighted the dangers of antipsychotics nearly four years ago, and the recent national audit showed positive steps are now being taken to reduce their use. This new study backs up the national audit’s findings that there is still some way to go to ensure patients across the country benefit from moves to reduce the use of these drugs. Though this research only looked at one area of the UK, these findings highlight the potential scale of the antipsychotics challenge and underline the need to keep up momentum on this issue.

“Antipsychotics should only be given to people with dementia when there is no other option for dealing with challenging behaviour, and their use must be carefully monitored. We know that doctors face a difficult task to tackle these symptoms, and safe, alternative treatments are urgently needed – such treatments can only come from research.”

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

Scientists in the US have developed a brain imaging ‘probe’ that may help detect Alzheimer’s in the very earliest stages of the disease. The probe works by binding to a protein called amyloid, a key feature of Alzheimer’s.

Researchers at Northwestern University and the University of Illinois developed the probe using an antibody that binds to amyloid, which is known to clump together in the brain and become toxic during Alzheimer’s. The researchers then combined this antibody with magnetic nanoparticles that show up during MRI scans.

Current brain scanning techniques can detect amyloid in the brain once it has formed into large, sticky plaques, but the researchers hope their new probe will help detect the toxic form of amyloid before these plaques have formed, potentially identifying people with Alzheimer’s at a much earlier stage. The scientists aim to develop a way of delivering the probe – which has so far been tested in the lab and in rodents – using a nasal spray.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“Though not yet published in full, this early study suggests that more sensitive brain scans capable of picking up Alzheimer’s before symptoms appear could be possible. It’s likely that new treatments will have the best chance of success if given early, and early detection will be vital for identifying the right people to take part in clinical trials. This particular probe has not yet been tested in people, so it remains to be seen how effective this method might be.

“With half a million people affected by Alzheimer’s, we still lack a treatment that can stop the disease in its tracks. New treatments can only come from research, and we must invest in research if we are to bring hope to those affected by the disease.”

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