Posts tagged dementia
Articles and news from the latest research reports.
Mechanism of Parkinson’s spread demonstrated
An international, interdisciplinary group of researchers led by Gabor G. Kovacs from the Clinical Institute of Neurology at the MedUni Vienna has demonstrated, through the use of a new antibody, how Parkinson’s disease spreads from cell to cell in the human brain. Until now, this mechanism has only been observed in experimental models, but has now been demonstrated for the first time in humans too.
At the focus of the study, recently published in the highly respected journal “Neurobiology of Disease”, is the protein α-synuclein. This protein is present in the human brain but develops into a pathologically modified form in the presence of Parkinson’s disease and a common type of age-related dementia (known as Lewy body dementia, responsible for up to a quarter of all dementia-related diseases).
This study, which was carried out by a team from the MedUni Vienna in collaboration with researchers from the USA, Germany and Hungary, demonstrates for the first time that human nerve cells take up the pathological α-synuclein and thereby transfer the disease from one cell to the next. “This explains why patients with Parkinson’s disease deteriorate more and more from a clinical perspective and develop new symptoms, because the disease is able to spread to other parts of the brain through this infection process,” says Gabor G Kovacs, commenting on the central finding of the study.
New antibody achieved major breakthrough
The researchers demonstrated this mechanism using an antibody that scientists from the MedUni Vienna played a key role in helping to develop in collaboration with the German biotech firm Roboscreen. As the study shows, this antibody is the first to distinguish between the physiologically present and disease-associated form of α-synuclein and reacts exclusively with the pathological form.
Mechanism of spread demonstrated for the first time could provide a basis for new treatments for Parkinson’s
"For patients with Parkinson’s disease, this means that α-synuclein’s mechanism of spread from cell to cell could serve as a point of therapeutic attack if we are able to block this cell-to-cell transfer mechanism", continues Kovacs. In diagnostic terms, this antibody also represents a major breakthrough, since the antibodies used previously were unable to distinguish between the physiological and disease-associated form, which meant that they could not be used as easily for diagnostic purposes, e.g. in body fluids.
New antibody improves diagnosis
The fact that this is now possible for the first time has been demonstrated by a further study, also recently published in the specialist publication “Clinical Neuropathology”. According to this study, the new antibody can be used to detect disease-associated α-synuclein in the cerebrospinal fluid of patients with brain disease associated with α-synuclein. This is of major importance for clinical practice, because it means it will be possible to clinically determine whether the dementia is caused by Lewy bodies or not. This study arose through close collaboration between the Clinical Institute of Neurology (Gabor G. Kovacs) and the University Department of Neurology (Walter Pirker) at the MedUni Vienna.
(Source: meduniwien.ac.at)
Researchers Reveal Pathway that Contributes to Alzheimer’s Disease
Researchers at Jacksonville’s campus of Mayo Clinic have discovered a defect in a key cell-signaling pathway they say contributes to both overproduction of toxic protein in the brains of Alzheimer’s disease patients as well as loss of communication between neurons — both significant contributors to this type of dementia.
Their study, in the online issue of Neuron, offers the potential that targeting this specific defect with drugs “may rejuvenate or rescue this pathway,” says the study’s lead investigator, Guojun Bu, Ph.D., a neuroscientist at Mayo Clinic, Jacksonville, Fla.
“This defect is likely not the sole contributor to development of Alzheimer’s disease, but our findings suggest it is very important, and could be therapeutically targeted to possibly prevent Alzheimer’s or treat early disease,” he says.
The pathway, Wnt signaling, is known to play a critical role in cell survival, embryonic development and synaptic activity — the electrical and chemical signals necessary for learning and memory. Any imbalance in this pathway (too much or too little activity) leads to disease — the overgrowth of cells in cancer is one example of overactivation of this pathway.
While much research on Wnt has focused on diseases involved in overactive Wnt signaling, Dr. Bu’s team is one of the first to demonstrate the link between suppressed Wnt signaling and Alzheimer’s disease.
“Our finding makes sense, because researchers have long known that patients with cancer are at reduced risk of developing Alzheimer’s disease, and vice versa,” Dr. Bu says. “What wasn’t known is that Wnt signaling was involved in that dichotomy.”
Using a new mouse model, the investigators discovered the key defect that leads to suppressed Wnt signaling in Alzheimer’s. They found that the low-density lipoprotein receptor-related protein 6 (LRP6) is deficient, and that LRP6 regulates both production of amyloid beta, the protein that builds up in the brains of AD patients, and communication between neurons. That means lower than normal levels of LRP6 leads to a toxic buildup of amyloid and impairs the ability of neurons to talk to each other.
Mice without LRP6 had impaired Wnt signaling, cognitive impairment, neuroinflammation and excess amyloid.
The researchers validated their findings by examining postmortem brain tissue from Alzheimer’s patients — they found that LRP6 levels were deficient and Wnt signaling was severely compromised in the human brain they examined.
The good news is that specific inhibitors of this pathway are already being tested for cancer treatment. “Of course, we don’t want to inhibit Wnt in people with Alzheimer’s or at risk for the disease, but it may be possible to use the science invested in inhibiting Wnt to figure out how to boost activity in the pathway,” Dr. Bu says.
“Identifying small molecule compounds to restore LRP6 and the Wnt pathway, without inducing side effects, may help prevent or treat Alzheimer’s disease,” he says. “This is a really exciting new strategy — a new and fresh approach.”
Simple test can help detect Alzheimer’s before dementia signs show
York University researchers say a simple test that combines thinking and movement can help to detect heightened risk for developing Alzheimer’s disease in a person, even before there are any telltale behavioural signs of dementia.
Faculty of Health Professor Lauren Sergio and PhD candidate Kara Hawkins who led the study asked the participants to complete four increasingly demanding visual-spatial and cognitive-motor tasks, on dual screen laptop computers. The test aimed at detecting the tendency for Alzheimer’s in those who were having cognitive difficulty even though they were not showing outward signs of the disease.
“We included a task which involved moving a computer mouse in the opposite direction of a visual target on the screen, requiring the person’s brain to think before and during their hand movements,” says Sergio in the School of Kinesiology & Health Science. “This is where we found the most pronounced difference between those with mild cognitive impairment (MCI) and family history group and the two control groups.”
Hawkins adds, “We know that really well-learned, stereotyped motor behaviours are preserved until very late in Alzheimer’s disease.” These include routine movements, such as walking. The disruption in communication will be evident when movements require the person to think about what it is they are trying to do.
For the test, the participants were divided into three groups – those diagnosed with MCI or had a family history of Alzheimer’s disease, and two control groups, young adults and older adults, without a family history of the disease.
The study, Visuomotor Impairments in Older Adults at Increased Alzheimer’s Disease Risk, published in the Journal of Alzheimer’s Disease, found that 81.8 per cent of the participants that had a family history of Alzheimer’s disease and those with MCI displayed difficulties on the most cognitively demanding visual motor task.
“The brain’s ability to take in visual and sensory information and transform that into physical movements requires communication between the parietal area at the back of the brain and the frontal regions,” explains Sergio. “The impairments observed in the participants at increased risk of Alzheimer’s disease may reflect inherent brain alteration or early neuropathology, which is disrupting reciprocal brain communication between hippocampal, parietal and frontal brain regions.”
“In terms of being able to categorize the low Alzheimer’s disease risk and the high Alzheimer’s disease risk, we were able to do that quite well using these kinematic measures,” says Hawkins. “This group had slower reaction time and movement time, as well as less accuracy and precision in their movements.”
Hawkins says the findings don’t predict who will develop Alzheimer’s disease, but they do show there is something different in the brains of most of the participants diagnosed with MCI or who had a family history of the disease.
World Alzheimer Report 2014: Evidence for dementia risk reduction
The World Alzheimer Report 2014 ‘Dementia and Risk Reduction: An analysis of protective and modifiable factors’, released today, calls for dementia to be integrated into both global and national public health programmes alongside other major non communicable diseases (NCDs).
Alzheimer’s Disease International (ADI) commissioned a team of researchers, led by Professor Martin Prince from King’s College London, to produce the report. ADI is publishing this report, in conjunction with World Alzheimer’s Day (21 September) and as a part of World Alzheimer’s Month, an international campaign to raise awareness and challenge stigma.
The report reveals that control of diabetes and high blood pressure as well as measures to encourage smoking cessation and to reduce cardiovascular risk, have the potential to reduce the risk of dementia even in late-life. The report found that diabetes can increase the risk of dementia by 50%. Obesity and lack of physical activity are important risk factors for diabetes and hypertension, and should, therefore, also be targeted.
While cardiovascular health is improving in many high income countries, many low and middle income countries show a recent pattern of increasing exposure to cardiovascular risk factors, with rising rates of diabetes, heart disease and stroke.
Smoking cessation is strongly linked in the report with a reduction in dementia risk. For example, studies of dementia incidence among people aged 65 years and over show that ex-smokers have a similar risk to those who have never smoked, while those who continue to smoke are at much higher risk.
Furthermore, the study revealed that those who have had better educational opportunities have a lower risk of dementia in late-life. Evidence suggests that education has no impact on the brain changes that lead to dementia, but reduces their impact on intellectual functioning.
The evidence in the report suggest that if we enter old age with better developed, healthier brains we are likely to live longer, happier and more independent lives, with a much reduced chance of developing dementia. Brain health promotion is important across the life span, but particularly in mid-life, as changes in the brain can begin decades before symptoms appear.
The report also urges NCD programs to be more inclusive of older people, with the message that it’s never too late to make a change, as the future course of the global dementia epidemic is likely to depend crucially upon the success or failure of efforts to improve global public health, across the population. Combining efforts to tackle the increasing global burden of NCDs will be strategically important, efficient and cost effective. Leading a healthier lifestyle is a positive step towards preventing a range of long-term diseases, including cancer, heart disease, stroke and diabetes.
However, survey data released by Bupa* has shown that many people are unclear about the causes and actions they can take to potentially reduce their risk of dementia. Just over a sixth (17%) of people realised that social interaction with friends and family could impact on the risk. Only a quarter (25%) identified being overweight as a possible factor, and only one in five (23%) said physical activity could affect the risk of developing dementia and losing their memories. The survey also revealed that over two thirds (68%) of people surveyed around the world are concerned about getting dementia in later life.
Professor Martin Prince, from King’s College London’s Institute of Psychiatry, Psychology & Neuroscience (IoPPN) and author of the report, commented: “There is already evidence from several studies that the incidence of dementia may be falling in high income countries, linked to improvements in education and cardiovascular health. We need to do all we can to accentuate these trends. With a global cost of over US$ 600 billion, the stakes could hardly be higher.”
Marc Wortmann, Executive Director, Alzheimer’s Disease International said: “From a public health perspective, it is important to note that most of the risk factors for dementia overlap with those for the other major non communicable diseases (NCDs). In high income countries, there is an increased focus on healthier lifestyles, but this is not always the case with lower and middle income countries. By 2050, we estimate that 71% of people living with dementia will live in these regions, so implementing effective public health campaigns may help to reduce the global risk.”
Professor Graham Stokes, Global Director of Dementia Care, Bupa, said: “While age and genetics are part of the disease’s risk factors, not smoking, eating more healthily, getting some exercise, and having a good education, coupled with challenging your brain to ensure it is kept active, can all play a part in minimising your chances of developing dementia. People who already have dementia, or signs of it, can also do these things, which may help to slow the progression of the disease.”
* These figures, unless otherwise stated, are from YouGov Plc. Total sample size was 8,513, from the UK (2,401), Australia (1,000), Chile (1,000), China (1,031), Poland (1,002), and Spain (1,077). Fieldwork was undertaken online, between 17–25 July 2014. The figures have been weighted and are representative of all adults (aged 18+) in each country. An even weighting was applied to each country to find a ‘Global Average’.
(Image caption: Shown are fMRI scans across all subjects in the study. The yellow and red areas in Section A represent parts of the brain that are activated while subjects are forming “gist memories” of pictures viewed. Section B represents areas of increased activation, shown in yellow and red, as detailed memories are being formed. Credit: Image courtesy of Jagust Lab)
Researchers find neural compensation in people with Alzheimer’s-related protein
The human brain is capable of a neural workaround that compensates for the buildup of beta-amyloid, a destructive protein associated with Alzheimer’s disease, according to a new study led by UC Berkeley researchers.
The findings, published today (Sunday, Sept. 14) in the journal Nature Neuroscience, could help explain how some older adults with beta-amyloid deposits in their brain retain normal cognitive function while others develop dementia.
“This study provides evidence that there is plasticity or compensation ability in the aging brain that appears to be beneficial, even in the face of beta-amyloid accumulation,” said study principal investigator Dr. William Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory.
Previous studies have shown a link between increased brain activity and beta-amyloid deposits, but it was unclear whether the activity was tied to better mental performance.
The study included 22 healthy young adults and 49 older adults who had no signs of mental decline. Brain scans showed that 16 of the older subjects had beta-amyloid deposits, while the remaining 55 adults did not.
The researchers used functional magnetic resonance imaging (fMRI) to track the brain activity of subjects in the process of memorizing pictures of various scenes. Afterwards, the researchers tested the subjects’ “gist memory” by asking them to confirm whether a written description of a scene – such as a boy doing a handstand – corresponded to a picture previously viewed. Subjects were then asked to confirm whether specific written details of a scene – such as the color of the boy’s shirt – were true.
“Generally, the groups performed equally well in the tasks, but it turned out that for people with beta-amyloid deposits in the brain, the more detailed and complex their memory, the more brain activity there was,” said Jagust. “It seems that their brain has found a way to compensate for the presence of the proteins associated with Alzheimer’s.”
What remains unclear, said Jagust, is why some people with beta-amyloid deposits are better at using different parts of their brain than others. Previous studies suggest that people who engage in mentally stimulating activities throughout their lives have lower levels of beta-amyloid.
“I think it’s very possible that people who spend a lifetime involved in cognitively stimulating activity have brains that are better able to adapt to potential damage,” said Jagust.
Can Your Blood Type Affect Your Memory?
People with blood type AB may be more likely to develop memory loss in later years than people with other blood types, according to a study published in the September 10, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology.
AB is the least common blood type, found in about 4 percent of the U.S. population. The study found that people with AB blood were 82 percent more likely to develop the thinking and memory problems that can lead to dementia than people with other blood types. Previous studies have shown that people with type O blood have a lower risk of heart disease and stroke, factors that can increase the risk of memory loss and dementia.
The study was part of a larger study (the REasons for Geographic And Racial Differences in Stroke, or REGARDS Study) of more than 30,000 people followed for an average of 3.4 years. In those who had no memory or thinking problems at the beginning, the study identified 495 participants who developed thinking and memory problems, or cognitive impairment, during the study. They were compared to 587 people with no cognitive problems.
People with AB blood type made up 6 percent of the group who developed cognitive impairment, which is higher than the 4 percent found in the population.
“Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia,” said study author Mary Cushman, MD, MSc, of the University of Vermont College of Medicine in Burlington. “Blood type is also related to other vascular conditions like stroke, so the findings highlight the connections between vascular issues and brain health. More research is needed to confirm these results.”
Researchers also looked at blood levels of factor VIII, a protein that helps blood to clot. High levels of factor VIII are related to higher risk of cognitive impairment and dementia. People in this study with higher levels of factor VIII were 24 percent more likely to develop thinking and memory problems than people with lower levels of the protein. People with AB blood had a higher average level of factor VIII than people with other blood types.
Why HIV patients develop dementia
Immune cells in the brain under suspicion
“HIV-associated neurocognitive disorders” (HAND) include disorders of the cognitive functions, motor capacities as well as behavioural changes. How exactly HAND occur has not, as yet, been fully understood. “Scientists assume that HIV is harmful to cells directly and that it also triggers indirect mechanisms that lead to nerve cell damage,” explains Dr Simon Faissner (RUB clinic for neurology, St. Josef-Hospital). The researchers strongly suspect that, once activated in the brain and the spinal cord, immune cells keep up a chronic inflammation level which then results in the destruction of nerve cells. An immune activation in peripheral tissue as well as therapeutic consequences may likewise contribute to nerve cell damage in the brain.
First steps of HIV infection are sufficient
The HI virus overcomes the blood-brain barrier hitchhiking on infected immune cells, the monocytes and probably the T cells. The researchers from Bochum tested the hypothesis that HIV-infected monocytes activate specific immune cells in the brain, the so-called microglial cells. These cells, in turn, respond by releasing harmful substances, such as reactive oxygen metabolites and inflammatory signalling molecules, i.e. cytokines. To test this hypothesis, the researchers developed a cell culture system in which they initially examined the effect of HIV-infected monocytes on microglial cells. The researchers simulated the individual steps of HIV infection and measured the concentration of the cytokines released at each stage. Thus, they were able to demonstrate that releasing the viral RNA in the monocytes was a sufficient trigger for maximal microglial activation. Subsequent infection phases – reverse transcription into DNA and the resulting formation of HIV proteins – did not augment activation any further.
Released substances result in neuronal cell death
In the second step, they analysed nerve cells from rat brains to determine if the substances released by the microglial cells could lead to cell death. Compared with the control group, the amount of cell death was indeed twice as high. Studies of liquor cerebrospinalis received from HIV-infected patients have shown a positive correlation with marker of neuronal degeneration in patients who did not as yet present any neurocognitive disorders.
Detailed understanding necessary for therapeutic strategies
“Thanks to our research, we have gained a better understanding of the mechanisms of HIV-associated neurodegeneration,” concludes Prof Dr Andrew Chan. “These results are likely to contribute to HAND biomarkers becoming established. In the long term, these data may be used to develop therapeutic strategies aiming at retarding HAND progression in HIV-infected patients.” Starting points may include activation of microglial cells – a method that is applied in other autoimmune diseases of the central nervous system, for example in multiple sclerosis.
Start-up through FoRUM funds
The research, which was initiated following a collaboration between clinics for neurology and dermatology, St. Josef Hospital, as well as the Department for Molecular and Medical Virology, has been made possible through start-up funding provided by the Faculty of Medicine at Ruhr-Universität (FoRUM). The collaboration has evolved into an international consortium of clinics and basic research organisations in Bochum, Langen, Strasbourg and Mailand. One objective of the follow-up study, for which an application for EU funds is pending, is going to be an in-depth analysis of inflammatory processes in the central nervous system. The researchers will attempt to inhibit inflammatory processes with different drugs. They are, moreover, planning to study direct cell-cell interaction by means of state-of-the-art microscopy, in collaboration with the University of Strasbourg.
(Image credit: Mehau Kulyk/Science Photo Library)
Focus on naturally occurring protein to tackle dementia
Scientists at the University of Warwick have provided the first evidence that the lack of a naturally occurring protein is linked to early signs of dementia.
Published in Nature Communications, the research found that the absence of the protein MK2/3 promotes structural and physiological changes to cells in the nervous system. These changes were shown to have a significant correlation with early signs of dementia, including restricted learning and memory formation capabilities.
An absence of MK2/3, in spite of the brain cells (neurons) having significant structural abnormalities, did not prevent memories being formed, but did prevent these memories from being altered.
The results have led the researchers to call for greater attention to be paid to studying MK2/3.
Lead researcher and author Dr Sonia Corrêa says that “Understanding how the brain functions from the sub-cellular to systems level is vital if we are to be able to develop ways to counteract changes that occur with ageing.
“By demonstrating for the first time that the MK2/3 protein, which is essential for neuron communication, is required to fine-tune memory formation this study provides new insight into how molecular mechanisms regulate cognition”.
Neurons can adapt memories and make them more relevant to current situations by changing the way they communicate with other cells.
Information in the brain is transferred between neurons at synapses using chemicals (neurotransmitters) released from one (presynaptic) neuron which then act on receptors in the next (postsynaptic) neuron in the chain.
MK2/3 regulates the shape of spines in properly functioning postsynaptic neurons. Postsynaptic neurons with MK2/3 feature wider, shorter spines (Fig.1) than those without (Fig2).
The researchers found that change, caused by MK2/3’s absence, in the spine’s shape restricts the ability of neurons to communicate with each other, leading to alterations in the ability to acquire new memories.
“Deterioration of brain function commonly occurs as we get older but, as result of dementia or other neurodegenerative diseases, it can occur earlier in people’s lives”, says Dr Corrêa. “For those who develop the early signs of dementia it becomes more difficult for them to adapt to changes in their life, including performing routine tasks.
“For example, washing the dishes; if you have washed them by hand your whole life and then buy a dishwasher it can be difficult for those people who are older or have dementia to acquire the new memories necessary to learn how to use the machine and mentally replace the old method of washing dishes with the new. The change in shape of the postsynaptic neuron due to absence of MK2/3 is strongly correlated with this inability to acquire the new memories”.
Dr Corrêa argues that “Given their vital role in memory formation, MK2/3 pathways are important potential pharmaceutical targets for the treatment of cognitive deficits associated with ageing and dementia.”
Dementia Risk Quadrupled in People with Mild Cognitive Impairment
In a long-term, large-scale population-based study of individuals aged 55 years or older in the general population researchers found that those diagnosed with mild cognitive impairment (MCI) had a four-fold increased risk of developing dementia or Alzheimer’s disease (AD) compared to cognitively healthy individuals. Several risk factors including older age, positive APOE-ɛ4 status, low total cholesterol levels, and stroke, as well as specific MRI findings were associated with an increased risk of developing MCI. The results are published in a supplement to the Journal of Alzheimer’s Disease.
“Mild cognitive impairment has been identified as the transitional stage between normal aging and dementia,” comments M. Arfan Ikram, MD, PhD, a neuroepidemiologist at Erasmus MC University Medical Center (Rotterdam). “Identifying persons at a higher risk of dementia could postpone or even prevent dementia by timely targeting modifiable risk factors.”
Unlike a clinical trial, the Rotterdam study is an observational cohort study focusing on the general population, instead of persons referred to a memory clinic. The Rotterdam study began in 1990, when almost 8,000 inhabitants of Rotterdam aged 55 years or older agreed to participate in the study. Ten years later, another 3,000 individuals were added. Participants undergo home interviews and examinations every four years.
“This important prospective study adds to the accumulating evidence that strokes, presumably related to so called ‘vascular’ risk factors, also contribute to the appearance of dementia in Alzheimer’s disease. This leads to the conclusion that starting at midlife people should minimize those risk factors. The recent results of the Finish FINGER study corroborate this idea. It should be remembered that delaying the onset of dementia by five years will reduce the prevalence of the disease by half. And of course, since there is no cure for AD, prevention is the best approach at present,” explains Professor Emeritus Amos D Korczyn, Tel Aviv University, Ramat Aviv, Israel, and Guest Editor of the Supplement.
To be diagnosed with MCI in the study, individuals were required to meet three criteria: a self-reported awareness of having problems with memory or everyday functioning; deficits detected on a battery of cognitive tests; and no evidence of dementia. They were categorized into those with memory problems (amnestic MCI) and those with normal memory (non-amnestic MCI).
Of 4,198 persons found to be eligible for the study, almost 10% were diagnosed with MCI. Of these, 163 had amnestic MCI and 254 had non-amnestic MCI.
The risk of dementia was especially high for people with amnestic MCI. Similar results were observed regarding the risk for Alzheimer’s disease. Those with MCI also faced a somewhat higher risk of death.
The research team investigated possible determinants of MCI, considering factors such as age, APOE-ɛ status, waist circumference, hypertension, diabetes mellitus, total and HDL-cholesterol levels, smoking, and stroke. Only older age, being an APOE-ɛ4 carrier, low total cholesterol levels, and stroke at baseline were associated with developing MCI. Having the APOE-ɛ4 genotype and smoking were related only to amnestic MCI.
When the investigators analysed MRI studies of the brain, they found that participants with MCI, particularly those with non-amnestic MCI, had larger white matter lesion volumes and worse microstructural integrity of normal-appearing white matter compared to controls. They were also three-times more likely than controls to have lacunes (3 to 15 mm cerebrospinal fluid (CSF)-filled cavities in the basal ganglia or white matter, frequently observed when imaging older people). MCI was not associated with total brain volume, hippocampal volume, or cerebral microbleeds.
“Our results suggest that accumulating vascular damage plays a role in both amnestic and non-amnestic MCI,” says Dr. Ikram. “We propose that timely targeting of modifiable vascular risk factors might contribute to the prevention of MCI and dementia.”
Reference:
Determinants, MRI Correlates, and Prognosis of Mild Cognitive Impairment: The Rotterdam Study. Renée F.A.G. de Bruijn, Saloua Akoudad, Lotte G.M. Cremers, Albert Hofman, Wiro J. Niessen, Aad van der Lugt, Peter J. Koudstaal, Meike W. Vernooij, M. Arfan Ikram. Journal of Alzheimer’s Disease, Volume 42/Supplement 3 (August 2014): 2013 International Congress on Vascular Dementia (Guest Editor: Amos D. Korczyn)
(Source: iospress.nl)
Link between vitamin D and dementia risk confirmed
Vitamin D deficiency is associated with a substantially increased risk of dementia and Alzheimer’s disease in older people, according to the most robust study of its kind ever conducted.
An international team, led by Dr David Llewellyn at the University of Exeter Medical School, found that study participants who were severely Vitamin D deficient were more than twice as likely to develop dementia and Alzheimer’s disease.
The team studied elderly Americans who took part in the Cardiovascular Health Study. They discovered that adults in the study who were moderately deficient in vitamin D had a 53 per cent increased risk of developing dementia of any kind, and the risk increased to 125 per cent in those who were severely deficient.
Similar results were recorded for Alzheimer’s disease, with the moderately deficient group 69 per cent more likely to develop this type of dementia, jumping to a 122 per cent increased risk for those severely deficient.
The study was part-funded by the Alzheimer’s Association, and is published in August 6 2014 online issue of Neurology, the medical journal of the American Academy of Neurology. It looked at 1,658 adults aged 65 and over, who were able to walk unaided and were free from dementia, cardiovascular disease and stroke at the start of the study. The participants were then followed for six years to investigate who went on to develop Alzheimer’s disease and other forms of dementia.
Dr Llewellyn said: “We expected to find an association between low Vitamin D levels and the risk of dementia and Alzheimer’s disease, but the results were surprising – we actually found that the association was twice as strong as we anticipated.
“Clinical trials are now needed to establish whether eating foods such as oily fish or taking vitamin D supplements can delay or even prevent the onset of Alzheimer’s disease and dementia. We need to be cautious at this early stage and our latest results do not demonstrate that low vitamin D levels cause dementia. That said, our findings are very encouraging, and even if a small number of people could benefit, this would have enormous public health implications given the devastating and costly nature of dementia.”
Research collaborators included experts from Angers University Hospital, Florida International University, Columbia University, the University of Washington, the University of Pittsburgh and the University of Michigan. The study was supported by the Alzheimer’s Association, the Mary Kinross Charitable Trust, the James Tudor Foundation, the Halpin Trust, the Age Related Diseases and Health Trust, the Norman Family Charitable Trust, and the National Institute for Health Research Collaboration for Leadership in Applied Research and Care South West Peninsula (NIHR PenCLAHRC).
Dementia is one of the greatest challenges of our time, with 44 million cases worldwide – a number expected to triple by 2050 as a result of rapid population ageing. A billion people worldwide are thought to have low vitamin D levels and many older adults may experience poorer health as a result.
The research is the first large study to investigate the relationship between vitamin D and dementia risk where the diagnosis was made by an expert multidisciplinary team, using a wide range of information including neuroimaging. Previous research established that people with low vitamin D levels are more likely to go on to experience cognitive problems, but this study confirms that this translates into a substantial increase in the risk of Alzheimer’s disease and dementia.
Vitamin D comes from three main sources – exposure of skin to sunlight, foods such as oily fish, and supplements. Older people’s skin can be less efficient at converting sunlight into Vitamin D, making them more likely to be deficient and reliant on other sources. In many countries the amount of UVB radiation in winter is too low to allow vitamin D production.
The study also found evidence that there is a threshold level of Vitamin D circulating in the bloodstream below which the risk of developing dementia and Alzheimer’s disease increases. The team had previously hypothesized that this might lie in the region of 25-50 nmol/L, and their new findings confirm that vitamin D levels above 50 nmol/L are most strongly associated with good brain health.
Commenting on the study, Dr Doug Brown, Director of Research and Development at Alzheimer’s Society said: “Shedding light on risk factors for dementia is one of the most important tasks facing today’s health researchers. While earlier studies have suggested that a lack of the sunshine vitamin is linked to an increased risk of Alzheimer’s disease, this study found that people with very low vitamin D levels were more than twice as likely to develop any kind of dementia.
“During this hottest of summers, hitting the beach for just 15 minutes of sunshine is enough to boost your vitamin D levels. However, we’re not quite ready to say that sunlight or vitamin D supplements will reduce your risk of dementia. Large scale clinical trials are needed to determine whether increasing vitamin D levels in those with deficiencies can help prevent the dementia from developing.”
(Source: exeter.ac.uk)