Evidence-Based Steps To Reduce Risk of Dementia by 20%

Your guide to reducing the risk of dementia

The jury is unfortunately still out on whether the crossword can help. You cannot alter your age or the genes you are born with, but there are lifestyle changes you can adopt which may reduce your chance of developing dementia by as much as 20%.


The BBC convened a panel of independent experts, chaired by the Alzheimer's Society, which evaluated more than 70 research papers and articles to come up with a series of tips for reducing your risk.


It may sound young, but the age of 35, they suggest, is high time to start thinking about these recommendations. If more of us acted on these, thousands of cases of dementia could be prevented in the future.
There is very strong evidence for the following:


EXERCISE
Prof Clive Ballard gives his top tips on how to cheat dementia
What is good for the heart is good for the brain. Exercise can have a beneficial effect at any age to help protect against dementia. To help reduce the risk at least 30 minutes of exercise, five times a week is suggested. It does not have to be the gym - a brisk walk is a perfectly acceptable alternative. Whatever form of exercise gets your heart pumping and leaves you somewhat out of breath is doing the trick. Exercise helps maintain a healthy weight and blood pressure, and so is indirectly thought to reduce the risk of dementia.
There is also growing evidence that regular exercise has other health effects such as promoting cell and tissue repair mechanisms including growth of new cells in the brain.


NOT BEING OBESE
Being seriously overweight is deemed a risk factor for developing dementia. This really matters in mid-life - between the ages of 35 and 65. Obesity increases the likelihood of developing Type 2 diabetes - believed to be a risk factor - but whether this causes the disease, or is simply more likely to develop in those who are also more prone to dementia is unclear. Obesity is also associated with higher cholesterol and blood pressure - again, known to be risk factors. You are deemed clinically obese - very overweight - if you have a BMI of 30 and above.


BRING DOWN HIGH BLOOD PRESSURE

The panel evaluated more than 70 research papers
Again, the key here is having consistently raised blood pressure in mid-life - anything above 140/90mmHg. It is thought that this increases the chance of dementia by causing damage to the brain. This may happen as a result of a stroke - in which blood supply to part or all of the brain is cut off - or due to microvascular disease, a condition which slows the flow of blood through the body thereby damaging cells and nerves in the brain. If you are over 40, or have a history of dementia or cardiovascular disease in your family, then get your blood pressure checked regularly.
REDUCE CHOLESTEROL
It is mid-life levels once more which appear to pose the greatest problem. Like high blood pressure, high levels of cholesterol raise the risk of stroke and microvascular disease. But cholesterol is also thought to be involved in the mechanism which causes amyloid protein plaques - the protein deposits that characterise Alzheimer's disease - to build up. Again if you are over 40 or have a family history, get your cholesterol checked. The Department of Health recommends a total cholesterol level of less than 5.0mmol/l.


NOT SMOKING
This had been an area of confusion, as some studies had suggested nicotine could have a protective effect - with the chemical reducing plaques when administered to animals in water. But the way in which we smoke tobacco, and the other chemicals inhaled in the process, negates this benefit. As well as raising the risk of vascular disease - a risk factor for dementia - smoking can result in low oxygen levels in the brain which in turn can promote the production of the protein found in brain plaques.
It is possible the following may have an impact:


ALCOHOL

There is no need to start drinking if you do not already
In fact the studies are quite clear that drinking a modest amount appears to protect against cognitive decline. Moderate drinking is defined as keeping within the recommended daily limits - up to two small glasses of wine for a woman, and three for a man. The problem is that these studies compare drinkers with non-drinkers - and people who abstain may do so for health reasons, which in turn may affect their chances of developing dementia. The message is if you are drinking within your weekly guidelines there is no need to stop, but there is no need to take up drinking or increase the amount you consume, as heavy drinking may in fact increase your risk.


FOLLOWING A MEDITERRANEAN DIET
Several recent studies have highlighted the potential for this diet to reduce the risk of Alzheimer's Disease. It involves eating lots of fruit and vegetables, whole grain foods, fish and plenty of olive oil, but it is relatively low in dairy products and processed foods. Further long term research is needed to confirm the effects of eating this way.
BEING SOCIALLY ACTIVE
Some evidence suggests that an active social life throughout life can be protective, with both the social ties one enjoys with others and non-physical leisure time deemed important. However, examining these factors and designing studies which can separate their effects is very difficult - consequently the conclusions which can be drawn from results are limited. One particular study has found that being single and living alone is a risk factor for dementia: social isolation is thought to have negative effects on health generally, increasing depression and cardiovascular disease.
Studies have also suggested that engaging in non-physical leisure activities such as gardening, and knitting may have a protective effect, a benefit that is likely to accumulate gradually over decades.
But the jury is out on:


BRAIN TRAINING
It sounds both attractive and plausible that giving your brain a "workout" could guard against dementia, and there is some evidence that very intensive brain training under strict conditions can improve specific functions like reasoning and problem solving. But there is no evidence as yet that doing a crossword a day or a number puzzle - or even learning a new language at 50 - will protect against dementia. That does mean they do not - simply that the proof that they do is presently lacking.
VITAMIN SUPPLEMENTS
There is no consistent evidence either way as to whether B vitamin supplements - folic acid, vitamin B12 or B6 - are effective in reducing the incidence of dementia. Research continues. However vitamin E supplements, which it was once hoped could prevent and even reverse early neurodegenerative changes, have not appeared to be effective in trials.

Escitalopram and Enhancement of Cognitive Recovery Following Stroke

The new issue of *Archives of General Psychiatry* (Vol. 67 No. 2)includes a study: "Escitalopram and Enhancement of Cognitive RecoveryFollowing Stroke."The authors are Ricardo E. Jorge, MD; Laura Acion, MS; David Moser, PhD;Harold P. Adams Jr, MD; & Robert G. Robinson, MD.

ContextAdjunctive restorative therapies administered during the first fewmonths after stroke, the period with the greatest degree of spontaneousrecovery, reduce the number of stroke patients with significant disability.

Objective: To examine the effect of escitalopram on cognitive outcome. Wehypothesized that patients who received escitalopram would show improvedperformance in neuropsychological tests assessing memory and executivefunctions than patients who received placebo or underwent ProblemSolving Therapy.DesignRandomized trial.SettingStroke center.

Participants: One hundred twenty-nine patients were treated within 3 months followingstroke. The 12-month trial included 3 arms: a double-blind placebo-controlled comparison of escitalopram (n = 43) with placebo (n = 45),and a nonblinded arm of Problem Solving Therapy (n = 41).Outcome MeasuresChange in scores from baseline to the end of treatment for theRepeatable Battery for the Assessment of Neuropsychological Status(RBANS) and Trail-Making, Controlled Oral Word Association, WechslerAdult Intelligence Scale-III Similarities, and Stroop tests.

Result: sWe found a difference among the 3 treatment groups in change in RBANStotal score (P < .01) and RBANS delayed memory score (P < .01). Afteradjusting for possible confounders, there was a significant effect ofescitalopram treatment on the change in RBANS total score (P < .01,adjusted mean change in score: escitalopram group, 10.0; nonescitalopramgroup, 3.1) and the change in RBANS delayed memory score (P < .01,adjusted mean change in score: escitalopram group, 11.3; nonescitalopramgroup, 2.5). We did not observe treatment effects in otherneuropsychological measures.

Conclusions: When compared with patients who received placebo or underwent ProblemSolving Therapy, stroke patients who received escitalopram showedimprovement in global cognitive functioning, specifically in verbal andvisual memory functions. This beneficial effect of escitalopram wasindependent of its effect on depression. The utility of antidepressantsin the process of poststroke recovery should be further investigated.

Neuroimaging May Shed Light On How Alzheimer's Disease Develops

ScienceDaily (Jan. 14, 2010) — Current Alzheimer's disease (AD) research indicates that accumulation of amyloid-beta (Aβ) protein plaques in the brain is central to the development of AD. Unfortunately, presence of these plaques is typically confirmed only at autopsy. In a special issue of the journal Behavioural Neurology, researchers review the evidence that Positron emission tomography (PET) can image these plaques during life. This exciting new technique provides researchers with an opportunity to test the amyloid hypothesis as it occurs in living patients.


In a review article with over 100 references, Dr. Gil Rabinovici and Dr. William Jagust from the University of California, San Francisco and Berkeley, summarize the results of experiments from their laboratories and others using the Aβ tracer Pittsburgh Compound-B (PIB). This compound binds to Aβ protein and allows the mapping of plaques in the brains of AD and non-AD volunteer subjects.
They report that PIB-PET can detect Aβ deposits in a significant proportion of cognitively normal older subjects and that these deposits are associated with brain atrophy even in the absence of cognitive symptoms. By the time patients develop mild cognitive impairment (MCI) amyloid load in the brain appears to have reached a plateau. As patients progress to dementia, neurodegeneration and cognitive decline proceed independently of further amyloid accumulation.


The authors interpret these results as consistent with a model in which amyloid deposition plays a critical early role on the path to AD, beginning years before onset of symptoms and triggering a series of events which ultimately leads to cognitive decline and dementia. While the use of PIB-PET is currently limited to research centers because of the compound's very short radioactive half-life (20 minutes), new amyloid imaging agents with longer half-lives are under development for more widespread use. Amyloid imaging is already playing an important role in the development of amyloid-based therapies for AD, and Dr. Rabinovici and Dr. Jagust speculate that in the future amyloid imaging will assist clinicians in identifying patients with mild or atypical symptoms who may be candidates for anti-amyloid treatments.


Writing in the article, the authors state, "PIB-PET has provided us with our first in vivo glance at the dynamic relationship between amyloid deposition, clinical symptoms, and structural and functional changes in the brain in the continuum between normal aging and AD…In the future, Aβ imaging will likely supplement clinical evaluation in selecting patients for anti-amyloid therapies both during drug development and in the clinic."

Exercise Associated With Preventing, Improving Mild Cognitive Impairment

ScienceDaily (Jan. 14, 2010) — Moderate physical activity performed in midlife or later appears to be associated with a reduced risk of mild cognitive impairment, whereas a six-month high-intensity aerobic exercise program may improve cognitive function in individuals who already have the condition, according to two reports in the January issue of Archives of Neurology, one of the JAMA/Archives journals.


Mild cognitive impairment is an intermediate state between the normal thinking, learning and memory changes that occur with age and dementia, according to background information in one of the articles. Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population. Previous studies in animals and humans have suggested that exercise may improve cognitive function.


In one article, Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues report the results of a randomized, controlled clinical trial involving 33 adults with mild cognitive impairment (17 women, average age 70). A group of 23 were randomly assigned to an aerobic exercise group and exercised at high intensity levels under the supervision of a trainer for 45 to 60 minutes per day, four days per week. The control group of 10 individuals performed supervised stretching exercises according to the same schedule but kept their heart rate low. Fitness testing, body fat analysis, blood tests of metabolic markers and cognitive functions were assessed before, during and after the six-month trial.
A total of 29 participants completed the study. Overall, the patients in the high-intensity aerobic exercise group experienced improved cognitive function compared with those in the control group.


These effects were more pronounced in women than in men, despite similar increases in fitness. The sex differences may be related to the metabolic effects of exercise, as changes to the body's use and production of insulin, glucose and the stress hormone cortisol differed in men and women.
"Aerobic exercise is a cost-effective practice that is associated with numerous physical benefits. The results of this study suggest that exercise also provides a cognitive benefit for some adults with mild cognitive impairment," the authors conclude. "Six months of a behavioral intervention involving regular intervals of increased heart rate was sufficient to improve cognitive performance for an at-risk group without the cost and adverse effects associated with most pharmaceutical therapies."


In another report, Yonas E. Geda, M.D., M.Sc., and colleagues at Mayo Clinic, Rochester, Minn., studied 1,324 individuals without dementia who were part of the Mayo Clinic Study of Aging. Participants completed a physical exercise questionnaire between 2006 and 2008. They were then assessed by an expert consensus panel, who classified each as having normal cognition or mild cognitive impairment.


A total of 198 participants (median or midpoint age, 83 years) were determined to have mild cognitive impairment and 1,126 (median age 80) had normal cognition. Those who reported performing moderate exercise -- such as brisk walking, aerobics, yoga, strength training or swimming -- during midlife or late life were less likely to have mild cognitive impairment. Midlife moderate exercise was associated with 39 percent reduction in the odds of developing the condition, and moderate exercise in late life was associated with a 32 percent reduction. The findings were consistent among men and women.


Light exercise (such as bowling, slow dancing or golfing with a cart) or vigorous exercise (including jogging, skiing and racquetball) were not independently associated with reduced risk for mild cognitive impairment.
Physical exercise may protect against mild cognitive impairment via the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vessel diseases, the authors note. "A second possibility is that physical exercise may be a marker for a healthy lifestyle," they write. "A subject who engages in regular physical exercise may also show the same type of discipline in dietary habits, accident prevention, adherence to preventive intervention, compliance with medical care and similar health-promoting behaviors."
Future study is needed to confirm whether exercise is associated with the decreased risk of mild cognitive impairment and provide additional information on cause and effect relationships, they conclude.

Neural Thermostat Keeps Brain Running Efficiently

ScienceDaily (Jan. 15, 2010) — Our energy-hungry brains operate reliably and efficiently while processing a flood of sensory information, thanks to a sort of neuronal thermostat that regulates activity in the visual cortex, Yale researchers have found.
actions of inhibitory neurons allow the brain to save energy by suppressing non-essential visual stimuli and processing only key information, according to research published in the January 13 issue of the journal Neuron.
"It's called the iceberg phenomenon, where only the tip is sharply defined yet we are aware that there is a much larger portion underwater that we can not see," said David McCormick, the Dorys McConnell Duberg Professor of Neurobiology at Yale School of Medicine, researcher of the Kavli Institute of Neuroscience and co-senior author of the study. "These inhibitory neurons set the water level and control how much of the iceberg we see. We don't need to see the entire iceberg to know that it is there."


The brain uses the highest percentage of the body's energy, so scientists have long wondered how it can operate both efficiently and reliably when processing a deluge of sensory information. Most studies of vision have concentrated on activity of excitatory neurons that fire when presented with simple stimuli, such as bright or dark bars. The Yale team wanted to measure what happens outside of the classical field of vision when the brain has to deal with more complex scenes in real life.
By studying brains of animals watching movies of natural scenes, the Yale team found that inhibitory cells in the visual cortex control how the excitatory cells interact with each other.
"We found that these inhibitory cells take a lead role in making the visual cortex operate in a sparse and reliable manner," McCormick said.
James Mazer was co-senior author of the paper with McCormick. Bilal Haider, a Yale graduate student, was lead author. Other Yale authors of the paper were Matthew R. Krause, Alvaro Duque, Yuguo Yu and Jonathan Touryan.


The work was funded by the National Eye Institute and the Kavli Foundation.