Back to Basics: Diet May Help Maintain Brain Function and Treat Brain Disorders
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NR-11-05 (11/14/05). For more information, please contact Sara Harris at (202) 462-6688 or sharris@sfn.org.
BACK TO BASICS: DIET MAY HELP MAINTAIN BRAIN FUNCTION AND TREAT BRAIN DISORDERS
WASHINGTON, DC, November 14, 2005 — What you eat—and how much of it—may affect how well your brain functions. New studies of the brain are beginning to suggest that some degree of caloric restriction may help reverse symptoms of Parkinson’s and Alzheimer’s. Additional studies are showing that your daily run not only can make you feel good, it may also make you think better.
“Select dietary factors and exercise can protect the brain against degenerative diseases and injuries encountered in daily living,” says Fernando Gómez-Pinilla, PhD, of UCLA and chair of a symposium on brain plasticity at this meeting. “Managed therapies based on the use of diet and exercise can be a powerful means to treat neurological problems.”
One possible treatment for Alzheimer’s sufferers may turn out to be a diet rich in almonds. Drugs currently used to treat the disease can have adverse side effects that include gastrointestinal bleeding, liver and kidney toxicity, and nausea. For that reason, chronic treatment with these drugs is discouraged; and they remain only mildly effective in treating the disease.
As possible alternatives to single-ingredient pharmaceutical drugs, Neelima Chauhan, PhD, of the University of Illinois-Chicago, has been looking at dietary-herbal alternatives and supplements that contain naturally balanced multi ingredients and have fewer or no adverse effects.
Some of these dietary-herbal alternatives are garlic, curcumin, berries, and nuts. Nuts in general are a rich source of selenium, magnesium, calcium, poly unsaturated fatty acids, including Omega-3 fatty acids like docosahexaenoic acid (DHA), and alpha tocopherol (Vitamin E). Vitamin E is a powerful antioxidant involved in scavenging free radicals, and alpha tocopherol is an effective form of this vitamin because it is maximally absorbed by the body and yields the greatest protective effects. DHA, one of the major constituents of neuronal and retinal membranes, regulates neuronal functions by modulating membrane properties such as neurotransmitter release, ion channel and enzyme regulation, and receptor-mediated transcription of genes involved in critical neuronal functions, such as memory.
Almonds, in particular, contain the highest amounts of alpha tocopherol in addition to calcium, magnesium, selenium, and DHA. Moreover, almonds have been demonstrated to produce estrogenic effects and properties similar to cholinesterase inhibitors, according to Chauhan. Thus, almonds contain a naturally balanced combination of ingredients, synthetic analogues of which are currently used in treating Alzheimer’s.
The almond diet has been shown to increase cerebral levels of cholinesterase and improve water maze performance in rodents. Consistent with these studies are the findings from Chauhan’s laboratory, which show that when Alzheimer’s transgenic mice are fed an almond-diet, their cerebral amyloid load is reduced and their performance in memory and learning tests improves. In addition, the amount of the protein amyloid, a hallmark of Alzheimer’s, is reduced.
“If our work can be validated pre-clinically, an almond diet may one day help prevent progression of Alzheimer’s in human beings,” says Chauhan.
Specific dietary components also play a critical role in the development and lifespan of the nervous system. Animal studies that involved restricting the daily intake of food by about 20 percent have resulted in a healthier animal that also lives longer. Further studies involving animal models of diseases that affect the brain, such as Parkinson’s and Huntington’s diseases, as well as animal models of stroke, have shown that, if the animal is first put on a restricted diet for a few months, there will be less damage to the brain in these disease models.
“These findings suggest that restricting the intake of food can be protective,” says Charles Meshul, PhD, and colleagues at the Portland Veterans Hospital and at Oregon Health and Science University. “But in the clinical setting, therapy is not initiated until after the patient suffers damage to the brain.”
He notes that studies have not been carried out to first damage the brain tissue and then restrict food intake to determine if dietary restriction can then reverse the effects of the tissue damage. “We have shown for the first time, that dietary restriction initiated after there is damage to the brain can result in a reverse of certain neurochemicals,” says Meshul, “although within the brain it has yet to be shown whether dietary restrictions in Parkinson’s disease patients would be useful in reversing some of the symptoms associated with the disease.”
Meshul and his colleagues treated a mouse model of Parkinson’s disease by injecting a toxin into the animal that specifically destroyed the same area of the brain that is affected in humans with this disease. Parkinson’s disease results from the loss of the neurotransmitter called dopamine. Symptoms of Parkinson’s do not appear in patients until about 70 to 80 percent of the dopamine is lost. However, other neurotransmitters, such as glutamate, in the brain are also affected.
In normal animals, dietary restriction results in a decrease in the levels of glutamate within the brain. In Meshul’s mouse model of Parkinson’s disease, there was a decrease in the brain levels of glutamate. But when the Parkinson’s mice were fed less food for three weeks, Meshul and his colleagues found that the brain levels of glutamate returned to the levels found in normal mice. In the Parkinson’s disease mouse, the 70 percent loss of dopamine in the brain was not affected by dietary restriction.
Similar dietary restrictions in experiments on mice suggest that the abnormal processes in the brain believed to cause Alzheimer’s disease can be slowed. Mark P. Mattson, PhD, and colleagues at the National Institute on Aging’s Laboratory of Neuroscience conducted studies, using newly developed “Alzheimer’s” mice that exhibited symptoms of Alzheimer’s, including poor performance in tests of learning and memory and increased anxiety. One-third of the mice received a normal diet, a third got 40 percent fewer calories, and a third fasted every other day. Half of the mice on each diet were tested for learning and memory as well as anxiety. In the older mice, those in the restricted calories and intermittent fasting diet groups exhibited higher levels of exploratory behavior (indicating less anxiety) and performed better in both the learning and memory tests.
Mattson and his fellow investigators are currently analyzing brains of these mice to determine if the beneficial effects of restricted calorie and intermittent fasting diets in the behavioral tests are associated with reductions in amyloid accumulation and other indicators of Alzheimer’s. They also plan to determine whether initiating dietary restriction after the Alzheimer’s mice are older and already symptomatic can slow down, or even reverse, the brain abnormalities. “If dietary restriction has similar beneficial effects in human beings,” says Mattson, “then it may be possible to reduce the risk of Alzheimer’s by cutting back on calories or by periodic fasting.”
Although much has been learned about the beneficial effects of exercise on cognitive function in humans and in rodents, surprisingly little is known about the molecular and cellular mechanisms governing these events. Research by Gómez-Pinilla and colleagues has found that brain-derived neurotrophic factor—or BDNF, a type of protein with a critical role in repair and maintenance of neural circuits—is increased in the hippocampus following voluntary exercise. The fact that the hippocampus is intimately involved with learning and memory provided the first clue that elevated BDNF levels resulting from exercise could impact cognitive function.
“We have recently identified important components of the pathways by which exercise and BDNF promote modifications at the molecular and cellular levels to result in permanent changes in cognitive function,” says Gómez-Pinilla. For example, he and his colleagues have determined that proteins involved with synaptic transmission and growth can mediate the action of BDNF in learning and memory. They have also found that animals with more BDNF in their hippocampi learn a spatial memory task faster than do those with less of this neurotrophin. “Our latest research shows that information obtained in the hippocampus applies to how the spinal cord can learn new tasks after injury,” he says.
“We are excited about our findings that exercise protects against the deleterious effects of some lifestyle factors on the brain,” says Gómez-Pinilla. “Our studies indicate that exercise protects the brain against the deleterious effects of insults such as a diet high in saturated fat and brain injury.”
