Prevention of Alzheimer's Disease
Here are the five possible preventions of Alzheimer's disease: (Information are from National Institute on Aging)
Today there is no way to prevent AD. A recent study of women living in a large retirement community reported that estrogen therapy may offer some protective benefit. The women who took estrogen replacement therapy (ERT) had an incidence of AD 40% lower than those who didn't (Alzheimer's Disease Education and Referral Center). Studies on rats support the benefit of estrogen on the brain. It appears to make nerve cells more sensitive to the hormone, NGF, and to stimulate production of acetylcholine, the chemical found in very reduced levels in AD patients. (In men, testosterone converts to estrogen in the brain, and because testosterone levels do not drop sharply with age, presumably protection continues for men).
Twin studies have shown a reduced risk of developing AD in those taking anti-inflammatory medicine. This has been followed by a series of short-term anti-inflammatory therapies in AD patients suggesting some benefit. Some further recent epidemiological studies of the association between anti-inflammatory medicine and lowered risk of developing AD have found even greater risk reduction for persons taking anti-inflammatory agents and type 2 histamine receptor blockers ( anti-ulcer medicine). The mechanism for the additive risk reduction may be that AD has an immune-mediated component of neuron damage potentially suppressible by anti-inflammatory agents, and that H2 receptor blockers reduce glutamate-mediated excitotoxic cell damage which is also postulated to be involved in AD neuropathology. The optimal doses and specific agents which best reduce risk for AD are not known, but are being investigated in clinical AD trials.
The generation of free radicals which can oxidatively damage brain cells is a response to a variety of insults which occur throughout life, and has been implicated as one of the mechanisms by which AD damages brain. In vitro studies show that neurons pretreated with free radical scavengers such as vitamins C or E are not damaged by exposure to free radicals. Clinically, antioxidants limit the amount of ischemic damage occurring during stroke. Antioxidants have also been tried in Parkinson's disease without success. The doses and types of antioxidants that may help reduce the risk of developing AD are not known, but it is known that for most people, antioxidants are safe and inexpensive. Some of the more widely known antioxidants are Vitamins C, E, and beta-carotene, gingko biloba extract, selegiline, antagonic stress, and coenzyme Q.
The Macarthur foundation has shown that persons over 75 who do regular cardiovascular exercise for about 30 minutes daily, such as briskly walking five miles a week, perform better on a variety of measures of cognitive function. The mechanism may be related to animal models of exercise in which rats which run the most on a treadmill show the highest levels of growth factors in their brains. Growth factors generally act to protect brain cells and their processes from damage.
Given the reduced risk of AD for persons with at least 8 years of education, it is reasonable to recommend active, regular use of thinking skills such as reading, writing and arithmetic. For example, research in the area of use-dependent plasticity has shown that persons who use language skills have larger, more elaborate connections in the areas of the brain related to language function. Also, we routinely see, clinically, patients with AD who have particular talents that are well preserved until moderately demented.
