Preventing Alzheimers

The Search for AD Prevention Strategies continued...

Expanding knowledge about estrogen. This hormone is produced by a woman's ovaries during her childbearing years. After this time, estrogen production declines dramatically. Over the past
25 years, some laboratory and animal research, as well as observational studies in women, have suggested that estrogen used by women to treat the symptoms of menopause also protects the brain.  Experts have wondered whether using estrogen could reduce the risk of AD or slow disease progression.

A number of clinical trials have shown that estrogen does not slow the progression of already-diagnosed AD. Clinical trials testing whether estrogen might prevent AD in women who have already gone through menopause have also found that using estrogen to treat or prevent AD may not be effective, if treatment is begun in later life. A large trial found that women older than 65 who took
estrogen (Premarin) alone or estrogen with a synthetic progestin were actually at increased risk of developing dementia, including AD. Some questions remain unanswered, however, such as
whether some forms of estrogen might help if started somewhat earlier than the older ages tested in this trial. These questions are now being investigated.

Researchers also are trying other ways to work with estrogen's potentially positive effects for the brain. For example, scientists have developed estrogen-like molecules called SERMs (selective
estrogen-receptor modulators) that protect against bone loss and other consequences of estrogen levels falling after menopause. These molecules may retain estrogen's neuron-protecting ability
but may not have some of its other harmful effects on the body. A large clinical trial tested a SERM called raloxifene, which is used in the prevention and treatment of osteoporosis. The study showed
that this SERM lowered the risk of MCI among a group of postmenopausal women with osteoporosis. A newly-funded clinical trial is ongoing to test whether raloxifene can slow the rate of AD progression.

Investigating ginkgo biloba. This readily available natural product has been proposed as a potential treatment or preventive agent for AD. A 1997 study in the U.S. suggested that a ginkgo extract may be of some help in treating the symptoms of AD and multi-infarctdementia, but no evidence exists that ginkgo biloba will prevent AD. At the NIH, the National Center for Complementary and Alternative Medicine and the NIA are currently supporting a large clinical trial to explore whether ginkgo has any effect on preventing AD or delaying cognitive decline in older adults.

Exploring immunization. Will a vaccine someday prevent AD? Early vaccine studies in mice were so successful in reducing deposits of beta-amyloid (the major component of the plaques that develop in the brains of people with AD) and improving brain performance on memory tests that investigators conducted preliminary clinical trials in humans with AD. These studies had to be stopped because of life-threatening inflammation that occurred in some participants. However, the pharmaceutical industry and NIHfunded scientists are continuing to refine this strategy in animal models of AD, hoping to find ways of maintaining the therapeutic effects while reducing the unwanted side effects. Several pharmaceutical companies have recently obtained permission from the FDA to test several of these new strategies for safety in early stage clinical trials.

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