Preventing Alzheimers
AD Risk Factors We Can't Control continued...
Genetics is the other known AD risk factor that a person can't control. Scientists have found genetic links to the two forms of AD. Early-onset AD is a very rare form of the disease that can occur in people between the ages of 30 and 65. In the 1980s and early 1990s, researchers found that mutations (or changes) in certain genes on three chromosomes cause early-onset AD. If a parent has any of these genetic mutations, his or her child has a 50-50 chance of inheriting the mutant gene and developing early-onset AD. Late-onset AD, the more common form, develops after age 65. In 1992, researchers found that certain forms of the apolipoprotein E (APOE) gene can influence AD risk:
- APOE e2, a rarely occurring form, may provide some protection;
- APOE e3, the most common form, plays a neutral role; and
- APOE e4, which is found in about 40 percent of people with AD; APOE e4 lowers the age of onset and thus increases risk.
(Having this gene form does not mean that a person will definitely develop AD; it only increases risk. Many people who develop AD do not have the APOE e4 form.)
Researchers are now intensively searching for other risk factor genes that may be linked to late-onset AD. Discovering these genes is essential for understanding the very early biological steps leading to AD and for pinpointing targets for drug development and other prevention or treatment strategies. It's also critical for developing better ways to identify people at risk and determining how AD risk factor genes may interact with other genes or with lifestyle or environmental factors to affect AD risk in any one individual.
In 2003, the NIA announced a major expansion of AD genetics research efforts. The AD Genetics Study is collecting genetic material from individuals in families with two or more living brothers or sisters who have late-onset AD. This valuable resource will allow geneticists to speed up the discovery of additional AD risk factor genes.
The Search for AD Prevention Strategies
Though we can't do much about our age or genetic profile, recent research suggests that maintaining good overall health habits may help lower the chances of developing several serious diseases,
including ones affecting the brain. This article describes a number of health, lifestyle, and environmental factors that could make a difference in AD and that are being actively studied by scientists.
Many of these potential factors have been identified in observational and animal studies. At present, they are only associated with changes in AD risk. Only further research, including clinical trials, will reveal whether, in fact, these factors can help to prevent AD. It is important to understand that the degree to which a person might be helped by any of these factors may be very slight, especially if the person has inherited a bad form of a risk factor gene. That is why it is so important to also focus on other parts of the AD prevention research mission. At the same time that scientists are examining lifestyle factors, many others are developing drugs that can enhance protective biochemical pathways or block pathways that lead to cognitive decline and AD.
Investigating heart disease risk. High levels of blood cholesterol are a known risk factor for heart disease. In recent years, basic research in laboratories as well as population and animal studies have suggested there may also be a connection between high levels of blood cholesterol and development of AD. These findings led scientists to wonder whether drugs that lower blood cholesterol progression. Recent population and animal studies have raised the
possibility that statins, the most commonly prescribed cholesterol lowering drugs, may reduce the risk of dementia. Other studies, though, have found no association between statins and dementia
risk. Thus, it is not clear at this time whether statins affect the onset or progression of AD. To help answer this question, the NIA is currently funding a clinical trial to determine whether one particular statin slows the progression of AD.
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