Alzheimer's Risk Factors & Prevention

In this section, you will find information on:

• Risk Factors
• Heredity & Alzheimer's Disease
• Building Brain Reserves

Risk Factors

Scientists have identified factors that appear to play a role in the development of Alzheimer’s disease (AD), but no definitive causes have been found for this complex disorder.

Known Risk Factors

• Age: The single greatest risk of developing Alzheimer’s is age. Approximately 5 percent of Americans between the ages of 65 and 74, and almost half of those 85 years and older are estimated to have AD.
  
  
• Genetics: The majority of Alzheimer’s cases are late-onset, usually developing after age 65, and this form of the disease shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. A gene called Apolipoprotein E (ApoE) appears to be a risk factor for the late-onset form of Alzheimer’s. There are three forms of this gene: ApoE2, ApoE3 and ApoE4. Roughly one in four Americans has ApoE4 and one in twenty has ApoE2. While inheritance of ApoE4 increases the risk of developing AD, ApoE2 substantially protects against the disease. Some current research is focused on the association between these two forms of ApoE and AD. Familial Alzheimer’s disease (FAD) or early-onset AD is an inherited, rare form of the disease, affecting less than 10 percent of AD patients. FAD develops before age 65, in people as young as 35. It is caused by one of three gene mutations on chromosomes 1, 14 and 21.

Potential Contributing Factors

• Cardiovascular disease: Risk factors associated with heart disease and stroke, such as high blood pressure and high cholesterol, may also increase the risk of developing AD. High blood pressure may damage blood vessels in the brain, disrupting regions that are important in decision-making, memory and verbal skills. This could contribute to the progression of AD. High cholesterol may inhibit the ability of the blood to clear protein from the brain.

• Type 2 Diabetes: There is growing evidence of a link between AD and type 2 diabetes. In Type 2 diabetes insulin does not work effectively to convert blood sugar into energy. This inefficiency results in production of higher levels of insulin and blood sugar which may harm the brain and contribute to the progression of AD.

• Oxidative Damage: Free radicals are unstable molecules that sometimes result from chemical reactions within cells. These molecules seek stability by attacking other molecules, which can harm cells and tissue and may contribute to the neuronal brain cell damage caused by AD.

• Inflammation: Inflammation is a natural, but sometimes harmful, healing bodily function in which immune cells rid themselves of dead cells and other waste products. As protein plaques develop in AD, inflammation results, but it is not known whether this process is damaging and a cause of AD, or part of an immune response attempting to contain the disease.

• Other Possible Risk Factors: Some studies have implicated prior traumatic head injury, lower education level and female gender as possible risk factors. AD may also be associated with an immune system reaction or a virus.

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Heredity and Alzheimer's Disease

Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited, rare form of the disease, affecting less than 10 percent of Alzheimer’s disease patients. FAD develops before age 65, in people as young as 35. It is caused by one of three gene mutations on chromosomes 1, 14 and 21. If even one of these mutated genes is inherited from a parent, the person will almost always develop FAD. All offspring in the same generation have a 50/50 chance of developing FAD if one parent has it.

The majority of Alzheimer’s disease cases are late-onset, usually developing after age 65. Late-onset Alzheimer’s disease has no known cause and shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. Although a specific gene has not been identified as the cause of late-onset Alzheimer’s disease, genetic factors do appear to play a role in the development of this form of the disease. A gene called Apolipoprotein E (ApoE) appears to be a risk factor for the late-onset form of AD. There are three forms of this gene: ApoE2, ApoE3 and ApoE4. Roughly one in four Americans has ApoE4 and one in twenty has ApoE2. While inheritance of ApoE4 increases the risk of developing AD, ApoE2 substantially protects against the disease. Scientists believe that several other genes may influence development of Alzheimer’s disease.  Two of these genes, UBQLN1 and SORL1, are located on chromosomes 9 and 11.  Researchers have also identified three genes on chromosome 10, one of which produces an insulin degrading enzyme, that may contribute to the disease.

Genetic risk factors alone are not enough to cause the late-onset form of Alzheimer’s disease, so researchers are actively exploring education, diet and environment to learn what role they might play in the development of this disease.

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Building Brain Reserves

Many people born between 1945 and 1964 or “baby boomers” are beginning to worry about Alzheimer’s disease. Millions are already caring for their parents and watching them fade away, and they realize they may be next in line. Although there is currently no cure, scientists believe there are ways to lower the risk of developing Alzheimer’s disease by continually “exercising” our brains. Some research suggests that shoring up mental reserves as we age may protect against the onslaught of Alzheimer's. This approach may also delay onset of the disease or possibly help retain cognitive function longer if it does strike.

Building cognitive reserves is a lifelong process that begins in childhood as we expand reading skills. According to classic neurological theory, during the early developmental stages of life, the human brain forms an enormous number of neurons, or nerve cells, but many of these cells also die. The neurons that survive do so by connecting with other neurons during the rapid-growth stage of the nervous system that occurs in childhood and adolescence. Reading progressively more challenging books, learning a musical instrument, creating art, playing chess and engaging in any mental activity all help form these vital neural connections that can last a lifetime, and appear to buffer people from cognitive decline later on.

Fortunately, according to the theory of "neuroplasticity," brain reserves can be expanded throughout life, even into advanced old age. A team of researchers led by Dr. David Bennett, M.D., director of the Rush Alzheimer’s Research Center, has studied neuroplasticity in adults. These scientists found that those who continue to learn, to embrace new activities, learn new skills – in essence, to exercise their brains -- continue to build up connections that in turn lower their risk of Alzheimer's disease. Perhaps they have begun to develop the disease, but they show no symptoms because they have brain cells to spare.

Another study led by Dr. Robert Friedland, of Case Western Reserve University School of Medicine, compared mental, physical and social activity levels in adults with rates of developing Alzheimer's disease. The researchers discovered that the more active adults, those who played a musical instrument, gardened, and played mentally engaging board games, for example, were significantly less likely to develop Alzheimer's disease. The benefit extended to those who were active between the ages of 40 and 60, so it’s never too late to start building intellectual muscle, and stimulating hobbies have a pay-off regardless of the age they are started.

It is never too late to start new and creative activities. Continue to enjoy favorite pastimes, but challenge yourself by learning something new. Try a foreign language, read books and newspapers, solve puzzles and brain teasers, sing, dance, play board and video games, correspond by mail and email and engage in conversation. The combination of social, mental and physical stimulation is really the best medicine we have for a healthy life.

Exercise your memory through these memory games and puzzles.

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Last Reviewed On: 11/20/08