Risk Factors

Scientists have identified factors that increase the risk of Alzheimer’s. The most important risk factors—age, family history and heredity—can't be changed, but emerging evidence suggests there may be other factors we can influence.



Family history

What you can do now


The greatest known risk factor for Alzheimer’s is advancing age. Most individuals with the disease are age 65 or older. The likelihood of developing Alzheimer’s doubles about every five years after age 65. After age 85, the risk reaches nearly 50 percent. One of the greatest mysteries of Alzheimer's disease is why risk rises so dramatically as we grow older.

Family history

Another strong risk factor is family history. Those who have a parent, brother, sister or child with Alzheimer’s are more likely to develop the disease. The risk increases if more than one family member has the illness. When diseases tend to run in families, either heredity (genetics) or environmental factors, or both, may play a role.

Aluminum not a cause

During the 1960s and 1970s, aluminum emerged as a possible suspect in causing Alzheimer’s disease. This suspicion led to concerns about everyday exposure to aluminum through sources such as cooking pots, foil, beverage cans, antacids and antiperspirants. Since then, studies have failed to confirm any role for aluminum in causing Alzheimer’s. Almost all scientists today focus on other areas of research, and few experts believe that everyday sources of aluminum pose any threat.

Potential Contributing Factors

Cardiovascular disease: Risk factors associated with heart disease and stroke, such as high blood pressure and high cholesterol, may also increase one's risk of developing Alzheimer's disease. 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 the disease. 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 Alzheimer's disease 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 Alzheimer's.

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 Alzheimer's.

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, inflammation results, but it is not known whether this process is damaging and a cause of Alzheimer's, 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. Alzheimer's disease may also be associated with an immune system reaction or a virus.


Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited and rare. It affects less than 10 percent of Alzheimer’s disease patients. Familial Alzheimer's disease develops before age 65, in people as young as 35. It is caused by 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 Familial Alzheimer's disease. All offspring in the same generation have a 50/50 chance of developing this type of Alzheimer's 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 Alzheimer's disease. 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 Alzheimer's disease, ApoE2 substantially protects against it.

Scientists believe that several other genes may influence the 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. A gene, called TOMM40, appears to significantly increase one’s susceptibility to developing Alzheimer’s when other risk factors are present, such as having the ApoE-4 gene. Several recently discovered genes that influence Alzheimer’s disease risk are CLU (also called APOJ) on chromosome 8, which produces a protein called clusterin, PICALM on chromosome 11 and CR1 on chromosome 1.

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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