I get a lot of questions about genes and the risk of getting AD. Many people with an AD parent are concerned about their risk. I, too, had an AD parent so I share your concerns.
The good news is that the majority of late-onset AD is not inherited and early-onset familial Alzheimer’s disease is rare.
We all know that there is currently no known prevention or cure for AD; however, you can act now to improve your health. Scientific data does support the benefit of a healthy diet, exercise, cognitive activity, and cardiovascular risk reduction. Read on . . .
Scientists have identified factors that appear to play a role in the development of Alzheimer’s disease, but no definitive causes have been found for this complex disorder.
Known Risk Factors
- Age: The single greatest risk of developing Alzheimer’s disease 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 Alzheimer’s.
- 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 the disease, ApoE2 substantially protects against it. Some current research is focused on the association between these two forms of ApoE and Alzheimer’s disease. Several other genes also appear to influence the development of Alzheimer’s disease, and more detailed information is available in the Heredity section.Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited, rare form of the disease, affecting less than 10 percent of patients. Familial Alzheimer’s Disease 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 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,
Alzheimer’s disease is a complex disorder, for which there is currently no known prevention or cure. Some research has generated hope that one day it might be possible to slow the progression of Alzheimer’s disease, delay its symptoms or even prevent it from occurring at all. Although there is preliminary data to support the benefit of some interventions, such as physical activity and cardiovascular risk reduction, nothing at this time has definitively been shown to prevent Alzheimer’s disease or other dementias. The scientific advisors of the American Health Assistance Foundation (AHAF) do not currently recommend or endorse any commercial nutritional supplement, exercise program, or cognitive training exercises for the purposes of preventing Alzheimer’s disease. In spite of this, AHAF encourages people to evaluate the role of these interventions on the overall health and spirits of both the patient and caregivers
A number of preliminary studies suggest that how we eat may raise or lower our risk of developing Alzheimer’s disease. Eating a diet that is high in whole grains, fruits, vegetables and that is low in sugar and fat can reduce the incidence of many chronic diseases, and researchers are continuing to study whether these dietary modifications are also applicable to Alzheimer’s disease. However, the strongest research supporting these modifications has been performed in animal studies, and remains to be rigorously established in randomized and controlled clinical trials.