Alzheimer's Prevention & Risk Factors
On this page, you will find the following:
Alzheimer's Risk Factors
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.
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Is Alzheimer's genetic?
Familial Alzheimer's disease (FAD) or early-onset Alzheimer's is 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.
In October of 2013, an international group of researchers reported on the identification of 11 new genes that offer important new insights into the disease pathways involved in Alzheimer's disease.The new genes (HLA-DRB5/HLA0DRB1, PTK2B, SLC24A4-0RING3, DSG2, INPP5D, MEF2C, NME8, ZCWPW1, CELF1, FERMT2 and CASS4) add to a growing list of gene variants associated with onset and progression of late-onset Alzheimer's.
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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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 BrightFocus Foundation 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, BrightFocus 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.
There are, however, some exciting reports, that though currently preliminary, may one day be shown to protect against Alzheimer's disease. Many of these modifications have also been shown to be part of overall healthy lifestyles that are likely to protect against other diseases as well. For example, researchers found that clinical trial participants who adhered to a Mediterranean diet have a slower decline on the mini-mental state examination (MMSE) cognitive decline. The Mediterranean diet may be protective against other diseases as well, including age-related macular degeneration. Also, vitamin D3 has been shown to have neuroprotective effects that may preserve cognitive function. This vitamin is produced naturally by the body from exposure to the sun, and is also being studied by BrightFocus supported scientists for its potential protective effects against glaucoma.
Some studies conducted in animals have shown that including blueberries, strawberries, and cranberries in the diet can lead to improved cognitive function, both in animals that age normally and in those that have been bred to develop “Alzheimer's disease.” Scientists are beginning to study what chemicals within these berries might be responsible for their beneficial effects.
Curcumin is a spice typically found in turmeric which is used to enhance the flavor of curries and meats in Indian cuisine. Currently researchers are studying the effects of curcumin on the human brain. Recent research implies that curcumin might actually reduce the amount of beta-amyloid plaques associated with Alzheimer's disease. The problem with curcumin is that, in its natural state it is very difficult for a human body to absorb curcumin consumed as food. Once in the blood stream, it is also quite difficult for curcumin pass from the blood to the brain. BrightFocus funded scientists are studying whether special preparations of curcumin might overcome these limitations. Similarly, a study conducted on green tea and Alzheimer's disease indicates that an antioxidant found in green tea, called epigallocatechin gallate (EGCG), has powerful anti-plaque ability and may actually prevent or delay Alzheimer's disease.
Switching from animal based oils and vegetable oil to extra virgin olive oil may also be a good habit to adopt. According to recent research, not only is extra virgin olive oil a generally healthy food, but it may prevent Alzheimer's disease as well. Studies suggest that oleocanthal, a naturally-occurring compound found in extra-virgin olive oil, changes the structure of Amyloid beta-Derived Diffusible Ligands (ADDLs). ADDLs are proteins that are toxic to nerve cells and may contribute to the symptoms of Alzheimer's disease. By structurally changing ADDLs, oleocanthal may be stopping the proteins' ability to damage nerve cells within the brain.
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Exercise is an important activity to add to a healthy lifestyle. BrightFocus encourages people to discuss exercise plans with their health care provider, so that an appropriate exercise program can be tailored for your specific needs. Studies conducted on those with mild cognitive impairment (MCI) indicate that aerobic exercise may improve cognitive agility. In one study, investigators looked at the relationship between physical activity and ones' risk of developing Alzheimer's disease. 1,700 adults aged 65 years and older were observed over a 6-year period in this study. Results showed that the risk of Alzheimer's disease was 35 to 40 percent lower in those who exercised for at least 15 minutes 3 or more times a week than in those who exercised fewer than 3 times a week.
While it is not proven that exercise could prevent Alzheimer's disease or slow its' progression, animal studies and preliminary human studies have produced significant interest amongst scientists. Larger, and more rigorous, randomized controlled trials will be necessary before a definitive statement on the role of exercise in the prevention of Alzheimer's disease can be made. In spite of this, developing an exercise program as part of an Alzheimer's disease patient's routine may also be helpful with maintaining muscle strength, decreasing frailty, and elevating mood.
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Building Brain Reserves & Social Engagement
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.
Each of these studies, though hopeful and promising, require replication before their impact on risk of Alzheimer's disease can be confirmed. But what does it hurt? While BrightFocus does not recommend any commercial products that advertise Alzheimer's disease prevention, learning new skills or enriching your life in study of a favorite topic is an act of empowerment that BrightFocus recommends for all people at any age.
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.
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Over the past couple of years, reports have been surfacing that NSAIDs like Ibuprofen, Naproxen and COX-2 inhibitors might actually prevent Alzheimer's disease. Researchers have been rigorously studying the relationship between NSAID use and Alzheimer's disease and no benefit has been demonstrated. Despite these results, scientists continue to look for ways to test how other anti-inflammatory drugs might affect the development or progression of Alzheimer's disease.
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Over the past several years, estrogen has been recognized as having a protective role in the brain. However, its' potential role in the development of Alzheimer's disease has yet to be determined. In fact, clinical trials have shown that estrogen does not slow the progression of already-diagnosed Alzheimer's disease and is not effective in treating or preventing AD if treatment is begun in later life.
One large trial found that women older than 65 who began taking estrogen in the form of Premarin® or PremPro® were actually at an increased risk of developing Alzheimer's disease and dementia. Although results from such studies were disappointing, many questions remain. For instance, would starting estrogen therapy closer to menopause be more effective in preventing Alzheimer's disease? These questions and other concerns related to estrogen's relationship with Alzheimer's disease are currently being studied in clinical trials.
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Disclaimer: The information provided is a public service of the BrightFocus Foundation and is not intended to constitute medical advice. It should not in any way substitute for the advice of a qualified healthcare professional. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. BrightFocus Foundation does not endorse any medical product or therapy.
Last Review: 04/15/14