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ALZHEIMER'S DISEASE

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WHAT IS ALZHEIMER'S DISEASE?

Alzheimer's disease is a degenerative disease of the brain from which there is no recovery. Slowly and inexorably, the disease attacks nerve cells in all parts of the cortex of the brain, as well as some surrounding structures, thereby impairing a person's abilities to govern emotions, recognize errors and patterns, coordinate movement, and remember. At the last, an afflicted person loses all memory and mental functioning.

WHO GETS ALZHEIMER'S DISEASE?

Alzheimer's disease (AD) is now the fourth leading cause of death in adults. Almost four million Americans and eight million more worldwide have it. Unless effective methods for prevention and treatment are developed, Alzheimer's disease will reach epidemic proportions, afflicting an estimated 14 million Americans within 50 years.

Age

Age is the biggest risk factor for AD. The number of cases of Alzheimer's disease doubles every five years in people over 65. By age 85, almost half of all people are afflicted.

Family History

People with a family history of the disease are at higher than average risk for AD. [ See Genetic Factors under What Causes Alzheimer's Disease?]

Gender

A number of studies suggest that women are more likely to develop AD, while one reported that men are more likely to suffer age-related brain damage. Studies are not consistent.

Population Differences

Few well-conducted studies have been conducted on differences among population groups.

African Americans and Hispanics may have a higher risk than Caucasian Americans.
Alzheimer's disease occurs less frequently in the Native American Crees and Cherokees and in Asians than in the general American population.

Genetic factors are at work in all groups but the same genes may have different effects depending on the ethnic population. Environmental factors also most likely play a role. For example, a study of Japanese men showed that their risk increased if they emigrated to America. And, the disease is much less common in West Africa than in African Americans, who share the same or higher risk with Caucasians Americans.

High Blood Pressure

Some studies have reported an association between Alzheimer's disease and systolic hypertension (the higher and first number in blood pressure measurement). Furthermore, lowering high blood pressure and cholesterol levels appear to reduce the risk of AD in elderly patients. Nevertheless, although hypertension is strongly linked to memory and mental difficulties, stronger evidence is needed to prove any causal relationship between hypertension and AD. For example, some studies, including a large community study, report no relationship.

High Cholesterol and Late-Onset Alzheimer's Disease (AD)

There has been research suggesting an association between high cholesterol levels and Alzheimer's disease (AD) in some people. A number of recent studies support the link between Alzheimer's disease and cholesterol by suggesting that certain cholesterol-lowing drugs statin drugs known as statins may be protective against AD.

Down's Syndrome

Nearly all patients who inherit Down's syndrome develop changes in the brain that resemble Alzheimer's if they live into their 40s, although onset varies and can occur as late as age 70. Women under the age of 35, but not older mothers, who give birth to children with Down's syndrome are also at much higher risk for Alzheimer's.

WHAT CAUSES ALZHEIMER'S DISEASE?

Researchers are finding specific biologic factors involved with Alzheimer's disease. Various environmental and genetic players appear to contribute to or trigger the process by which these factors destroy nerve cells leading to this disease.

Biologic Factors in the Brain

Imaging techniques in patients with AD have found significant loss of brain cells and volume in the regions of the brain devoted to memory and higher mental functioning. Important abnormalities have specifically been observed during biopsies:

Twisted nerve cell fibers, known as neurofibrillary tangles.
A sticky protein called beta amyloid .
Other factors also play a role.

The Effects of Neurofibrillary Tangles and Beta Amyloid in Alzheimer's. These biologic factors appear to be involved in the development Alzheimer's disease in the following ways:

Neurofibrillary tangles are the damaged remains of microtubules, the support structure that allows the flow of nutrients through the neurons (nerve cells). A key component in these tangled fibers is an abnormal form of the tau protein, which in its healthy version helps in the assembly of the microtubule structure. The defective tau, however, appears to block the actions of the normal version.
Beta Amyloid (also called A beta) is the second significant finding. This insoluble protein accumulates and forms sticky patches called neuritic plaque, which are found surrounded by the debris of dying nerve cells in the brains of Alzheimer's victims.
Amyloid precursor protein (APP) is a large nerve-protecting protein that is the source of beta amyloid. In Alzheimer's certain enzymes, particularly those called gamma-secretases, snip APP into beta amyloid pieces. This process is controlled by factors called presenilin proteins. (Genetic abnormalities that affect either APP or presenilin proteins occur in some inherited cases of early onset Alzheimer's.)
High levels of beta amyloid are associated with reduced levels of the neurotransmitter acetylcholine. (Neurotransmitters are chemical messengers in the brain.) Acetylcholine is part of the cholinergic system , which is essential for memory and learning, and which is progressively destroyed in Alzheimer's patients.
Beta amyloid may also disrupt channels that carry sodium, potassium, and calcium. These elements serve the brain as ions, producing electric charges that must fire regularly in order for signals to pass from one nerve cell to another. If the channels that carry ions are damaged, an imbalance can interfere with nerve function and signal transmission.

Other Proteins. Researchers have now identified other important proteins in the areas of the brain affected by Alzheimer's disease.

ERAB (endoplasmic-reticulum associated binding protein) appears to combine with beta amyloid, which in turn attracts new beta amyloid from outside the cells. High amounts of ERAB may also enhance the nerve-destructive power of beta amyloid.
AMY plaques resemble beta amyloid so closely that researchers were able to detect them only with the use of highly sophisticated techniques.
Elevated levels of a protein called prostate apoptosis response-4 (Par-4) may cause nerve cells to self-destruct.

Oxidation and the Inflammatory Response

Researchers are also attempting to discover why beta amyloid is so toxic to nerve cells. Some researchers are focusing on two processes in the body that may be involved with Alzheimer's disease: oxidation and the inflammatory process . One scenario for their role in Alzheimer's is as follows:

As beta amyloid breaks down it releases unstable chemicals called oxygen-free radicals. Once released, oxygen-free radicals bind to other molecules through a process called oxidation.
Oxidation is the result of many common chemical processes in the body, but when oxidants are overproduced, they can cause severe damage in cells and tissue, including even affecting genetic material in cells (its DNA). Oxidation is known to play a role in many serious diseases, including coronary artery disease and cancers, and experts believe it may also contribute to Alzheimer's.
One result of oxidation is the marshaling of immune factors to repair any injury. Overproduction of some of these immune factors, however, produces so-called inflammatory response, in which these factors can actually damage the body's own cells themselves.
Inflammatory factors of specific interest in Alzheimer's research are the enzyme cyclooxygenase (COX) and its products called prostaglandins. Excess amounts of these factors may increase levels of glutamate. Glutamate is an amino acid that excites nerves and, when overproduced, is a powerful nerve-cell killer.
The inflammatory process has also recently been associated with the release of soluble toxins called amyloid beta derived diffusible ligands, which some investigators believe may prove to key players in the destructive process.

Genetic Factors

Major research targets in Alzheimer's disease are the factors responsible for beta amyloid build-up and concentration in certain people and not in others. Genetic factors are believed to play a role in many cases.

The ApoE Gene and Late-Onset Alzheimer's. The major target in genetic research on late-onset Alzheimer's disease has been apolipoprotein E (ApoE), which plays a role in the movement and distribution of cholesterol for repairing nerve cells during development and after injury.

The gene for ApoE comes in three major types:

ApoE4. Studies have reported the greatest deposits of beta amyloid in people with ApoE4, which is now believed to be a major risk factor for late-onset Alzheimer's. Some experts theorize that one function of the ApoE protein is to remove beta amyloid and that the ApoE4 variant does so less efficiently than other ApoE genetic types. (ApoE4 has been studied for years as a risk factor for coronary artery disease, although the relationship between heart disease and Alzheimer's is uncertain. Some studies have found a higher risk for heart disease in people with Alzheimer's disease who carry two copies of the ApoE4 genotype.)
ApoE3. Fewer beta amyloid deposits have been observed in people with the ApoE3 gene. Some research indicates that ApoE3 in combination with ApoE4 may induce changes in beta amyloid that trigger the inflammatory response in the brain.
ApoE2. The fewest deposits have been observed in people with ApoE2, which may actually be protective.

People inherit a copy of one type from each parent, but Alzheimer's disease is not inevitable even in people with two copies of the ApoE4 gene. Reports vary widely in estimating the extent of risk:

People without ApoE4 have an estimated risk for developing Alzheimer's by age 85 of between 9% and 20%.
In people with one copy of the gene, the risk is between 25% and 60%.
In people with two copies, the risk ranges from 50% to 90%. Only 2% of the population carry two copies of the ApoE4 gene.

Some researchers suspect that some specific variation of the ApoE4 gene may be the actual culprit or combinations with other genes are critical for the disease, since many people who carry the ApoE4 exhibit no signs of Alzheimer's. For example, an apolipoprotein called Apo(a) may be involved in amplifying the effects of ApoE4.

Other Genetic Factors in Late-Onset Alzheimer's. Most people with late-onset Alzheimer's disease do not carry the ApoE4 gene. Increasingly, researchers believe that many cases of late-onset Alzheimer's disease are a result of a collaboration of genetic factors that participate in the process of producing or degrading beta amyloid. Some under investigation are the following:

Researchers are now targeting chromosome 10 as a possible location for genetic factors involved with AD. (The ApoE4 gene is on chromosome 19.)
Researchers have detected mutations in the proteins amyloid precursor protein (APP) and ubiquitin-B (Ubi-B), which may account for some cases of late- and early-onset Alzheimer's. Such mutations are not inherited, however, but appear to be genetic mistakes that occur during transcription, the coding process in which DNA establishes the pattern for the production of its proteins and other molecules.
One 2000 study of an Arab community with a high incidence of Alzheimer's has found evidence for a recessive gene, which means that both parents must carry it in order for the disease to be passed on. (Surprisingly, the ApoE4 gene showed up in this population at the lowest levels on record.)

Genetic Factors for Early-Onset Alzheimer's. Scientists are coming closer to identifying defective genes responsible for early-onset Alzheimer's, an uncommon, but extremely aggressive form of the disease.

Mutations in genes known as presenilin-1 (PS1) and presenelin-2 (PS2) account for most cases of early onset inherited Alzheimer's disease. The defective genes appear to accelerate beta amyloid plaque formation and apoptosis, a natural process by which cells self-destruct.
Genetic mutations in the genes that control amyloid precursor protein (APP) are also being targeted as causes of early-onset Alzheimer's. The genetic disease Down's syndrome, for example, overproduces beta-amyloid precursor protein (APP), the source of beta amyloid, and almost always leads to early Alzheimer's. Other APP mutations are being identified.

Estrogen Loss and Mental Decline

Estrogen, the primary female hormone, appears to have properties that protect against the memory loss and lower mental functioning associated with normal aging. Investigators are trying to determine if estrogen loss after menopause increases the risk for Alzheimer's disease in older women. Among estrogen's effects on the brain are the following:

Laboratory studies suggested that estrogen may help block production of beta-amyloid, the source of the sticky plaques found in Alzheimer's brains.
Estrogen may trigger the temporary growth of nerve pathways in the memory portion of the brain.
Estrogen may stimulate production of the neurotransmitters acetylcholine and serotonin, which are depleted in Alzheimer's patients.
Estrogen also appears to smooth, relax, and open blood vessels, which may help blood flow in the brain.
Estrogen is also an antioxidant. That is, it helps clean up free-oxygen radicals, the unstable particles thought to play a role in Alzheimer's.

Studies have been mixed on the association between natural estrogen levels and mental functioning in older women, however. For example, one 2001 study reported no association between the risk for dementia and a longer reproductive life in women, suggesting that longer exposure to estrogen did not protect against mental decline. On the other hand, a 2002 study reported poorer mental status in women with lower levels of estrogen.

Environmental Factors

Also of interest to researchers are the environmental factors (e.g., infections, metals, industrial or other toxins) that may trigger oxidation, inflammation, and the disease process, particularly in people with genetic susceptibility to Alzheimer's.

Infectious Organisms. Slow, infectious viruses cause a number of other degenerative neurologic diseases, such as kuru and Creutzfeldt-Jakob disease. Although no specific virus has been linked to Alzheimer's, some researchers theorize that people with a genetic susceptibility to Alzheimer's may be vulnerable to the actions of certain viruses, particularly under circumstances when the immune system may be weakened. Studies that help support this theory are as follows:

Evidence in one British research center has suggested that presence of herpesvirus (HSV) 1 increases the risk for AD in individuals who carry ApoE4. (HSV1 is a form of herpes that can invade the central nervous system). In one study, the risk was normal in those with only one of these factors. Furthermore, research is finding that parts of the HSV1 protein strongly resemble beta amyloid and, in laboratory studies, even have been observed to kill brain cells and develop sticky plagues.
Chlamydia pneumoniae is a common organism that causes respiratory infections. Researchers are finding that it may have very powerful inflammatory affects in blood vessels. And some studies (but not all) have found evidence of the organism in parts of the brain affected by late-onset Alzheimer's. More research is needed to determine the significance of these findings.

Metals. Some laboratory studies have reported excessive amounts of metal ions such as zinc, copper in AD brain. Such ions may possibly change the chemical architecture of normal beta amyloid, making it more harmful. A mildly acidic environment appears to be important in the process that binds these metals to beta amyloid. Experts observe that such conditions (acidic environment and higher levels of zinc and copper) commonly occur as part of the inflammatory response to local injury.

Electromagnetic Fields. Some studies on people exposed to intense electromagnetic fields (EMF) have reported a higher incidence of Alzheimer's. Some researchers believe that magnetic fields may interfere with the concentration of calcium inside cells, and others believe that they may increase production of beta amyloid. In any event, the association is between EMF and Alzheimer's is very weak.

Other Factors Associated with AD

Vitamin B Deficiencies and Homocysteine. Some studies suggest that deficiencies of the B vitamins B6, B12, and folate may be a risk factor for Alzheimer' diseases. Such vitamins are related to nerve protection. In addition, deficiencies of these vitamins increase levels of the amino acid homocysteine, which is considered to be a risk factor for heart disease and has now been associated with a higher risk for AD as well. Researchers theorize that homocysteine impairs the ability of DNA to repair nerve cells. The weakened cells are then more vulnerable to the harmful effects of oxidized beta amyloid.

Depression. There is a significant overlap between depression and dementia in the elderly. Some evidence suggests that there may even be common genetic factors in people who have both early depression and AD.

Head Injury. Some studies have found an association between serious head injuries in early adulthood and the development of Alzheimer's. It is not yet known if such injuries directly cause Alzheimer's or simply accelerate the disease in people who are already susceptible to it.

Lower Education and Economic Groups. A number of studies have reported either a higher risk for Alzheimer's disease in people with less education or a lower risk for AD in those who remain mentally active. Some experts speculate that learning itself may stimulate more neurons to grow and thus create a larger reserve in the brain so that it takes longer for brain cells to be destroyed.

Another possible reason for the association may lie in results such as those reported by a 2002 study, in which people who have small heads plus the ApoE4 gene had 14 times the risk for AD than those without this combination. Some researchers suggest that people with smaller heads have less brain volume so as genetic changes begin to occur AD symptoms develop earlier in smaller brains. Small brain size, in turn, is controlled not only by genetics but also by early malnutrition and infection, which is more likely to occur in lower income and educational groups. This theory is further supported by studies reporting a higher risk of AD in people who suffered malnutrition at any early age.

HOW CAN ALZHEIMER'S DISEASE BE PREVENTED?

There have been no proven methods for preventing Alzheimer's disease since the cause of it is still unknown. Still, certain factors are showing some evidence of reducing risk.

Male and Female Hormone Replacement Therapy

Hormone Replacement Therapy. Observational studies have suggested that hormone replacement therapy (HRT) may help prevent mental decline after menopause. It should noted that women who take HRT tend to be healthier and better educated to begin with, which may bias the results.

The following include other studies on the effects of HRT and mental decline.

A 2001 major analysis of 29 studies suggested a 40% to 60% reduction in the risk of dementia in women who took supplemental hormones. In addition, women who experienced mental symptoms after menopause, such as forgetfulness or problems in concentration, reported improvement after taking HRT. (Women who did not have these symptoms, however, reported no differences in mental functioning from HRT.) Experts pointed out that most of these studies had limitations and were not controlled trials, which are the gold standards of medical research. Most also did not distinguish among regimens or hormonal preparations.
Two major controlled studies are currently underway, although to date early results have been disappointing and finding no difference in mental performance between conjugated estrogen users and non-users.
One 2000 study on Japanese women found modest benefits from unopposed estrogen therapy but greater mental decline with combined therapies containing progestin and estrogen.
Two 2001 controlled studies reported no protection from Alzheimer's disease in women taking either estrogen or estrogen-progestin combination therapies.
Studies investigating ERT as a treatment for women with existing Alzheimer's have also reported no benefits to date either for improving symptoms or slowing progression. Some experts believe that the negative effects were due to a devastating effect of sudden estrogen exposure on brains that had been estrogen deprived for years.
Such negative study results and other evidence suggest that although estrogen depletion is associated with mental decline, other factors in the brain may also decline that are needed to interact with estrogen. Therefore taking estrogen as a supplement may have no significant effect. In fact, continuous exposure to estrogen in the brain may itself pose problems.

Testosterone. Animal studies have suggested that testosterone might be helpful in reducing levels of beta amyloid. Some experts believe that giving testosterone to elderly men and combinations of testosterone and estrogen to older women may prove to be protective. More research is warranted.

DHEA. Dehydroepiandrosterone (DHEA). DHEA is a male-like hormone in the body that declines with age. Some evidence suggests that it may help reduce mental decline in older women, but not in older men. Studies are underway.

Nonsteroidal Anti-Inflammatory Drugs

Evidence is building that ibuprofen (Advil, Motrin) and other similar agents (known as nonsteroidal anti-inflammatory drugs, or NSAIDs) have properties that prevent beta amyloid accumulation in the brain. In addition to ibuprofen, prescription NSAIDs, including sulindac (Clinoril) and indomethacin (Indocin), may have similar benefits. The longer they are used, the more protective they are. (It is not clear what dosage level is protective, but evidence suggests that even low-doses may be beneficial). Not all NSAIDs are protective. Other common NSAIDs, including aspirin, naproxen (Aleve, Naprosyn, Naprelan, Anaprox) and the new COX-2 inhibitor celecoxib (Celebrex), may not have these AD-protective actions although evidence is lacking to confirm or refute the benefits of specific NSAIDs. Unfortunately, chronic use of NSAIDs poses a high risk for bleeding and ulcers in the gastrointestinal tract, so until clinical trials have been conducted no one should take long-term NSAIDs simply to protect against AD.

Newer NSAIDs called COX-2 inhibitors (Vioxx, Celebrex) may have nerve-protecting properties without as severe side effects, but long-term studies are needed to determine this.

Statins

Some studies are reporting up to 70% lower risk for Alzheimer's disease and dementia in people who take cholesterol-lowering drugs called statins. (High cholesterol and risk for the disease have been linked in a number of studies.) The most positive results to date are with lovastatin (Mevacor) and pravastatin (Pravachol). (High cholesterol and risk for the disease have been linked previously.) They are currently being studied for treating AD.

Dietary Factors

Because of differences in AD rates among different populations, investigators are looking at dietary factors for protection. Caloric intake itself may play a role in brain health. In one study on animals, restricting calories below normal (but above starvation levels) helped prevent age-related nerve degeneration. It should be pointed out, however, that in patients with existing Alzheimer's, weight loss is a strong indicator of mental decline.

Fats and Oils. The following are some studies suggesting an association between fat and AD.

In China and Nigeria, where fat intake is low, the risk of developing Alzheimer's is 1% at age of 65 compared to 5% in the US.
A study in the Netherlands reported an association between dementia and diets high in total fat, saturated fat, and cholesterol.
A 2001 animal study indicated that high-fat diets alter ApoE processing of beta amyloid. This helps support population studies suggesting that a high-fat diet in people who carry the ApoE4 gene may confer a particularly high risk. For example, in one 2000 US study, adults who carried the ApoE4 gene and whose diet consisted of 40% fat calories had 29 times the risk for Alzheimer's compared to non-ApoE4 carriers on the same high-fat diet.

It should be noted that fats that contain omega-3 fatty acids, in particular the compound docosahexaenoic acid (DHA), may help protect the aging brain. These fatty acids are found in oily fish such as salmon, halibut, swordfish, and mackerel. People can also obtain DHA in supplements.

The recommended dietary goal is to limit total fat intake to 30% or fewer calories from fat. Everyone should avoid saturated fats found in animal products) and trans-fatty acids (found in fast foods and commercial baked goods). People should also eat fish twice a week and choose polyunsaturated and monounsaturated oils (canola and olive oil). [ For more information, see the Report, Heart Healthy Diet.]

Dark-Colored Fruits and Vegetables. According to several studies, eating plenty of darkly colored fruits and vegetables may slow brain aging. Of interest was a 1999 study on animals, in which extracts taken from blueberries and strawberries actually reversed age-related decline in brain function. Blueberries were the most effective. Dark-colored fruits and vegetables are recommended in any case for good health.

Soy. Soy has estrogen-like properties and animal studies suggest it may might be protective against AD, particularly in postmenopausal women. Of some concern, however, were one population and a few animal studies suggest that soy intake may actually pose a risk for greater mental among older men. More research is needed to confirm the effects of soy on the aging brain and to determine if there are gender differences.

Alcohol. Some studies have suggested that moderate intake of alcohol (one or two drinks a day) of any kind may protect the aging brain, possibly by releasing acetylcholine, the chemical in the brain that is deficient in AD. Although most studies have focused on wine, a 2001 Dutch study found that light to moderate alcohol intake, regardless of alcohol type, helped protect against dementia, including Alzheimer's. Not all studies have been positive. One, for example, suggested that wine may have some protective properties for noncarriers of ApoE4 but actually increase the risk for carriers of the gene. In any case, heavy alcohol consumption offers no protection and is dangerous. Alcohol also may increase the risk for breast cancer in women and should never be consumed during pregnancy.

Folate and Vitamin B12. The B vitamins folate and vitamin B12 prevent elevated levels of homocysteine, a chemical that appears to increase the risk for AD and heart disease. Both vitamins may be important for protection against AD. Both vitamins are added to cereal products Foods containing folate include avocados, bananas, oranges, asparagus, green leafy vegetables, and dried beans. B12 is found only in animal products. (Oily fish are very high in B12 and also have other nerve-protective properties.). People who are folate deficient may need supplements of folate (natural form) or folic acid (its synthetic from), which is twice as potent at folate. Some experts recommend 400 mcg of folic acid to reduce homocysteine, although one study suggested 800 mcg (.8 mg) a day is necessary to reduce homocysteine levels.

Antioxidant Vitamins. Much research on Alzheimer's disease has indicated that oxidation (release of damaging unstable particles) may play an important role in the disease process. Some reports have suggested that a combination of the antioxidants vitamins C and E (but not the use of them separately) may be protective against mental decline. However, no strong evidence to date has found any protection from antioxidant supplements.

Exercise

Aerobic exercise (such as walking or jogging) is very important for helping to protect against mental decline during aging. A number of studies are reporting that regular exercise may protect specifically against Alzheimer's as well other forms of mental deterioration and dementia. And the more exercise, the better.

Investigative Vaccines

Of great interest is the investigation of vaccines that use antibodies to attach to beta amyloid molecules. Antibodies are immune factors that target and attack specific molecular invaders in the body. Researchers hope that these antibodies will alert the immune system to attack and destroy the beta amyloid molecules, which are considered to be the building blocks of the nerve-destroying deposits in Alzheimer's brains. Animal studies are promising, but clinical trials on humans have been suspended due to side effects.

WHAT ARE THE SYMPTOMS OF ALZHEIMER'S DISEASE?

Mild impairment in thinking is now believed to be a significant sign of early-stage Alzheimer's in older people. The early symptoms of Alzheimer's disease may be overlooked because they resemble signs of natural aging. These symptoms include:

Forgetfulness.
Loss of concentration.
Unexplained weight loss.
Motor problems, including mild difficulties in walking.

In healthy individuals, similar symptoms can result from a number of common aging problems:

Fatigue.
Grief or depression.
Illness.
Vision or hearing loss.
The use of alcohol or certain medications.
Simply the burden of too many details to remember at once.

[See Table , Differences between Normal Signs of Aging and Dementia, below.]

DIFFERENCES BETWEEN NORMAL SIGNS OF AGING AND DEMENTIA
Early Signs of Alzheimer's
NORMAL	DEMENTIA
Memory And Concentration	Memory And Concentration
Periodic minor memory lapses or forgetfulness of part of an experience. Occasional lapses in attention or lapses in attention or concentration.	Misplacement of important items. Confusion about how to perform simple tasks. Trouble with simple arithmetic problems. Difficulty making routine decisions. Confusion about month or season.
Mood And Behavior	Mood And Behavior
Temporary sadness or anxiety based on appropriate and specific cause. Changing interests. Increasingly cautious behavior.	Unpredictable mood changes. Increasing loss of outside interests. Depression, anger, or confusion in response to change. Denial of symptoms.
Later Signs of Alzheimer's Disease
NORMAL	DEMENTIA
Language And Speech.	Language And Speech.
Unimpaired language skills.	Difficulty completing sentences or finding the right words. Inability to understand the meaning of words. Reduced and/or irrelevant conversation.
Movement/ Coordination	Movement/ Coordination
Increasing caution in movement. Slower reaction times.	Visibly impaired movement or coordination, including slowing of movements, halting gait, and reduced sense of balance.
Other Symptoms	Other Symptoms
Normal sense of smell. No abnormal weight changes in either men or women.	Impaired sense of smell. Severe weight loss, particularly in female patients. (Evidence suggests it indicates that these symptoms occur in AD patients who have the ApoE gene.)
Source of most of the data: Alzheimer's Disease: Early Warning Signs and Diagnostic Resources. The Junior League of NYC, Inc, 1988

Many medical and psychological conditions can also cause Alzheimer's symptoms. About 20% of suspected Alzheimer's cases, in fact, turn out to be some other disorder, half of which are potentially treatable or controllable. [ See How Is Alzheimer's Disease Diagnosed?, below.]

HOW IS ALZHEIMER'S DISEASE DIAGNOSED?

Ruling Out Other Causes Memory Loss or Dementia

A definitive test to diagnose Alzheimer's disease, even in patients showing signs of dementia, has not yet been devised, so the first step is to rule out other conditions that might be causing memory loss or dementia. There are a number of causes for dementia in the elderly:

Alzheimer's disease.
Vascular dementia (abnormalities in the vessels that carry blood to the brain).
Lewy bodies variant (LBV), also called dementia with Lewy bodies.
Parkinson's disease.

Experts currently believe that 60% of cases of dementia are due to Alzheimer's, 15% to vascular injuries, and the rest are a mixture of the two or caused by other factors. As yet, it is very difficult to differentiate among these dementias. Other diseases, many common in the elderly, can also cause symptoms that resemble Alzheimer's disease.

Vascular Dementia. Vascular dementia is primarily caused by either multi-infarct dementia (multiple small strokes) or Binswanger's disease (which affects tiny arteries in the midbrain). One major analysis suggests that patients with vascular dementia have better long term verbal memory than Alzheimer's patients, but poorer executive function (less ability to integrate and organize).

Lewy Bodies Variant. Lewy bodies are abnormalities found in the brains of patients with both Parkinson's disease and Alzheimer's. They can also be present in the absence of either disease; in such cases, the condition is called Lewy bodies variant (LBV). In all cases, the presence of Lewy bodies is highly associated with dementia. LBV was defined in 1997 and some experts believe it may be responsible for about 20% of people who have been diagnosed with Alzheimer's. They can be difficult to distinguish. Compared to AD patients, those with LBV may be more likely to have hallucinations and delusions early on, to walk with a stoop (similar to Parkinson's disease), to have more fluctuating attention problems, and to perform better than AD patients on verbal recall but less well organizing objects.

Parkinson's Disease. Dementia is about six times more common in the elderly Parkinson patient than in the average older adult. It is most likely to occur in older patients who have had major depression. Unlike in Alzheimer's, language is not usually affected in Parkinson's related dementia. Visual hallucinations occur in about a third of people on long-term medications. [For more details, see report Parkinson's Disease.]

Other Conditions that Cause Similar Symptoms. Some elderly people have a condition called mild cognitive impairment, which involves more severe memory loss than normal but no other symptoms of Alzheimer's. A number of conditions, including many medications, can produce symptoms similar to Alzheimer's:

Severe depression.
Drug abuse.
Thyroid disease.
Severe vitamin B12 deficiency.
Blood clots.
Hydrocephalus (excessive accumulation of spinal fluid in the brain).
Syphilis.
Huntington's disease.
Creutzfeldt-Jakob disease.
Brain tumors.

It is important that the physician recognize any treatable conditions that might be causing symptoms or worsening existing dementia caused by Alzheimer's or vascular abnormalities.

Psychological Testing. A number of psychologic tests are used or being developed to assess difficulties in attention, perception, and memory and problem-solving, social, and language skills.

Two commonly used tests that are very useful in identifying individuals who may be at risk for Alzheimer's are the Mini-Mental State Exam (MMSE) and the Mattis Dementia Rating Scale. One study suggests that missing recall items on the MMSE in combination with a cluster of other symptoms is a very reliable way of identifying Alzheimer's at an early stage. The symptoms include difficulty in calculation, repetition, getting lost while driving, forgetting relatives' names, and poor judgment.
A clock drawing test is also a good test for AD. The patient is given a piece of paper with a circle on it and is first asked to write the numbers in the face of a clock and then to show "10 minutes after 11." The score is based on spacing between the numbers and the positions of the hands. In the study, scoring eight or less identified 71% of Alzheimer's patients and correctly ruled out 82% of subjects without the disease.

Electroencephalography

Electroencephalography (EEG) traces brain-wave activity; in some Alzheimer's patients this test reveals "slow waves." Although other diseases may evidence similar abnormalities, EEG data helps distinguish a potential Alzheimer's patient from a severely depressed person, whose brain waves are normal.

Imaging Tests

Imaging tests include computerized tomography (CT) and magnetic resonance imaging (MRI and the more advanced techniques single photon emission computed tomography (SPECT), and positron-emission tomographic (PET). The are sometimes used to rule out other disorders such as multi-infarct dementia, stroke, blood clots, tumors, or hydrocephalus. Eventually imaging techniques, particularly PET or SPECT, may be able to specifically detect AD in early stages, but at this time attempts to accurately identify AD changes in the brain are limited to trials.

Investigative Tests.

Blood Tests. High blood levels of a substance called p97 may prove to help detect the presence of Alzheimer's, but more research is needed. Other blood tests may rule out metabolic abnormalities.

Cerebrospinal Fluid Test. A screening test the detects high levels of beta-amyloid proteins in the cerebrospinal fluid is expected to be approved in 2002 in Europe. The manufacturers are hoping to eventually develop a blood test that can give similar results.

Odor Test. Investigators are also using the impairment of smell in AD to develop tests that require patients to distinguish between odors.

Determining Severity after a Diagnosis Has Been Made

Once a diagnosis has been made, some experts observe that certain factors at the time of diagnosis indicate a higher risk for a more rapid decline:

Older age.
Being male.
The presence of high blood pressure.
Signs of loss of motor control and coordination.
Tremor.
Social withdrawal.
Loss of appetite and severe weight loss.
Accompanying sensory problems, such as hearing loss and a decline in reading ability.
General physical debility.

WHAT ARE THE LATEST DRUG TREATMENTS FOR ALZHEIMER'S DISEASE?

Most drugs currently being used or that are under investigation to treat Alzheimer's are aimed at slowing progression. To date, none are cures. In fact, the improvements from some of these drugs may be so modest that even the patients and their families are not aware of them. Even in these cases, however, the drugs may delay the need for admission to nursing homes. Since nearly all the studies are conducted on Alzheimer's patients in mild to moderate stages of the disease, it is important to seek out clinical drug trials as soon as Alzheimer's disease is diagnosed. Caregivers need to be available to help patients comply with any experimental therapies.

Drugs that Protect the Cholinergic System

The standard drugs used for Alzheimer's are designed to protect the cholinergic system, which is essential for memory and learning and is progressively destroyed in Alzheimer's. The benefits of these drugs are far from dramatic, however. About half of patients with mild to moderate disease show slight improvement These agents, however, do not appear to affect the basic destructive disease process involve beta amyloid. When patients go off the drugs the deterioration continues. All drugs have gastrointestinal side effects, including nausea.

Donepezil. Donepezil (Aricept) boosts the levels of acetylcholinesterase, the important enzyme in the cholinergic system. It is taken once a day and has only modest benefits but it does help slow loss of function and reduce caregiver burden. It works equally in patients with or without ApoE4. It may even have some advantage for patients with moderate to severe AD.
Rivastigmine. Rivastigmine (Exelon) boosts levels of two enzymes (the major one, acetylcholinesterase, and butyrylcholinesterase). It is taken twice a day. This agent may be particularly beneficial for patients with rapidly progressing disease. This drug has slowed or slightly improved disease status even in patients with advanced disease. (Rivastigmine may cause significantly more side effects than donepezil, including nausea, vomiting, and headache.) As with all anticholinergics, the drug is not a cure.
Galantamine (Reminyl). Galantamine not only protects the cholinergic system but also acts on nicotine receptors, which are also depleted during Alzheimer's. [See also Nicotine Replacement Agents below.] Its effects on mental functioning are similar to those of Aricept and Exelon, and it also has been helpful for improving function. One promising study found that the benefits of galantamine persisted and perhaps even improved over time.
Tacrine. Tacrine (Cognex) was the first cholinergic protective drug. It needs to be taken four times a day, has only modest benefits, and has no benefits for patients who carry the ApoE4 gene. In high doses, it can also injure the liver. In general, newer cholinergic protective drugs that do not pose as great a risk for the liver are now used for Alzheimer's.

Comparative studies are needed to determine which of these agents are most beneficial with least side effects. Many experts have reservations about developing more drugs that affect the cholinergic system since, at best, they only slow progression, but will never cure the disease. Of note, elderly AD patients often need medications that inhibit the cholinergic system and offset the effects of the AD pro-cholinergic agents. (Anticholinergics include antihistamines, antipsychotic drugs, and some anti-incontinence drugs.)

Nonsteroidal Anti-Inflammatory Drugs as Treatment

Nonsteroidal anti-inflammatory drugs (NSAIDs are being studied for treatment as well as prevention of Alzheimer's).

Nicotine Replacement

Nicotine enhances the actions of the cholinergic system (which is depleted in Alzheimer's disease) and is known to improve concentration and memory in the short term. Some studies have suggested that nicotine may protect nerve cells and help prevent the formation of beta amyloid. One study indicated that nicotine might help protect against Alzheimer's disease in carriers, but not noncarriers, of the ApoE4 gene. Research to date, however, has found no strong evidence of improvement with nicotine replacement methods. Smoking itself makes little difference in the risk for Alzheimer's, and, in fact, the risk for dementia is slightly higher in smokers.

Alternative Treatments

Ginkgo Biloba. Ginkgo biloba is a common herb that has antioxidant properties and appears to increase blood flow to the brain. Studies are reporting that ginkgo biloba extracts may slightly improve the memory of patients with mild to moderate AD. It does not appear to be as effective as the standard AD agents (donepezil, rivastigmine, metrifonate). Ginkgo has only minimal side effects. The agent poses a small risk for bleeding, which may be hazardous in combination with other blood-thinning medications, such as warfarin or high-doses of vitamin E. The herb is available over the counter. (Although there are no standards in the US by which to regulate it, the website www.naturaldatabase.com compares brands by quality of ingredients.)

Turmeric. Interestingly, studies suggest that curcumin, a compound found in the spice turmeric, has properties that may protect against AD disease process.

Melatonin. Melatonin, a natural hormone involved in sleep regulation, is of interest. It is an antioxidant, it may break down beta amyloid, and it is able to pass through blood-brain barrier. Deficiencies have been observed in patients with AD. It may be helpful, particularly for improving sleep habits in these patients.

Other Investigative Agents

A number of other agents are being investigated and show promise in early or late trials. Intense areas of research are focusing on agents that prevent beta amyloid build-up, its toxic effects on nerve cells, or other mechanisms of the disease process. Among them are the following:

Nerve growth factors that stimulate nerve activity in the brain. Cerebrolysin (Cere) is an example of such drugs and is showing promise in European clinical trials in improving mental function. Leteprinim potassium (Neotrofin) activates genes that produce nerve-growth factor in the brain. Early human trials are suggesting that it may have positive effects on memory and behavior.
Drugs that boost butyrylcholinesterase, an enzyme in the cholinergic system that might a play additional role in AD.
N-methyl-D-aspartate (NMDA) blockers. NMDA blockers, such as memantine, bind to glutamate, an amino acid that excites nerves and, in excess, is a powerful nerve-cell killer. Early small studies report that it reduces severe dementia and improves function.
Insulin growth factor. Insulin and insulin growth factors may prevent beta amyloid accumulation.
Antioxidants. Indole-3-propionic acid (IPA) is a natural agent that may interfere with enzymes that contribute to the AD disease process.
Researchers investigating the use of the antibiotic clioquinoline, which binds to metals in beta amyloid plaques. Studies on mice were promising and human trials are underway.

Investigative Procedures

Low-flow ventriculoperitoneal shunts are implanted devices that drain cerebrospinal fluid from the brain. The theory is that a low flow clearance will also carry off beta amyloid as well. Early studies show some promise, although the procedure is invasive.

Treating Symptoms Associated with Alzheimer's

Depression. Major depression with dementia that occurs in elderly people may be an early sign of Alzheimer's; in such cases, it precedes Alzheimer's by two years or less. Some experts believe that disease progression may even be delayed by treating such people with both an antidepressant and a drug, such as donepezil, currently used for Alzheimer's. The antidepressants known as selective serotonin reuptake inhibitors (SSRIs) may be particularly effective in relieving depression, irritability, and restlessness associated with Alzheimer's.

Apathy. Depression is often confused with apathy, which according to one study is more common than depression in Alzheimer's patients and responds to stimulants, such as methylphenidate (Ritalin), rather than antidepressants. An apathetic patient lacks emotions, motivation, interest, and enthusiasm while a depressed patient is generally very sad, tearful, and hopeless.

Symptoms of Psychosis (Wandering, Irritability, Aggression, and Hallucinations). Verbally or physically aggressive behavior, wandering, and hallucinations have been traditionally treated with standard antipsychotic drugs, such as haloperidol (Haldol), but they have severe side effects. Newer, so-called atypical antipsychotics, including risperidone (Risperdal) and olanzapine (Zyprexa), appear to significantly decrease symptoms of psychosis and aggression while posing a very low risk for severe side effects. They are now the drugs of choice. Carbamazepine or valproate, anti-seizure drugs, may also be effective for agitation and dementia.

Disturbed Sleep. Alzheimer's patients commonly experience disturbances in their sleep/wake cycles. Moderately short-acting sleeping agents, such as temazepam (Restoril), zolpidem (Ambien) or zaleplon (Sonata) or sedating antidepressants such as trazodone (Desyrel, Molipaxin) may be useful in managing insomnia. Some research suggests that exposure to brighter-than-normal artificial light during the day for patients with normal vision may help reset wake/sleep cycles and prevent nighttime wandering and sleeplessness. Trials on melatonin, a natural hormone that helps trigger sleep at night, are in progress.

WHAT ARE THE PHASES OF ALZHEIMER'S DISEASE AND THEIR MANAGEMENT?

The remaining life span of an Alzheimer's victim is generally reduced, although a patient may live anywhere from three to twenty years after diagnosis. The final phase of the disease may last from a few months to several years, during which time the patient becomes increasingly immobile and dysfunctional. Caregivers should understand the phases of this illness in order to help determine their own capacities for dealing with this painfully sad disease.

Home Treatment in Early Stages

Telling the Patient. Often physicians will not tell patients that they have Alzheimer's. Studies indicate that progression may be slowed down with intellectual effort and most investigative drug trials are performed in early stages. If an Alzheimer's patient expresses a need to know the truth, it should be disclosed. Both the caregiver and the patient can then begin to address issues of this disabling disease that can be controlled, such as access to support groups and drug research.

Mood and Emotional Behavior. Alzheimer's patients display abrupt mood swings and many become aggressive and angry. Some of this erratic behavior is caused by chemical changes in the brain. But certainly, it can also be attributed to the terrible and real experience of losing the knowledge and understanding of one's surroundings, causing fear and frustration that they can no longer express verbally.

The following recommendations for caregivers may help soothe patients and avoid agitation:

Keep environmental distractions and noise at a minimum if possible. (Even normal noises, such as people talking outside a room, may seem threatening and trigger agitation or aggression.)
Speak clearly. Most experts recommend speaking slowly to an Alzheimer's patient, but some caregivers report that Alzheimer's patients respond better to clear, quickly spoken, short sentences that they can more easily remember.
Use a combination of facial expression, voice tones, and words for communicating emotions. (One interesting study suggested that Alzheimer's patients may have difficulty in recognizing the meaning of facial expressions, particularly those signaling sadness, surprise, and disgust.)
Limit choices (such as clothing selection).
Offer diversions, such as a snack or car ride, if the patient starts shouting or exhibiting other disruptive behavior.
Simply touching and talking may also help.
Maintain as natural an attitude as possible. Alzheimer's patients can be highly sensitive to the caregiver's underlying emotions and react negatively to patronization or signals of anger and frustration.
Showing movies or videos of family members and events from the patient's past may be comforting.

Although much attention is given to the negative emotions of Alzheimer's patients, some become extremely gentle, retaining an ability to laugh at themselves or appreciate simple visual jokes even after their verbal abilities have disappeared. Some appear not unhappy, but to be in a drug-like or "mystical" state focusing on the present experience as their past and future slip away. Encouraging and even enjoying such states may bring some comfort to a caregiver.

There is no single Alzheimer's personality, just as there is no single human personality. All patients must be treated as the individuals they continue to be, even after their social self has vanished.

Appearance and Cleanliness. For the caregiver, grooming the Alzheimer's patient may be an alienating experience. For one thing, many patients resist bathing or taking a shower. Some spouses find that showering with their afflicted mate can solve the problem for a while. Often the Alzheimer's patient loses the sense of color and design and will put on odd or mismatched clothing. This may be very frustrating to a loved one, particularly since (certainly in the beginning) embarrassment is a common and painful emotion experienced by the caregiver. It is important to maintain a sense of humor and perspective and to learn which battles are worth fighting and which ones are best abandoned.

Driving. As soon as Alzheimer's is diagnosed, the patient should be prevented from driving. A Swedish study found that over half of elderly people involved in fatal accidents had some degree of neurologic damage.

Wandering. A potentially dangerous trait is the Alzheimer's patient's tendency to wander. At the point the patient develops this tendency, many caregivers feel it is time to seek out nursing homes or other protective institutions for their loved ones. For those who remain at home, the following precautions are recommended:

Locks should be installed outside the door, which the caregiver can open, but the patient cannot.
Alarms might be installed at exits.
A daily exercise program should be implemented, which may help tire the patient out; one study showed that walking 30 minutes, three times a day also improved communication.
The caregiver should contact organizations, such as Alzheimer's Association or Medic Alert, for identification supplies and procedures that help locate patients who wander away from home and become lost. [See Where Else Can Help Be Found for Alzheimer's Disease?, below.]
Speech Problems. Some evidence suggests that speech therapy combined with AD medications may be helpful for maintaining verbal skills patients with mild symptoms.

Sexuality. In many cases, the Alzheimer's patient becomes uninhibited sexually; at the same time, the patient's physical deterioration and receding capacity to recognize the spouse as a known and loved individual can make sexual activity despairing and repellent for the caregiving spouse. Other patients may lose interest in sex. If sexual issues are a problem, they should be discussed openly with the physician, and ways should be found to maintain non-sexual physical affection that can bring comfort to both the patient and the spouse.

Home Treatment During Later Stages

The Alzheimer's patient needs 24-hour a day attention. Even if the caregiver has the resources to keep the Alzheimer's patient at home during later stages of the disease, outside help is still essential. If available, home visits by a health profession appear to have a favorable impact on survival and delay in needing a nursing home. Medicare is now covering many Alzheimer's services and patients should be able to stay at home longer than previously.

Incontinence. An Alzheimer's patient's incontinence is generally devastating to the caregiver and a primary reason why many caregivers decide to seek nursing home placement when the patient reaches this stage. When the patient first shows signs of incontinence, the doctor should ascertain that it is not caused by an infection. Urinary incontinence may be controlled for some time by trying to monitor times of liquid intake, feeding, and urinating. Once a schedule has been established, the caregiver may be able to anticipate incontinent episodes and get the patient to the toilet before they occur.

Immobility and Pain. As the disease progresses, Alzheimer's victims become immobile, literally forgetting how to move. Eventually, they become almost entirely wheelchair-bound or bedridden. Bedsores can be a major problem. Sheets must be kept clean, dry, and free of food. The patient's skin should be washed frequently, gently blotted thoroughly dry, and moisturizers applied. The patient should be moved every two hours and the feet kept raised with pillows or pads. Exercises should be administered to the legs and arms to keep them flexible. One expert reported that 62% of patients with mild to moderate dementia report pain, usually in joints, yet very few patients in late-stage dementia receive pain medication, even though there is no evidence that they are not experiencing the same pain.

Dehydration. Dehydration can become a problem; it is essential to encourage fluid intake equal to eight glasses of water daily. It should be noted that coffee and tea are diuretics and will deplete fluid.

Eating Problems. Weight loss and the gradual inability to swallow are two major related problems in late-stage Alzheimer's and are associated with an increased risk of death. Weight gain, however, is linked to a lower risk of dying. The patient can be fed through a feeding syringe, or the caregiver can encourage chewing action by pushing gently on the bottom of the patient's chin and on the lips. The caregiver should offer the patient foods of different consistency and flavor in case the patient can handle one form better than another. Because choking is a danger, the caregiver should learn to administer the Heimlich maneuver, which may be taught by the local Red Cross. In very late stages, some caregivers choose feeding tubes for the patient. They should be aware that feeding tubes have no measurable impact on survival.

Care for the Caregiver

Few diseases disrupt a patient and his or her family so completely or for so long a period of time as Alzheimer's. The patient's family endures two separate losses and grieves twice:

First, they must grieve for the on-going disappearance of the personality they recognize. Dealing with the Alzheimer's patient throughout the course of the disease is like Alice's fall down the rabbit hole into Wonderland. No sooner has the caregiver grappled with one set of problems, when the patient's further deterioration creates new and more intractable ones.
Finally, the caregiver must grieve the actual death of the person.

Often, caregivers themselves begin to show signs of mental disorder or ill health. The disease may even have negative effects on the immune systems of the patients' partners. Depression, empathy, exhaustion, guilt, and anger can play havoc with even a healthy individual faced with the care of a loved one suffering from Alzheimer's. And the care-giving spouse is usually elderly and often frail. Children are likely to be grown-up and may live far away.

Although the great majority of caregivers have expressed their need for good information, in a 2001 study only 28% of caregivers believe they have received thorough and helpful information from their doctors. No one should endure such agony alone. It is important for the caregivers to receive counseling and support for themselves as well. In fact, according to one study, when caregivers took part in support programs, institutionalization of the patient was delayed by a year. National and local Alzheimer's associations are available and can provide important support and other services. [See Where Else Can Help for Alzheimer's Disease Be Obtained?.]

Nursing Homes and Other Outside Services

A point comes when the most devoted caregiver will probably need to institutionalize the Alzheimer's patient. That point is determined not only by the caregiver's emotional endurance, but also by his or her physical strength and stamina, as an Alzheimer's adult typically takes on the random, undisciplined behavior of a very young child. Financial considerations in finding a nursing home are often paramount, but the kind of care is equally important. Although fully half of all nursing home patients are victims of Alzheimer's, not all nursing homes have programs specifically designed for them. Some institutions may claim that they do, but often they simply group patients together without offering any special programs. If a caregiver manages to find a facility that offers good services, it may be located far from home, making visits difficult. The caregiver must then decide whether superior care at a distant institution is worth seeing the patient less frequently, still one more painful issue. A hospice program, if it is available, offers a more humane and compassionate option than the nursing home or hospital during the final months of a terminal illness.

Twelve Steps for Caregivers

1. Although I cannot control the disease process, I need to remember I can control many aspects of how it affects my relative.

2. I need to take care of myself so that I can continue doing the things that are most important.

3. I need to simplify my lifestyle so that my time and energy are available for things that are really important at this time.

4. I need to cultivate the gift of allowing others to help me, because caring for my relative is too big a job to be done by one person.

5. I need to take one day at a time rather than worry about what may or may not happen in the future.

6. I need to structure my day because a consistent schedule makes life easier for me and my relative.

7. I need to have a sense of humor because laughter helps to put things in a more positive perspective.

8. I need to remember that my relative is not being difficult on purpose; rather that his/her behavior and emotions are distorted by the illness.

9. I need to focus on and enjoy what my relative can still do rather than constantly lament over what is gone.

10. I need to increasingly depend upon other relationships for love and support.

11. I need to frequently remind myself that I am doing the best that I can at this very moment.

12. I need to draw upon the Higher Power, which I believe is available to me.

Source: The American Journal of Alzheimer's Care and Related Disorders & Research, Nov/Dec 1989

WHERE ELSE CAN HELP FOR ALZHEIMER'S DISEASE BE OBTAINED?

Alzheimer's Disease Education and Referral Center (ADEAR Center), National Institute on Aging, PO Box 8250, Silver Spring, MD 20907-8250. Call (800-438-4380) or (http://www.alzheimers.org/)
The center offers information on Alzheimer's disease and institutions that offer clinical trials. The web site offers good up to date news.

Alzheimer's Association, 919 North Michigan Ave., Suite 1100, Chicago, IL 60611. Call (800-272-3900) or (312-335-8700) or (http://www.alz.org/)
This is the primary Alzheimer's disease organization; it provides names of local chapters, fact sheets, and advice. It also provides information for Safe Return, a program for wandering Alzheimer's victims.

Alzheimer's Disease International (http://www.alz.co.uk/)

Alzheimer's Research Forum (http://www.alzforum.org/)

American Academy of Neurology, 1080 Montreal Avenue, St. Paul, Minnesota 55116. Call (651-695-1940) or (http://www.aan.com/)

National Institute of Neurological Disorders and Stroke, Office of Scientific and Health Reports, Bethesda, MD 20824. Call (800-352-9424) or (http://www.ninds.nih.gov/)
The institute provides information on clinical trials.

Medic Alert, 2323 Colorado Ave., Turlock, CA 95382. Call (888-633-4298) or (209-668-3333 from outside US) or (http://www.medicalert.org)
This organization provides bracelets or neck chain emblems with critical personal medical information. Also keeps computerized medical records.

National Institute on Aging and Eldercare Locator. Call (800-677-1116) or (http://www.eldercare.gov).
Eldercare Locator is a service of the National Association of Area Agencies on Aging. It provides information about and referrals to respite care and other home and community services.

American Health Assistance Foundation (AHAF), 15825 Shady Grove Rd., Ste. 140, Rockville, MD 20850 Call (800-437-2423) or (http://www.ahaf.org/)
This organization provides information, support, and referrals to families affected by Alzheimer's disease.

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