there is no general agreement. As it stands, there is treatment, but no cure. As many as 4.5 million Americans suffer from AD which usually begins after age 60 with the risk increasing with age.
Younger people also may get AD, but it is much less common. About 5 % of men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease.
Nevertheless, AD is not a normal part of aging.
AD is named after Dr. Alois Alzheimer, a German doctor who in 1906 noted changes in the brain tissue of a woman who had died of an unusual mental illness. He found abnormal clumps, now
called “amyloid plaques,” and tangled bundles of fibers, now called “neurofibrillary tangles” in her brain tissue when examined under the microscope. Today, these plaques and tangles in the
brain are considered diagnostic of AD. There are other brain changes in people with AD. For example, nerve cells die in areas of the brain that are important to memory and other mental abilities,
and connections between nerve cells are disrupted. There also are lower levels of some of the chemicals in the brain that carry messages back and forth between nerve cells. AD may impair
thinking and memory by disrupting these messages.
Probably there is no one single cause, but several factors that affect each person differently. Age is the most important known risk factor for AD. The number of people with the disease
doubles every 5 years beyond age 65. Another risk factor is a family history of the disease. Genetics may play some role in many AD cases. For example, early-onset familial AD, a rare form that
usually occurs between the ages of 30 and 60, is inherited. The more common form of AD is known as “late-onset.” It occurs later in life, and no obvious inheritance pattern is seen in most
families. Several risk factor genes may interact with each other and with non-genetic factors to cause the disease. The only risk factor gene identified for late-onset AD is a gene that makes one
form of a protein called apolipoprotein E (ApoE). Everyone has ApoE, which helps carry cholesterol in the blood. About 15 percent of people have the form that increases the risk of AD. It is likely
that other genes also may increase the risk of AD, or protect against AD, but they are not yet identified. We still need to learn more about what causes AD. It appears that education, diet, and
environment may play some role. Some of the risk factors for heart disease and stroke, such as high blood pressure, high cholesterol, and low levels of the vitamin folate, may also increase the
risk of AD. Evidence for physical, mental, and social activities as protective factors against AD is also increasing.
AD begins slowly. At first, the only symptom may be mild forgetfulness, easily confused with age-related memory change. Most people with mild forgetfulness do not have AD. In the early
stage of AD, people have trouble remembering recent events, activities, or the names of familiar people or things and they may not be able to solve simple math problems. Such difficulties
usually they do not cause alarm. As the disease goes on, symptoms become more obvious and become serious enough to cause people with AD or their family members to seek medical help.
In the middle stages of AD simple skills like brushing their teeth and combing hair may be lost. They can no longer think clearly and fail to recognize familiar people and places. Problems
speaking, understanding, reading, or writing begin to appear. In the later stages anxiety or aggressiveness may appear and often the affectd person may wander away from home. Eventually,
patients need total care.
The only definite way to diagnose AD is to find out whether there are plaques and tangles in brain tissue. To look at brain tissue, however, doctors usually must wait until they can do an
autopsy, that is an examination of the body after a person dies. Therefore, doctors can only make a diagnosis of “possible” or “probable” AD while the person is still alive. Experienced doctors
can diagnose AD correctly up to 90 percent of the time. Recently a special blood protein (phosphorylated tau protein) has been identified which seems to correlate with the later development of
AD. This may turn out to be predictive of AD.
On average, AD patients live from 8 to 10 years after they are diagnosed, though some people may live with AD for as many as 20 years. No treatment can stop AD, however, for some
people in the early and middle stages of the disease, the drugs tacrine (Cognex, which is still available but no longer actively marketed by the manufacturer), donepezil (Aricept), rivastigmine
(Exelon), or galantamine (Razadyne, previously known as Reminyl) may help prevent some symptoms from becoming worse for a limited time. Another drug, memantine (Namenda), has been
approved to treat moderate to severe AD, although it also has only limited effects. Also, some medicines may help control behavioral symptoms of AD such as sleeplessness, agitation,
wandering, anxiety, and depression. Treating these symptoms often makes patients more comfortable and makes their care easier for caregivers.
Several years ago, a clinical trial showed that vitamin E slowed the progress of some consequences of AD by about 7 months. Additional studies are investigating whether
antioxidants—vitamins E and C—can slow AD. Another clinical trial is examining whether vitamin E and/or selenium supplements can prevent AD or cognitive decline. Early studies suggested
that extracts from the leaves of the ginkgo biloba tree may be of some help in treating AD symptoms. There is no evidence yet that ginkgo biloba will cure or prevent AD, but scientists now are
trying to find out in a clinical trial whether ginkgo biloba can delay cognitive decline or prevent dementia in older people.
There is evidence that inflammation in the brain may contribute to AD
damage. Some studies have suggested that drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) might help slow the progression of AD, but clinical trials thus far have not
demonstrated a benefit from these drugs. Scientists are testing a number of drugs to see if they prevent AD, slow the disease, but no real progress has yet been reported.
Chelation therapists commonly observe that people who are chelated regularly experience a slow-down in the progression of their disease and that some seem to stop progressing. Hormone therapy is also useful, especially pregnenolone and human growth hormone (HGH) when deficiencies can be documented. There seems to be a strong correlation with heavy metal toxicity, especially aluminum and cadmium. This is probably why chelation therapy is of benefit to many. Of course, Alzheimer’s patients can experience vascular disease as well as anyone else and when this happens, the combination of poor blood supply to the brain with Alzheimer’s is devastating. Once again, chelation therapy is effective in most cases in increasing blood supply to all organs. The best hope for Alzheimer’s patients, at this time, appears to be chelation therapy combined with nutrient and hormone therapy.
Mild Cognitive Impairment
During the past several years, scientists have focused on a type of memory change called mild cognitive impairment (MCI), which is different from both AD and normal age-related memory
change. People with MCI have memory problems, but they do not have other losses such as confusion, attention problems, and difficulty with language.