Alzheimer’s disease is the most common cause of dementia, the progressive decline in intellectual function. It is estimated that two to four million Americans suffer from AD, and as many as 14 to 20 million will have it by the middle of the 21^st century as the population ages. The incidence of AD increases with age. Approximately 3% of people between the ages of 65 and 74 years suffer from the disease. The incidence increases to 19% between the ages of 75 and 84. Alzheimer’s disease affects approximately 47% of the population age 85 and older.

Early symptoms of Alzheimer’s disease are occasional forgetfulness and mild memory loss. The onset of symptoms is so insidious that the disease is usually suspected only in hindsight, after loss of intellectual function becomes obvious to family members. The patient is usually oblivious to the progressive functional decline which eventually impairs his or her ability to manage basic self care and activities of daily living.

The diagnosis of AD is based on the clinical symptoms as there are no laboratory tests or imaging procedures which can determine if a person does or does not have the disease. The diagnosis is made by the presence of a compatible history of onset, typical abnormalities on cognitive testing, and the absence of any other explanation. Early in the course, AD may be difficult to diagnose. As symptoms advance, the diagnosis becomes obvious. From the stand point of the health care professional, the primary concern in evaluating a patient with suspected AD is to rule out treatable conditions which may mimic the symptoms of AD (such as thyroid disease, vitamin deficiencies, depression, strokes). Therefore brain imagining procedures and laboratory tests are frequently performed to rule out other medical conditions.

The cause of Alzheimer’s disease is unknown. Microscopic examination of brains from AD patients reveal characteristic abnormalities known as neurofibrillary tangles and senile plaques. Neurofibrillary tangles are tufts of twisted proteins seen within the nerve cells in the brain. Senile plaques are clumps of nerves surrounding deposits of beta-amyloid protein. It is not know whether these microscopic changes are the cause of the dementing process or merely a consequence of the pathologic process.

At one time, environmental factors such as pollution and aluminum toxicity were suspected causes of AD . However these associations have not been born out in population studies. In a subset of cases, genetic factors appear to play role, as familial patterns of AD are well recognized. In addition to age, risk factors are a family history of AD and Down’s Syndrome.

There is no cure for Alzheimer’s disease, although some medications seem to temporarily improve the symptoms in the early stages. Two medications, tacrine (Cognex) and donepezil (Aricept), which inhibit the breakdown of the neurotransmitter acetylcholine, improve cognitive and social functioning when dementia symptoms are mild. The degree of improvement is slight, but noticeable. Gingko extract, widely prescribed in Europe for circulatory disorders, also improved the symptoms of dementia in recent studies performed in the United States. (1) An herbal supplement derived from Cats Claw (as a proprietary formulation designated PTI 00703) inhibited the formation of amyloid plaques in animal models of Alzheimer’s disease in rats. (2) Further investigation of this herb in Alzheimer’s patients has been proposed.

At the present time, there is no certain prevention of Alzheimer’s disease. However, some of the treatments currently under investigation appear promising and hold hope for the future.

1.  Le Bars P, et. al. Journal of the American Medical Association 1997; 298:1327-1332,

2. Herb May Help Alzheimer’s Experiment Show