Alzheimer

Alzheimer disease (AD) is an incurable degenerative disease of the brain first described in 1906 by the German neuropathologist Alois Alzheimer. It is the most common cause of dementia in adults and is estimated to affect more than 2 million men and women over the age of 65 in the United States. AD is a progressive illness, with memory loss usually the initial and major symptom. Other symptoms include impairments in language, abstract reasoning, and the ability to find one's way. Personality changes ranging from apathy to restless agitation are common, and depression, delusions, and hallucinations may also occur. The cognitive parts of the brain are especially affected, while regions that detect sensations and control muscular movement are usually spared. The symptoms worsen gradually every year, and in the later stages the patient is usually unable to live independently. Although it is difficult to predict the course of decline in a given individual, death usually occurs ten years or more after onset. 

The hallmarks of AD in the brain are structures called neurofibrillary tangles that are found in dying nerve cells and plaques composed of degenerating nerve-cell elements surrounding a core of amyloid protein. Other biochemical abnormalities include disrupted nerve-cell membrane phospholipid metabolism and decreases in neurotransmitter substances such as acetylcholine. 

The cause of AD is unknown, but there are a number of risk factors for developing the disease; advanced age is the most important. Although the risk of developing AD is less than 1 percent before 50 years of age, it increases steeply with each successive decade of life to reach 30 percent or more by the age of 90. Genetic factors are also important. Mutations in several genes have been associated with patients who have rare familial types of AD. In these individuals the abnormal genes appear to influence the production of amyloid protein, which triggers the development of the disease. The gene apolipoprotein-E (apoE) somewhat influences an individual's susceptibility to AD. One form of this gene appears to protect people from getting AD, while another confers a greater risk. 

Until the exact cause of AD is determined, a cure will remain elusive. There are no treatments that reverse the primary cognitive impairments or that retard the course of illness. Some experimental drug trials have sought to improve memory symptoms by treating the deficits in acetylcholine neurotransmission, and two drugs have been approved for use, although their effectiveness is limited. Other potential treatments include vitamin E and nonsteroidal antiinflammatory agents.