Alzheimer's disease is the most common form of dementia , a group of disorders that impairs mental functioning. (Dementia literally means loss of mentation, or thinking.) At the moment, Alzheimer's is progressive and irreversible. Abnormal changes in the brain worsen over time, eventually interfering with many aspects of brain function. Memory loss is one of the earliest symptoms, along with a gradual decline of other intellectual and thinking abilities, called cognitive functions, and changes in personality or behavior.
Alzheimer's advances in stages, progressing from mild forgetfulness and cognitive impairment to widespread loss of mental abilities. In advanced Alzheimer's, people become dependent on others for every aspect of their care. The time course of the disease varies by individual, ranging from five to 20 years. The most common cause of death is infection.

What Causes Alzheimer's Disease?
Scientists have made significant progress in understanding the possible causes of Alzheimer's disease, but many questions remain. It is likely that many factors, both inherited and environmental, interact in complex, poorly understood ways to cause the disease. (Also see Risk Factors below.)
In addition to investigating what might trigger Alzheimer's in some people, scientists have identified a number of brain changes that are associated with Alzheimer's. These include the characteristic plaques and tangles around and inside nerve cells that were first described by the German physician Alois Alzheimer in 1906. (More detail below in What happens to the brain in Alzheimer's disease?)
Click here to learn what scientific research is revealing about the possible causes of Alzheimer's disease.

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What Happens To The Brain in Alzheimer's Disease?
The progressive loss of cognitive function in Alzheimer's disease is accompanied by pathologic (disease-associated) changes in the brain. One of these is the formation of plaques - sometimes described as tiny "brillo pads" - in the space between nerve cells. The plaques are comprised of a brain protein called beta amyloid . Another protein, called tau, which normally channels chemical messages inside nerve cells, deforms and collapses into neurofibrillary tangles that appear like twisted bits of thread inside nerve cells.
As the disease progresses, nerve cells in several brain areas shrink and die, including cells that normally produce critical neurotransmitters , the chemical messengers that relay brain signals from one nerve cell (neuron ) to another. Acetylcholine is a neurotransmitter that is deficient in people with Alzheimer's. As nerve cells continue to die, the brain itself shrinks and the wrinkles along its surface become smoother.

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Who Is Affected by Alzheimer's Disease?
Today, it is estimated that about five million* Americans suffer from Alzheimer's disease, and about 360,000 people are newly diagnosed every year. Alzheimer's affects about 10 percent of people ages 65 and up, and the prevalence doubles roughly every 10 years after age 65. Half of the population ages 85 and up may have Alzheimer's.
Because the population of the U.S. is aging, the number of people with Alzheimer's will continue to rise unless something can be done to stem the rise. At current rates, experts believe that as many as 16 million Americans will have the disease by the year 2050.
The financial cost of caring for someone with Alzheimer's disease can be overwhelming and is estimated to be about $50,000 per year in direct medical expenses. Multiplied by five million (the estimated number of people with Alzheimer's), total direct costs in the U.S. exceed $250 billion per year. When indirect costs such as lost wages and decreased productivity of sufferers and their caregivers are included, the annual costs of Alzheimer's rise astronomically - high enough to potentially bankrupt the nation's entire healthcare system.
*Sources: Evans D., International Conference on Alzheimer's Disease and Related Disorders, July 22, 2002; Evans et al, The Milbank Quarterly, 1990; Brookmeyer et al, American Journal of Public Health, 1998