Alzheimer's Disease

Alzheimer's Disease

Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, or neurons, resulting in loss of memory, thinking and language skills, and behavioral changes. 


           

These neurons, which produce the brain chemical, or neurotransmitter,

acetylcholine, break connections with other nerve cells and ultimately die.

For example, short-term memory fails when Alzheimer's disease first

destroys nerve cells in the hippocampus, and language skills and judgment

decline when neurons die in the cerebral cortex. 


           

Two types of abnormal lesions clog the brains of individuals with 

Alzheimer's disease: Beta-amyloid plaques—sticky clumps of protein fragments and cellular material that form outside and around neurons; and neurofibrillary tangles—insoluble twisted fibers composed largely of the protein tau that build up inside nerve cells. Although these structures are hallmarks of the disease, scientists are unclear whether they cause it or a byproduct of it. 


           

Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older. Alzheimer's disease is not a normal part of aging. 


           

Origin of the term Alzheimer's disease dates back to 1906 when Dr. Alois Alzheimer, a German physician, presented a case history before a medical meeting of a 51-year-old woman who suffered from a rare brain disorder. A brain autopsy identified the plaques and tangles that today characterize Alzheimer's disease. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles).

Plaques and tangles in the brain are two of the main features of Alzheimer’s disease. The third is the loss of connections between nerve cells (neurons) in the brain.

Although we still don’t know how the Alzheimer’s disease process begins, it seems likely that damage to the brain starts a decade or more before problems become evident. During the preclinical stage of Alzheimer’s disease, people are free of symptoms but toxic changes are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons begin to work less efficiently.

Over time, neurons lose their ability to function and communicate with each other, and eventually they die. Before long, the damage spreads to a nearby structure in the brain called the hippocampus, which is essential in forming memories. As more neurons die, affected brain regions begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.

Scientists don’t yet fully understand what causes Alzheimer’s disease, but it has become increasingly clear that it develops because of a complex series of events that take place in the brain over a long period of time. It is likely that the causes include some mix of genetic, environmental, and lifestyle factors. Because people differ in their genetic make-up and lifestyle, the importance of any one of these factors in increasing or decreasing the risk of developing Alzheimer’s may differ from person to person.

Most people with Alzheimer’s disease have “late-onset” Alzheimer’s, which usually develops after age 60. Many studies have linked the apolipoprotein E (APOE) gene to late-onset Alzheimer’s. This gene has several forms. One of them, APOE ε4, seems to increase a person’s risk of getting the disease. However, carrying the APOE ε4 form of the gene does not necessarily mean that a person will develop Alzheimer’s disease, and people carrying no APOE ε4 can also develop the disease.

Research suggests that a host of factors beyond basic genetics may play a role in the development and course of Alzheimer’s disease. There is a great deal of interest, for example, in associations between cognitive decline and vascular and metabolic conditions such as heart disease, stroke, high blood pressure, diabetes, and obesity. Understanding these relationships and testing them in clinical trials will help us understand whether reducing risk factors for these conditions may help with Alzheimer’s as well.

Further, a nutritious diet, physical activity, social engagement, and mentally stimulating pursuits can all help people stay healthy as they age. New research suggests the possibility that these and other factors also might help to reduce the risk of cognitive decline and Alzheimer’s disease.