Alzheimer's Disease

From Psy3242

Revision as of 14:26, 9 April 2008

Someone develops Alzheimer's Disease every 71 seconds. Alzheimer's Disease is a progessive neuro de-generative disorder that accelerates cell loss. In recent years researchers have found that exercise improves memory,concentration, and abstract reasoning among older adults, and may even delay the onset of Alzheimer's disease. Aerobic exercise increases blood flow to the brain which nourishes brain cells and allows them to function more effectively. A recent study showed that exercise actually promotes the growth of new neurons(brain cells) in the hippocampus--the part of the brain that controls memory and learning. Scientists previously believed that once brain cells died, they were not replaced. According to previous research, chemicals, obesity, and smoking have all been linked to Alzheimer's. People who described themselves as goal-oriented and able to control impulses were less likely to develop Alzheimer's Disease according to a study of 997 people. Baby monkeys exposed to lead showed Alzheimer's like symptoms including amyloid plague, years later, according to a recent study. At the University of Alabama at Birmingham, mice who drank the equivalent of five sodas a day for six months did worse on memory tasks than those who drank water. The mice that had sodas had more than twice the amyloid plaque in their brains (which is a sign of Alzheimer's) than the others.The treatment costs of Alzheimer's Disease(AD) in the United States is estimated to be 100 billion. AD is the fourth common cause of death after heart disease, cancer and stroke. The neurobehavioral hallmark of probable AD is a gradual onset and continuous cognitive decline. The neuropathology of AD can only be confirmed by biopsy or autospy which includes the presence of neurofibillary tangles and amyloid or senile plaques. They occur in normal elderly persons but they occur in much larger numbers throughout the brains of AD patients and affect the functioning of the hippocampi. The brains of AD victims also have large numbers of granulovascuolar organelles which are small clusters of dead brain cell material that collect in the neurons in the hippocampi. Atrophy or shriveled cortex or shrunken cortex is a sign of dead nuerons that are present in Alzheimer's Disease.

Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.

• Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd). Tangles are twisted fibers of another protein called tau (rhymes with “wow”).

• Tangles form inside dying cells. Though most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions.

Scientists are not absolutely sure what role plaques and tangles play in Alzheimer’s disease. Most experts believe they somehow block communication among nerve cells and disrupt activities that cells need to survive.

At a scientific meeting in November 1906, German physician Alois Alzheimer presented the case of “Frau Auguste D.,” a 51-year-old woman brought to see him in 1901 by her family. Auguste had developed problems with memory, unfounded suspicions that her husband was unfaithful, and difficulty speaking and understanding what was said to her. Her symptoms rapidly grew worse, and within a few years she was bedridden. She died in Spring 1906, of overwhelming infections from bedsores and pneumonia.

Dr. Alzheimer had never before seen anyone like Auguste D., and he gained the family’s permission to perform an autopsy. In Auguste’s brain, he saw dramatic shrinkage, especially of the cortex, the outer layer involved in memory, thinking, judgment and speech. Under the microscope, he also saw widespread fatty deposits in small blood vessels, dead and dying brain cells, and abnormal deposits in and around cells.

The condition entered the medical literature in 1907, when Alzheimer published his observations about Auguste D. In 1910, Emil Kraepelin, a psychiatrist noted for his work in naming and classifying brain disorders, proposed that the disease be named after Alzheimer.