Dangers of Alzheimer disease

Alzheimer Disease 
Alzheimer disease (AD) is a disorder characterized by a gradual loss of reason that begins with memory lapses and ends with an inability to perform any type of daily activity. Personality changes signal the onset of AD. A normal 50- to GO-year-old adult might forget the name of a friend not seen for years. People with AD, however, forget the name of a neighbor who visits daily. With time, they have trouble travel­ing and cannot perform simple errands. People afflicted with AD become confused and tend to repeat the same question. Signs of mental disturbances eventually appear, and patients gradually become bedridden and die of a complication, such as pneumonia.
A normal neuron (nerve cell), and a neuron damaged by Alzheimer disease (AD), are shown in figure 8A. The AD neu­ron has two abnormalities not seen in the normal neuron: (1) Bundles of fibrous protein, called neurofibrillary tangles, surround the nucleus in the cell, and (2) protein-rich accu­mulations, called amyloid plaques, envelop the axon branches. These abnormal neurons are especially seen in the portions of the brain that are involved in reason and memory (frontal lobe and limbic system). To see the abnormal brain neurons, brain tissue must be examined microscopically after the patient dies.
A chemical test can be used to check brain tissue for the presence of a protein called Alzheimer disease associated pro­tein (ADAP), which is believed to be the protein contained in the neurofibrillary tangles. If ADAP is proven to be the protein involved in AD, individuals could be tested for this protein by obtaining a spinal tap of cerebrospinal fluid.
Over a life span of 100 years, the likelihood of developin~ AD is 16% for people with no family history of AD, and 240 ­for those having first-degree relatives with AD. This differenc in susceptibility suggests that AD might have a genetic basic Researchers have discovered that in some families whose members have a 50% chance of AD, a genetic defect exists or:. chromosome 21. This is of extreme interest because Dow-I; syndrome results from the inheritance of three copi of chromosome 21, and people with Down syndrome tend to develop AD. Further, the genetic defect affects the normal production of amyloid precursor protein (APP), which may be th cause of the amyloid plaques.
Acetylcholine is a chemical that stimulates neurons to carry nerve impulses, and it appears that this chemical may be in short supply in the brains of patients with AD. Drugs tha: enhance acetylcholine production are currently being tested iG AD patients. Experimental drugs that prevent neuron degener­ation are also being tested. For example, it is possible tha: nerve growth factor, a substance that is made by the body an that promotes the growth of neurons, will one day be available to AD patients.