Tangles are long, slender tendrils found inside nerve cells, or neurons. Scientists have learned that when a protein called tau becomes altered, it may cause the characteristic tangles in the brain of an Alzheimer’s patient. In healthy brains, tau provides structural support for neurons, but in Alzheimer’s patients this structural support collapses.

Plaques, or clumps of fibers, form outside the neurons in the adjacent brain tissue. Scientists found that a type of protein, called amyloid precursor protein, forms toxic plaques when it is cut in two places. Researchers have isolated the enzyme beta-secretase, which is believed to make one of the cuts in the amyloid precursor protein. Researchers also identified another enzyme, called gamma secretase, that makes the second cut in the amyloid precursor protein. These two enzymes snip the amyloid precursor protein into fragments that then accumulate to form plaques that are toxic to neurons.

Scientists have found that tangles and plaques cause neurons in the brains of Alzheimer’s patients to shrink and eventually die, first in the memory and language centers and finally throughout the brain. This widespread neuron degeneration leaves gaps in the brain’s messaging network that may interfere with communication between cells, causing some of the symptoms of Alzheimer’s disease.

Alzheimer’s patients have lower levels of neurotransmitters, chemicals that carry complex messages back and forth between the nerve cells. For instance, Alzheimer’s disease seems to decrease the level of the neurotransmitter acetylcholine, which is known to influence memory. A deficiency in other neurotransmitters, including somatostatin and corticotropin-releasing factor, and, particularly in younger patients, serotonin and norepinephrine, also interferes with normal communication between brain cells.

IV  Causes

The causes of Alzheimer’s disease remain a mystery, but researchers have found that particular groups of people have risk factors that make them more likely to develop the disease than the general population. For example, people with a family history of Alzheimer’s are more likely to develop Alzheimer’s disease.

Some of the most promising Alzheimer’s research is being conducted in the field of genetics to learn the role a family history of the disease has in its development. Scientists have learned that people who are carriers of a specific version of the apolipoprotein E gene (apoE gene), found on chromosome 19, are several times more likely to develop Alzheimer’s than carriers of other versions of the apoE gene. The most common version of this gene in the general population is apoE3. Nearly half of all late-onset Alzheimer’s patients have the less common apoE4 version, however, and research has shown that this gene plays a role in Alzheimer’s disease. Scientists have also found evidence that variations in one or more genes located on chromosomes 1, 10, and 14 may increase a person’s risk for Alzheimer’s disease. Scientists have identified the gene variations on chromosomes 1 and 14 and learned that these genes produce mutations in proteins called presenilins. These mutated proteins apparently trigger the activity of the enzyme gamma secretase, which splices the amyloid precursor protein.

Researchers have made similar strides in the investigation of early-onset Alzheimer’s disease. A series of genetic mutations in patients with early-onset Alzheimer’s has been linked to the production of amyloid precursor protein, the protein in plaques that may be implicated in the destruction of neurons. One mutation is particularly interesting to geneticists because it occurs on a gene involved in the genetic disorder Down syndrome. People with Down syndrome usually develop plaques and tangles in their brains as they get older, and researchers believe that learning more about the similarities between Down syndrome and Alzheimer’s may further our understanding of the genetic elements of the disease.

Some studies suggest that one or more factors other than heredity may determine whether people develop the disease. One study published in February 2001 compared residents of Ibadan, Nigeria, who eat a mostly low-fat vegetarian diet, with African Americans living in Indianapolis, Indiana, whose diet included a variety of high-fat foods. The Nigerians were less likely to develop Alzheimer’s disease compared to their U.S. counterparts. Some researchers suspect that health problems such as high blood pressure, atherosclerosis (arteries clogged by fatty deposits), high cholesterol levels, or other cardiovascular problems may play a role in the development of the disease.

Other studies have suggested that environmental agents may be a possible cause of Alzheimer’s disease; for example, one study suggested that high levels of aluminum in the brain may be a risk factor. Several scientists initiated research projects to further investigate this connection, but no conclusive evidence has been found linking aluminum with Alzheimer’s disease. Similarly, investigations into other potential environmental causes, such as zinc exposure, viral agents, and food-borne poisons, while initially promising, have generally turned up inconclusive results.

Some studies indicate that brain trauma can trigger a degenerative process that results in Alzheimer’s disease. In one study, an analysis of the medical records of veterans of World War II (1939-1945) linked serious head injury in early adulthood with Alzheimer’s disease in later life. The study also looked at other factors that could possibly influence the development of the disease among the veterans, such as the presence of the apoE gene, but no other factors were identified.

 

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