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May 17, 2007

New Clue to Alzheimer's Cause

One of the key differences between the human and non-human brain is a phenomenon called myelination. Myelination is the production of myelin, a part-fat, part-protein substance that coats part of our neurons. It allows for speedier transmission of signals within the brain and, ultimately, higher levels of cognitive functioning.

Until we are about 50 years old, myelination continues to occur, gradually improving our brains, After 50, myelination slows and the myelin coating around the neurons begins to degenerate.

Early or excessive loss of myelin may happens in MS (multilple sclerosis), transverse myelitis and several other nervous system diseases.

Now, a report in the April 2007 issue of the journal Alzheimer's & Dementia by Dr. George Bartzokis, UCLA professor of neurology, suggests that age-related loss of myelin causes the buildup in the brain of toxic deposits made of amyloid that are the hallmark of Alzheimer's disease.

This buildup goes on to further damage myelin, crippling brain function and causing Alzheimer's. By improving our understanding of the process behind Alzheimer's, Bartzokis's research may point the way toward new treatments for this terrible disease.

"Myelination of the brain follows an inverted U-shaped trajectory, growing strongly until middle age. Then it begins to breakdown," said Bartzokis. "Before the advent of modern medicine, very few persons lived beyond age 50 and therefore, as a species, we evolved to continue myelinating over our entire natural life span."

The amount of myelinated "white matter" in the brain peaks at about age 50, then slowly begins to decline as we age. The myelin that is produced in adulthood becomes spread thinner and thinner. This makes it more susceptible to environmental and genetic damage.

"The myelin breakdown process mimics the developmental process of myelination, but this time in reverse," Bartzokis said, noting that a similar progression is seen in the cognitive, functional and neurologic declines that characterize Alzheimer's disease.
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