Researchers from UCLA believe Alzheimer’s disease may result from a natural aging process that causes the breakdown myelin, the outer insulating layer of nerves.
Myelin is a fatty sheath that coats the axons of the nerves, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functioning.
Myelination continues sheathing axons until we reach the age of about 50, but in these later stages, the myelin becomes more and more susceptible to damage.
In a report in the April issue of the journal Alzheimer’s & Dementia, Dr. George Bartzokis, UCLA professor of neurology, suggests that it is the breakdown of this late-stage myelin that promotes the buildup of toxic amyloid-beta fibrils that eventually deposit in the brain and become the plaques which have long been associated with Alzheimer’s disease.
These amyloid products in turn destroy more and more myelin, according to Bartzokis, disrupting brain signaling and leading to cell death and the classic clinical signs of Alzheimer’s. If correct, the research suggests a broader approach to therapeutic interventions for the disease.
And in a unique twist for modern-day science, Bartzokis tested his myelin model of Alzheimer’s by comparing modern imaging results with maps of cortical myelination that were published in the medical journal The Lancet — back in 1901.
“Myelination is the single most unique aspect in which the human brain differs from those of other species,” said Bartzokis, who also directs the UCLA Memory Disorders and Alzheimer’s Disease Clinic.
Myelin is produced by oligodendrocytes, specialized glial cells that themselves become more vulnerable with age.
“Myelination of the brain follows an inverted U-shaped trajectory, growing strongly until middle age. Then it begins to breakdown,” Bartzokis said.
“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.”