Breakdown of late-stage myelin promotes Alzheimers disease

A new study has found that the breakdown of late-stage myelin promotes Alzheimers disease, as it builds up toxic amyloid-beta fibrils that eventually deposit in the brain and become plaques.

Washington, May 12 : A new study has found that the breakdown of late-stage myelin promotes Alzheimer's disease, as it builds up toxic amyloid-beta fibrils that eventually deposit in the brain and become plaques.

Myelin is the fatty sheath that coats the axons of the nerves, allowing for efficient conduction of nerve impulses. This process called myelination, is key to the fast processing speeds that underlie our higher cognitive functioning, including wisdom.

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.

The study was conducted by a team of researchers led by Dr. George Bartzokis at the University of California, Los Angeles.

Oligodendrocytes and myelin have the highest levels of iron of any brain cells. According to researchers, evidence supported the possibility that brain iron levels might be a risk factor for age-related neurodegenerative diseases like Alzheimer's.

Researches suggested that myelin breakdown in the late-myelinating regions releases iron, which promotes the development of the toxic amyloid oligomers and plaques, which in turn destroy more myelin.

As part of the study, to test this hypothesis, researchers examined published images of amyloid deposition acquired in living individuals. The images were made using radiolabeled ligands, molecules that bind to amyloid plaques in the brains of Alzheimer's patients.

Researchers found that physical location of these plaques perfectly matched much earlier work published in a 1901 edition of The Lancet that mapped the locations in the brain where late-stage myelination occurs.

"It was pretty striking. And the results are easily testable using currently available imaging methods. What's important is that these results have implications for novel therapeutic interventions that could target oligodendrocytes, myelin and iron deposits in the brain," Bartzokis said.

"Myelination of the brain follows an inverted U-shaped trajectory, growing strongly until middle age. Then it begins to breakdown. 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," Bartzokis said.

According to researchers, as a result, the volume of myelinated white matter increases to a peak at about age 50, and then slowly begins to reverse and decline in volume with the increasing age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters, and so spreads itself thinner and thinner. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down.

The findings of the research were published in the April issue of the journal Alzheimer's and Dementia.

ANI