Recent research from the Max Planck Institute has revealed that degenerating myelin, the protective sheath around nerve cells in the brain, significantly contributes to Alzheimer’s disease progression. Alzheimer’s disease is a prevalent and irreversible form of dementia that primarily affects the elderly, with the risk doubling every five years after age 65. As myelin deteriorates with age, it promotes the pathological changes typical of Alzheimer’s, including the accumulation of amyloid-beta peptides that form amyloid plaques—a hallmark of the disease.
The study utilized mouse models to examine the interplay between myelin degradation and amyloid plaque deposition. Findings indicated that diminished myelin accelerates plaque buildup by stressing nerve fibers, which in turn leads to increased production of amyloid peptides. Compromised myelin also distracts immune cells, called microglia, from effectively removing plaques, as they prioritize dealing with the damaged myelin instead.
These insights suggest that addressing age-related myelin degradation may offer new avenues for preventing or slowing Alzheimer’s disease, emphasizing the critical role of intact myelin in maintaining normal brain function. The study highlights potential therapeutic strategies focused on targeting myelin health to combat Alzheimer’s progression.
