fbpx
Home Health Alzheimer’s: Is brain inflammation the missing trigger?

Alzheimer’s: Is brain inflammation the missing trigger?

0
Alzheimer’s: Is brain inflammation the missing trigger?

THE difference between people with amyloid brain plaque who develop Alzheimer’s disease and those who do not appears to be inflammation.

An excessive activation of the brain’s microglial cells encourages the growth of tau protein tangles that characterize the disease.

The study suggests combination therapies address-ing both amyloid plaque buildup and neuroinflam-mation may prove effective against Alzheimer’s disease.

Doctors regard amyloid plaque lodged between the brain’s nerve cells and tangled tau protein fibers forming within the cells as the hallmark of Alz-heimer’s disease.

However, amyloid plaque — consisting of broken pieces of protein that clump together — is also pre-sent in the brains of older adults who do not develop Alzheimer’s, suggesting another factor is triggering the disease.

A new study finds that inflammation in the brain drives the progression from the presence of amyloid plaque and tau tangles to the onset of dementia and Alzheimer’s disease.

Lead author of the study, Dr. Tharick Pascoal, Ph.D., assistant professor of psychiatry and neurol-ogy at the University of Pittsburgh School of Medi-cine, PA, explains:

“Many [older adults] have amyloid plaques in their brains but never progress to developing Alzheimer’s disease. We know that amyloid accumulation on its own is not enough to cause dementia — our results suggest that it is the interaction between neuroin-flammation and amyloid pathology that unleashes tau propagation and eventually leads to widespread brain damage and cognitive impairment.”

The study appears in Nature MedicineTrusted Source.

While scientists have observed neuroinflammation in people with Alzheimer’s before, the new study reveals for the first time its critical role in the devel-opment of the disease.

The research finds that activating the brain’s im-mune cells — its microglial cells — promotes the spread of tangled tau proteins that comprise amyloid plaque.

Heather M. Snyder, Ph.D., Alzheimer’s Association vice president of medical and scientific relations, who was not involved in the study, explained the purpose of neuroinflammation to Medical News Today.