Alzheimer's disease may be linked to the brain's attempt to battle past infections, according to a new study suggesting that debris left over from the fight leads to the condition, reported
The New York Times.
Many researchers frustrated by the seemingly intractable condition are jumping on the theory's bandwagon.
The study in the journal Science Translational Medicine proposed that in an effort to fight off infections the brain's defense system creates a sticky cage made of protein called beta amyloid to trap invading microbes. The remains of those cages over time become the plaque commonly associated with Alzheimer's.
"It's interesting and provocative," said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer's Disease Neuroimaging Initiative, according to the Times.
"Our findings raise the intriguing possibility that (beta) amyloid may play a protective role in innate immunity and infectious or sterile inflammatory stimuli may drive amyloidosis," said the
study's abstract. "These data suggest a dual protective/damaging role for (beta amyloid) as has been described for other antimicrobial peptides."
Robert D. Moir, of Harvard Medical School and Massachusetts General Hospital, had been examining the role of amyloid proteins – which had been thought of as garbage that accumulates in the brain with age, noted the Times – and theorized that the protein could be part of a primitive immune system that acts as the first line of defense against infections crossing the blood-brain barrier which begins to break down as people get older.
The study's results could impact the future of Alzheimer's therapies currently in development, which are largely based upon the premise that beta amyloid is pathological, said the
Cure Alzheimer's Fund.
"Instead of eradicating amyloid from the brains of Alzheimer's patients, a safer approach may be therapies that are designed to lower amyloid levels without destroying them entirely."
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