"By the time symptoms begin creating problems, the disease has been unfolding in the brain for years. Microscopic amyloid-beta plaques have accumulated between neurons, and later threads of neurofibrillary tau proteins have tangled themselves into tight knots inside brain cells. The two abnormalities - first described in 1906 by the German physician Alois Alzheimer - have become the twin hallmarks of the disease."
"The results are somewhat unclear. In trials, FDA-approved drugs that target amyloid plaques slow cognitive decline by about 30 percent but do not halt or reverse the disease. Many have the plaques but never display symptoms. But new technologies - artificial intelligence that may be able to identify new genetic determinants of the disease, blood tests for proteins in the brain, and real-time brain monitoring that reveals how individual neurons die - are finding new ways to understand and possibly help treat Alzheimer's."
Alzheimer's begins years before symptoms, with amyloid-beta plaques accumulating between neurons and neurofibrillary tau tangles forming inside brain cells. FDA-approved drugs that target amyloid slow cognitive decline by about 30 percent but do not halt or reverse the disease, and many people with plaques remain asymptomatic. Emerging tools include artificial intelligence to identify genetic determinants, blood tests for brain proteins, and real-time neuronal monitoring to observe cell death. Additional research explores lithium deficiency as a possible factor in onset and progression. The aging population is projected to increase Alzheimer's cases dramatically, heightening urgency for effective treatments.
Read at Harvard Gazette
Unable to calculate read time
Collection
[
|
...
]