"Alzheimer's disease has proved to be a tricky target, and researchers and drug developers have been pursuing effective treatments for decades. Debates rage over the disorder's underlying causes, and various approaches have faced one hurdle after another. But the field has reached a turning point. Over the past four years the U.S. Food and Drug Administration has approved several therapies that address some of the condition's potential biological roots rather than merely mitigating symptomsa key scientific milestone. Despite the advances, however, there is still a long list of open questions and so much work to be done."
"The brains of people who die with Alzheimer's show a distinct biology: clumps or plaques of amyloid beta proteins in spaces between neurons and tangles of tau proteins that accumulate primarily within the nerve cells. One prevailing theory holds that amyloid builds up early, and tau tangles develop when nerve cell damage is underway but cognitive symptoms are not yet apparent. Over time these pathogenic, or disease-causing, proteins disrupt nerve cell communication."
"The newest treatmentslecanemab and donanemabbind to amyloid beta proteins, clear them from the brain and modestly slow cognitive decline."
Alzheimer's disease is characterized by extracellular amyloid-beta plaques and intracellular tau tangles that interfere with neuronal communication. Amyloid often accumulates decades before symptoms appear, with a common 20- to 30-year lag between initial detection and obvious cognitive decline. Two recently approved therapies, lecanemab and donanemab, bind amyloid beta, reduce brain plaque burden, and modestly slow cognitive deterioration. Amyloid and tau also occur in other neurodegenerative disorders, making progression from protein accumulation to dementia inexact. Numerous biological uncertainties remain, and further research is required to improve timing, targeting, and long-term clinical benefit.
Read at www.scientificamerican.com
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