BrightFocus-Funded Researcher Sheds Light on Why Alzheimer's Medications Rarely Help
July 10, 2013
Source: Journal of Biological Chemistry
BrightFocus Foundation’s Alzheimer’s Disease Research program funded Dr. Zhefeng Guo, who is an assistant professor of neurology at the David Geffen School of Medicine at UCLA and a member of UCLA's Brain Research Institute and Molecular Biology Institute.
Zhefeng Guo, Ph.D.
Photo courtesy of UCLA
Current medications do not treat Alzheimer's or stop it from progressing; they only temporarily lessen symptoms, such as memory loss and confusion.
Current Alzheimer's drugs aim to reduce the amyloid plaques —sticky deposits that build up in the brain—that are a visual trademark of the disease. These plaques are made of long fibers of a protein called amyloid beta, or Aβ. Recent studies, however, suggest that the real culprit behind Alzheimer's may be small Aβ clumps called oligomers that appear in the brain years before plaques develop.
In unraveling oligomers' molecular structure, UCLA scientists discovered that Aβ has a vastly different organization in oligomers than in amyloid plaques. Their finding could shed light on why Alzheimer's drugs designed to seek out amyloid plaques have no effect on oligomers.
The UCLA study suggests that recent experimental Alzheimer's drugs failed in clinical trials because they zero in on plaques and do not work on oligomers. Future studies on oligomers will help speed the development of new drugs specifically aiming at Aβ oligomers, the researchers say.
Adapted from UCLA
Summary in the Journal of Biological Chemistry
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