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Aβ fibrils, TEM
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  • David B. Teplow, Ph.D.
  • Professor of Neurology
  • Director, Biopolymer Laboratory
  • David Geffen School of Medicine at UCLA

Right target, but missing the bulls-eye for Alzheimer's

UCLA researchers discover new point of attack for drug therapy

Abeta, with hairpin turn between orange and red arrows

Alzheimer's disease is the most common cause of late-life dementia. The disorder is thought to be caused by a protein known as amyloid-beta, or Abeta, which clumps together in the brain, forming plaques that are thought to destroy neurons. This destruction starts early, too, and can presage clinical signs of the disease by up to 20 years.

For decades now, researchers have been trying, with limited success, to develop drugs that prevent this clumping. Such drugs require a “target" — a structure they can bind to, thereby preventing the toxic actions of Abeta.

Now, a new study out of UCLA suggests that while researchers may have the right target in Abeta, they may be missing the bull's-eye. Reporting in the Jan. 23 issue of the Journal of Molecular Biology, UCLA neurology professor David Teplow and colleagues focused on a particular segment of a toxic form of Abeta and discovered a unique hairpin-like structure that facilitates clumping.

Now, a new study out of UCLA suggests that while researchers may have the right target in Abeta, they may be missing the bull's-eye. Reporting in the Jan. 23 issue of the Journal of Molecular Biology, UCLA neurology professor David Teplow and colleagues focused on a particular segment of a toxic form of Abeta and discovered a unique hairpin-like structure that facilitates clumping.

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Research Interests:

The Teplow laboratory seeks to understand and treat diseases associated with the aging process. These include Alzheimer's disease (AD), Parkinson's disease, Huntington's disease, and Lou Gehrig's disease. The laboratory has special expertise in AD, the most common cause of late-life dementia. A key cause of AD is thought to be a protein called the amyloid beta-protein (Abeta). This protein deposits in the brain to form what are called “amyloid plaques." Our group has worked to understand how these plaques form and to use this knowledge to design drugs to prevent or treat the disease. Our studies have revealed that Abeta shares properties with other proteins linked to human diseases of aging, therefore the work done on AD is likely to advance efforts to understand and treat these disorders.

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