Stanford Research Targets Amyloid Role in Alzheimer's

Researchers at Stanford are seeking to unravel and reverse the mystery of Amyloid protein accumulation. Amyloids accumulate in the brains of Alzheimer's Disease candidates, eventually triggering the progression of the disease in concert with biochemical factors occurring at the molecular level. Understanding these interactions are key to developing a solution to the Disease.

(AP)A potential new therapeutic approach to Alzheimer's disease protects brain cells in culture by drastically reducing the neurotoxic amyloid protein aggregates that are critical to the development of the disease. The treatment involves dispatching a small molecule into the cell to enlist the aid of a larger “chaperone” protein to block the accumulation of the brain-clogging protein.

The new "Trojan horse" technique overcomes a major challenge in drug design - namely, the limited ability of molecules small enough to enter a cell to interfere with interactions between much larger proteins. The researchers said it might also be possible to use this new approach to sabotage proteins central to pathogenic organisms, such as human immunodeficiency virus (HIV).

"We achieved much better protective effects than have been achieved by pharmaceutical companies and by other academic groups using other approaches,"
said Gerald R. Crabtree.

Led by Howard Hughes Medical Institute investigator Gerald R. Crabtree, the researchers reported their findings in the October 29, 2004, issue of the journal Science. First author Jason Gestwicki and senior author Isabella Graef are both members of Crabtree's laboratory at Stanford University School of Medicine.

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