Published in Blood Weekly, May 3rd, 1999
The fibrillar aggregates making up the amyloid plaque that characterizes Alzheimer's disease may be formed by cells in an attempt to isolate proposed "toxic intermediates," the hypothesis proposes. If this is so, then new drugs being designed to inhibit fibril formation could do more harm than good by allowing the toxin to accumulate in the brain.
The hypothesis is the brainchild of Peter T. Lansbury of Harvard Medical School, Boston, Massachusetts. In the scenario he proposes, normal protein folding proceeds without...
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Source: Blood Weekly (1999-05-03)
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