Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid β‐protein
DJ Selkoe - Annals of the New York Academy of Sciences, 2000 - Wiley Online Library
Annals of the New York Academy of Sciences, 2000•Wiley Online Library
A central challenge of research on Alzheimer's disease (AD) is to assemble the enormous
body of scientific observations about the disorder, some of them seemingly in conflict with
others, into a coherent and credible mechanism of pathogenesis. In this article, I attempt to
synthesize the disparate findings on AD into a unified sequence that essentially begins with
alterations in the production or clearance of the amyloid β‐protein (Aβ). Mounting evidence
from many laboratories supports an Aβ accumulation in limbic and association cortices as …
body of scientific observations about the disorder, some of them seemingly in conflict with
others, into a coherent and credible mechanism of pathogenesis. In this article, I attempt to
synthesize the disparate findings on AD into a unified sequence that essentially begins with
alterations in the production or clearance of the amyloid β‐protein (Aβ). Mounting evidence
from many laboratories supports an Aβ accumulation in limbic and association cortices as …
Abstract: A central challenge of research on Alzheimer's disease (AD) is to assemble the enormous body of scientific observations about the disorder, some of them seemingly in conflict with others, into a coherent and credible mechanism of pathogenesis. In this article, I attempt to synthesize the disparate findings on AD into a unified sequence that essentially begins with alterations in the production or clearance of the amyloid β‐protein (Aβ). Mounting evidence from many laboratories supports an Aβ accumulation in limbic and association cortices as the fundamental initiator of the disease, with attendant therapeutic implications.
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