The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.

John Hardy; Dennis J Selkoe (Profiled Authors: Selkoe, Dennis J; Hardy, John)

Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA.
Science (New York, N.Y.) 2002;297(5580):353-6.

PubMed

Abstract

It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.

Scientific Context

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