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PMID: 12130773 Published · ppublish English Journal Article Review

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

Science (New York, N.Y.) ·Vol. 297 ·No. 5580 ·2002-07-19 ·Pages 353-6

Hardy J, Selkoe DJ

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.

MeSH Terms
Alzheimer Disease/drug therapy,etiology,genetics,pathology Amino Acid Sequence Amyloid beta-Peptides/metabolism Amyloid beta-Protein Precursor/chemistry,genetics,metabolism Animals Anti-Inflammatory Agents/therapeutic use Anticholesteremic Agents/therapeutic use Brain/metabolism,pathology Clinical Trials as Topic Humans Molecular Sequence Data Nerve Degeneration Neurofibrillary Tangles/metabolism,pathology Neurons/pathology Plaque, Amyloid/pathology Protease Inhibitors/therapeutic use tau Proteins/metabolism
Chemicals
Amyloid beta-Peptides Amyloid beta-Protein Precursor Anti-Inflammatory Agents Anticholesteremic Agents Protease Inhibitors tau Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hardy John
Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA.
Selkoe Dennis J
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
1095-9203
Published
2002-07-19
Pages
353-6
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Corrections
ErratumIn
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CommentIn
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