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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

Science · 2002 · Vol. 297(5580) · pp. 353–356
John HardyDennis J. Selkoe

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.

Alzheimer's disease research and treatmentsPrion Diseases and Protein MisfoldingCholinesterase and Neurodegenerative DiseasesNeurodegenerationPathogenesisAmyloid (mycology)DiseaseNeuroscienceBiochemistry of Alzheimer's diseaseAlzheimer's diseaseAmyloid betaAmyloid βMedicine

MeSH terms

Alzheimer DiseaseAmino Acid SequenceAnimalsAnti-Inflammatory AgentsAnticholesteremic AgentsBrainClinical Trials as TopicHumansMolecular Sequence DataNerve DegenerationNeuronsProtease InhibitorsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorNeurofibrillary Tangles
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