The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.
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.
Hardy
John
J
Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA.
Selkoe
Dennis J
DJ
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D000595:Amino Acid Sequence; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002986:Clinical Trials as Topic; D006801:Humans; D008969:Molecular Sequence Data; D009410:Nerve Degeneration; D016874:Neurofibrillary Tangles / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000473:pathology; D058225:Plaque, Amyloid / Q000473:pathology; D011480:Protease Inhibitors / Q000627:therapeutic use; D016875:tau Proteins / Q000378:metabolism
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D000893:Anti-Inflammatory Agents; D000924:Anticholesteremic Agents; D011480:Protease Inhibitors; D016875:tau Proteins