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

Science (New York, N.Y.)

metabolism, tau Proteins, therapeutic use, Protease Inhibitors, pathology, Plaque, Amyloid, Neurons, Neurofibrillary Tangles, Nerve Degeneration, Molecular Sequence Data, Humans, Clinical Trials as Topic, Brain, Anticholesteremic Agents, Anti-Inflammatory Agents, Animals, genetics, chemistry, Amyloid beta-Protein Precursor, Amyloid beta-Peptides, Amino Acid Sequence, etiology, drug therapy, Alzheimer Disease

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      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.

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