Abstract
The amyloid cascade hypothesis, which posits that amyloid-β accumulation is the key event in Alzheimer disease neurodegeneration, has dominated the field for 20 years. Recent findings, however, show that neuronal-injury biomarkers are independent of amyloid-β, calling for reconsideration of the pathological cascade and assessment of alternative therapeutic strategies.
MeSH terms
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Alzheimer Disease / complications
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology*
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Amyloid beta-Peptides / metabolism*
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Amyloidosis / metabolism
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Brain / metabolism
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Brain / pathology*
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Brain Injuries / etiology
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Brain Injuries / metabolism
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Cognition Disorders / etiology
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Cognition Disorders / metabolism
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Cognition Disorders / pathology
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Humans