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The Amyloid Hypothesis of Cognitive Dysfunction

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Neuroinflammation

Part of the book series: Contemporary Neuroscience ((CNEURO))

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Abstract

The amyloid hypothesis of Alzheimer’s disease posits that a critical event in the pathogenesis of the disorder is the deposition of amyloid fibrils containing the amyloid β (Aβ) peptide derived from the processing of the amyloid precursor protein. This hypothesis is the subject of multiple reviews (1,2). The greatest support for this hypothesis derives from the genetics of familial Alzheimer’s disease, where all mutations known to cause Alzheimer’s disease share the capacity to increase production of the long form of the Aβ peptide (3). Still, acceptance of this hypothesis is far from universal (see ref. 4 and affiliated commentaries). Importantly, Alzheimer’s disease is, by definition, a cognitive disorder, requiring a patient to have a graded deterioration in multiple cognitive domains before a diagnosis can be made. In the absence of biopsy, pathological criteria for the disorder can only be met by autopsy. Thus, a critical question in the context of the amyloid hypothesis is the role of amyloid in the cognitive dysfunction of Alzheimer’s disease.

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Authors
  1. Dave Morgan
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  2. Marcia N. Gordon
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  1. Oxon Medica, South San Francisco, CA, USA

    Paul L. Wood

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Morgan, D., Gordon, M.N. (2003). The Amyloid Hypothesis of Cognitive Dysfunction. In: Wood, P.L. (eds) Neuroinflammation. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-297-5_14

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  • DOI: https://doi.org/10.1007/978-1-59259-297-5_14

  • Publisher Name: Humana Press, Totowa, NJ

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