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The Pathogenesis of Alzheimer Disease: An Alternative to the Amyloid Hypothesis

Open access
Terry, Robert D.·1996·Journal of Neuropathology and Experimental Neurology

Abstract

This paper attempts to put together in the form of a flow sheet (Fig. 1) the several known alterations, both chemical and structural, of brain tissue in Alzheimer disease, which ultimately result in dementia. While most investigators in the field believe strongly that amyloid deposition is at the core of the disease, this writer finds that a more coherent, and thus more satisfying, schema can be based on the centrality of cytoskeletal abnormality. Not only do all four identified genes interact one way or another with the cytoskeleton, but abnormality of the latter leads to alterations of the Golgi apparatus with effects on protein processing, and on axoplasmic flow such that one can expect loss of synapses and subsequent loss of neurons with consequent disconnection and loss of neurotransmitters. Dementia is the result.

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Metadata

Authors
Terry, R. D.
Venue
Journal of Neuropathology and Experimental Neurology
Published
1996-10
Volume
55
Issue
10
Pages
1023-1025
ISSN
0022-3069 (ISSN-L)
OpenAlex
W2057013121
Cited by
299
References
0
FWCI
7.13
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: The Pathogenesis of Alzheimer Disease: An Alternative to the Amyloid Hypothesis. https://app.cochat.ai/papers/10.1097/00005072-199610000-00001
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Terry, R. D. (1996). The Pathogenesis of Alzheimer Disease: An Alternative to the Amyloid Hypothesis. Journal of Neuropathology and Experimental Neurology. https://doi.org/10.1097/00005072-199610000-00001

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.