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Cited by 130Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 47 of the 49 references it cites were found in a registry or an index.

A plasticity-based theory of the pathogenesis of Alzheimer's disease.

MESULAM, M.‐MARSEL·2000·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2000.tb05559.x
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Abstract

Amyloid plaques (APs) and neurofibrillary tangles (NFTs) are the two diagnostic markers of Alzheimer's disease (AD). The neuropsychological features of AD are closely correlated with the distribution of the NFTs and therefore favor a disease process revolving around neurofibrillary degeneration. The genetics, however, favor a disease process revolving around the APs, principally because mutations in the amyloid precursor protein (A beta PP) are sufficient to cause AD. The inability to reconcile these two aspects of AD has prevented the formulation of a unified theory of pathogenesis. It is interesting to note that all genetic causes and risk factors of AD can increase the physiological burden of neuroplasticity. My hypothesis is that the resultant intensification of the plasticity burden leads to an initially adaptive upregulation of tau phosphorylation and A beta PP turnover, to the subsequent formation of NFTs and APs as independent consequences of excessive plasticity-related cellular activity, and to the eventual loss of neurons, dendrites, and synapses as the ultimate expression of plasticity failure. The two pathological markers of AD are therefore independent manifestations of a more fundamental process through which the many different genotypes of AD trigger an identical clinical and neuropathological phenotype.

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Research works printed but not linked: 2

  1. Masliah E. et al.1995. Abnormal synaptic regeneration in hAPP695 transgenic and APOE knockout mice.InResearch Advances in Alzheimer's Disease and Related Disorders. K. Iqbal J. A. Mortimer B. Winbladet al. Eds.: 406–414. John Wiley and Sons. New York.
  2. Trojanowski J.Q., 1993, From pathological marker to potential mediator of neuronal dysfunction and degeneration in Alzheimer's disease, Clin. Neurosci., 1, 184

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Metadata

Authors
MESULAM, M. ‐.
Affiliations
Northwestern University (US)
Corresponding author
MESULAM, M.‐MARSEL
ORCID
MESULAM, M.‐MARSEL
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2000-12
Volume
924
Issue
1
Pages
42-52
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2000.tb05559.x
OpenAlex
W2061837100
Cited by
130
References
49
Citations by year
2025: 2 · 2024: 5 · 2023: 7 · 2021: 6 · 2020: 3 · 2019: 8 · 2018: 4 · 2017: 4 · 2016: 7 · 2015: 5 · 2014: 7 · 2013: 8 · 2012: 10
FWCI
0.74
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1881 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns020285-15)
  • National Institute on Aging (AG13854, P30AG013854)
  • National Institute of Neurological Disorders and Stroke (NS 20285)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease pathogenesis, neuroplasticity, amyloid plaques, neurofibrillary tangles, tau phosphorylation, amyloid precursor protein, synaptic loss, neurodegeneration, genotype-phenotype correlation
MeSH terms
Alzheimer Disease, Brain, Humans, Neuronal Plasticity

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