Cited by 358Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Neuritic pathology and dementia in alzheimer's disease

McKee, A. C., Kosik, K. S., Kowall, N. W.·1991·Annals of Neurology

Abstract

Previous studies of Alzheimer's disease (AD) have correlated the severity of dementia with either the number of senile plaques or neurofibrillary tangles. We used antibodies raised against amyloid β/A4 protein of senile plaque cores and tau protein as well as thioflavine S and the Campbell‐Switzer modification of the Hicks silver method to examine the hippocampal formation and five neocortical regions from 22 nondemented elderly control subjects and 34 demented patients with cerebral senile plaques and neurofibrillary tangles, without complicating disease processes. Ten control subjects (46%) had no β/A4 protein deposition. Twelve control subjects (54%) had widespread β/A4 protein deposition but no neocortical neuritic pathology. Of the 34 patients with AD‐type changes, 27 (79%) had widespread senile plaques and neurofibrillary tangles, while 7 (21%) had neocortical senile plaques with few neurofibrillary tangles. All demented patients had widespread β/A4 protein deposition and neocortical tau‐immunoreactive, Hicks silver‐positive dystrophic neurites. The neurites were found both free in the neuropil as well as surrounding senile plaques. Quantitative analysis showed that dystrophic neurites were significantly increased in patients with AD compared with control subjects and the number of dystrophic neurites and neurofibrillary tangles correlated with the clinical severity of dementia. Widespread cerebral β/A4 protein deposition may be necessary but by itself is insufficient for the development of dementia in AD.

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Crossref · 10.1002/ana.410300206

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  • Numerous studies have documented a strong link between neocortical NFTs and cognitive loss.

    “On the other hand, numerous studies have documented a strong link between neocortical NFTs and cognitive loss[26, 46, 48, 97, 123, 160, 169].”

    From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [97]

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Authors
McKee, A. C., Kosik, K. S., & Kowall, N. W.
Affiliations
  • Harvard University (US)
  • Brigham and Women's Hospital (US)
Corresponding author
McKee, A. C.
Venue
Annals of Neurology
Publisher
Wiley
Published
1991-08
Volume
30
Issue
2
Pages
156-165
ISSN
  • 0364-5134 (ISSN-L)
  • 1531-8249
OpenAlex
W2065327124
Cited by
358
References
44
Citations by year
2026: 1 · 2025: 3 · 2024: 1 · 2023: 3 · 2022: 5 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 5 · 2014: 5 · 2013: 4 · 2012: 8
FWCI
19.19
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5k08ns001368-02, 5r01ag006601-13)
  • National Institute on Aging (AG 06601, P50AG005134, AG 05134)
  • National Institute of Neurological Disorders and Stroke (NS 01368-01)
Topics
  • Health Sciences › Medicine › Physiology › 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, dementia severity, amyloid plaques, neurofibrillary tangles, tau protein, dystrophic neurites, hippocampus, neocortex, thioflavine S
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Antibodies, Monoclonal, Cerebral Cortex, Hippocampus, Humans, Immunohistochemistry, Microtubule-Associated Proteins, Middle Aged, Nerve Tissue Proteins, Neurofibrils, Reference Values, Amyloid beta-Peptides, tau Proteins

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