Regional Distribution of Neurofibrillary Tangles and Senile Plaques in the Cerebral Cortex of Elderly Patients: A Quantitative Evaluation of a One-Year Autopsy Population from a Geriatric Hospital
Abstract
Detailed analyses of the neuropathologic changes in the cerebral cortex of elderly individuals and Alzheimer's disease patients have demonstrated that certain components of the neocortical and hippocampal circuits are likely to be selectively vulnerable. Based on the distribution of neurofibrillary tangles (NFTs) and senile plaques, it has been proposed that a global corticocortical disconnection leads to the loss of integrated functions observed in Alzheimer's disease. In order to investigate the distribution of lesions associated with aging as well as with the earliest symptoms of senile dementia, we performed a quantitative neuropathologic evaluation of a large series of elderly patients representing the entire autopsy population for the year 1989 from a geriatric hospital. Among the 145 cases quantitatively assessed, there were 102 nondemented patients, 33 patients presenting clinically with globally intact intellectual function but early signs of impairment of specific cognitive functions, and 10 cases with senile dementia of the Alzheimer type. All of the cases had NFTs in layer II of the entorhinal cortex, regardless of their clinical diagnosis, and most cases had some NFTs in the CA1 field of the hippocampus. Severe pathologic changes within the inferior temporal neocortex were observed only in the demented cases. The extent of amyloid deposition was not correlated with the clinical diagnosis and seemed to be present in the neocortical areas earlier than in the hippocampal formation. Also, several cases contained NFTs without amyloid deposition, but amyloid never occurred without NFTs. These results suggest that involvement of certain structures within the hippocampal formation is a consistent feature of aging. Thus, involvement of the hippocampal formation may be a necessary, but not sufficient, condition for the clinical expression of dementia, which is likely to be more closely related to the progressive degeneration of select neuronal populations in the neocortex.
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A modest number of medial temporal lobe NFTs are universally present in subjects older than 70 years, even in persons who have intact cognition.
“a modest number of medial temporal lobe NFTs are universally present in subjects older than 70 years (33), even in persons who have intact cognition.”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [33]
We are aware of no reported case of truly intact cognition despite extremely severe AD pathologic changes (i.e. widespread neocortical NFTs) measured with quantitative pathologic analysis.
“We are aware of no reported case of truly intact cognition despite extremely severe AD pathologic changes (i.e. widespread neocortical NFTs) measured with quantitative pathologic analysis, although many persons with intact cognition have been assessed in autopsy series (33, 42, 54, 133, 142, 148, 151-166).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [33]
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Self-citation
- Authors
- Bouras, C., Hof, P. R., Giannakopoulos, P., Michel, J.-P., & Morrison, J. H.
- Affiliations
- University of Geneva (CH)
- Icahn School of Medicine at Mount Sinai (US)
- Venue
- Cerebral Cortex
- Publisher
- Oxford University Press (OUP)
- Published
- 1994
- Volume
- 4
- Issue
- 2
- Pages
- 138-150
- ISSN
- 1047-3211 (ISSN-L)
- 1460-2199
- OpenAlex
- W2018354461
- Cited by
- 280
- References
- 54
- Citations by year
- 2025: 8 · 2024: 6 · 2023: 7 · 2022: 5 · 2021: 3 · 2020: 4 · 2019: 25 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 8 · 2014: 12 · 2013: 10 · 2012: 13
- FWCI
- 9.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cerebral Cortex (publishedVersion)
- PubMed (publishedVersion)
- reroDoc Digital Library (submittedVersion)
- Funders
- National Institute on Aging (AG 05138, P50AG005138, AG-06647)
- 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
- neurofibrillary tangles, amyloid plaques, Alzheimer's disease, entorhinal cortex, hippocampal CA1, amyloid deposition, inferior temporal cortex, senile dementia, elderly patients
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Amyloid, Cerebral Cortex, Female, Geriatrics, Hippocampus, Hospitals, Special, Humans, Male, Neurofibrillary Tangles
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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