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Neurodegenerative basis of age-related cognitive decline
Open accessAbstract
OBJECTIVE: To assess the contribution of dementia-related neuropathologic lesions to age-related and disease-related change in cognitive function. METHODS: A total of 354 Catholic nuns, priests, and brothers had annual clinical evaluations for up to 13 years, died, and underwent brain autopsy. The clinical evaluations included detailed testing of cognitive function from which previously established composite measures of global cognition and specific cognitive functions were derived. As part of a uniform neuropathologic evaluation, the density of neurofibrillary tangles was summarized in a composite measure and the presence of Lewy bodies and gross and microscopic cerebral infarction was noted. RESULTS: During follow-up, rate of global cognitive decline was gradual at first and then more than quadrupled in the last 4 to 5 years of life consistent with the onset of progressive dementia. Neurofibrillary tangles, cerebral infarction, and neocortical Lewy bodies all contributed to gradual age-related cognitive decline and little age-related decline was evident in the absence of these lesions. Neurofibrillary tangles and neocortical Lewy bodies contributed to precipitous disease-related cognitive decline, but substantial disease-related decline was evident even in the absence of these lesions. CONCLUSION: Mild age-related decline in cognitive function is mainly due to the neuropathologic lesions traditionally associated with dementia.
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“Since the publication of the 2011 guidelines, data have continued to accumulate indicating that the cognitive decline in AD occurs continuously over a long period [6–8]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [7]
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“Even in extreme old age, the presence of many neocortical NFTs correlates with antemortem cognitive decline (105, 188-191).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [190]
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Metadata
- Authors
- Wilson, R. S., Leurgans, S. E., Boyle, P. A., Schneider, J. A., & Bennett, D. A.
- Affiliations
- Rush University Medical Center (US)
- Venue
- Neurology
- Published
- 2010-09-21
- Volume
- 75
- Issue
- 12
- Pages
- 1070-1078
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC2942064
- OpenAlex
- W2057852669
- Cited by
- 234
- References
- 30
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 12 · 2023: 15 · 2022: 15 · 2021: 32 · 2020: 9 · 2019: 12 · 2018: 11 · 2017: 13 · 2016: 10 · 2015: 12 · 2014: 13 · 2013: 20 · 2012: 26
- FWCI
- 12.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG015819, P30AG010161, R01AG034374)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- age-related cognitive decline, dementia, neurofibrillary tangles, Lewy bodies, cerebral infarction, neuropathology, cognitive function, progressive dementia, brain autopsy
- MeSH terms
- Age Factors, Aging, Brain, Cognition, Cognition Disorders, Dementia, Female, Humans, Longitudinal Studies, Male, Nerve Degeneration, Neuropsychological Tests, Lewy Bodies, Neurofibrillary Tangles, Disease Progression
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