Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease

Morris, John C.; Price, Joseph L.

doi:10.1385/jmn:17:2:101

Cited by 513Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease

Morris, John C., Price, Joseph L.·2001·Journal of Molecular Neuroscience

DOI 10.1385/jmn:17:2:101

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Abstract

The results of studies from the Washington University Alzheimer Disease (AD) Research Center and those from other centers and investigators regarding the neuropathologic correlates of normal aging and early-stage AD are reviewed. We conclude that widespread amyloid plaques in the neocortex best distinguishes very early stage AD, including "MCI" stage, and preclinical stages, from healthy brain aging. Other AD lesions, including increased formation of neurofibrillary tangles and neuronal degeneration appear to result from the amyloid-initiated pathologic process, although they may have a more immediate effect on expression and severity of dementia. These data provide strong support for anti-amyloid intervention as a preventive therapy for AD. It is now critical to develop methods to detect preclinical AD during life.

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Aβ can accumulate as toxic plaques and soluble oligomers in the brains of individuals with AD a decade or more before the initial symptoms are identified.
“Aβ can accumulate as toxic plaques and soluble oligomers in the brains of individuals with AD a decade or more before the initial symptoms are identified (2).”
From Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans (2011) · cites this paper as [2]
Aβ accumulation and deposition in the AD brain can begin 10 y before the appearance of the first symptoms.
“Aβ accumulation and deposition in the AD brain can begin 10 y before the appearance of the first symptoms (2, 32).”
From Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans (2011) · cites this paper as [2]

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Authors: Morris, J. C., & Price, J. L.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Morris, John C.
ORCID: Morris, John C.
Venue: Journal of Molecular Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2001
Volume: 17
Issue: 2
Pages: 101-118
ISSN: 0895-8696 (ISSN-L)
DOI: 10.1385/jmn:17:2:101
OpenAlex: W2065592408
Cited by: 513
References: 116
Citations by year: 2026: 3 · 2025: 2 · 2024: 11 · 2023: 10 · 2022: 18 · 2021: 21 · 2020: 14 · 2019: 15 · 2018: 13 · 2017: 13 · 2016: 25 · 2015: 34 · 2014: 29 · 2013: 22 · 2012: 38
FWCI: 10.36
Type: journal article
Language: en
Open access: closed
Locations: Journal of Molecular Neuroscience (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (AG03991, AG 05681, P50AG005681, P01AG003991)
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, mild cognitive impairment, normal brain aging, amyloid plaques, neurofibrillary tangles, neurodegeneration, preclinical Alzheimer's disease, anti-amyloid therapy, dementia, neuropathology
MeSH terms: Aged, Aging, Alzheimer Disease, Cerebral Cortex, Diagnosis, Differential, Humans, Middle Aged, Neurofibrillary Tangles, Disease Progression, Plaque, Amyloid

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Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease

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