The DOI matches its Crossref record; 116 of the 116 references it cites were found in a registry or an index.
Pathologic Correlates of Nondemented Aging, Mild Cognitive Impairment, and Early-Stage Alzheimer's Disease
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 (2).”
From Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans (2011) · cites this paper as [2]
In the citing paper
“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]
Citations
Cites
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Self-citationMild Cognitive Impairment: Clinical Characterization and Outcome
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(2007) · Elsevier eBooks · doi:10.1016/b978-012373657-4/50008-8
Mistlberger, R. E., & Kent, B. A. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.734840494.793555104
An intergenerational analysis of cognitive impairment in healthy elders
Gupta, D., Vir, D., Sood, P., Kumar, H., & Panda, N. K. (2022) · Annals of Geriatric Education and Medical Sciences · doi:10.18231/j.agems.2022.005
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Abrahamson, E. E., Kofler, J. K., López, O. L., Cohen, A. D., Gogola, A., Aizenstein, H. J., Karikari, T. K., Mufson, E. J., Villemange, V., & Ikonomović, M. D. (2026) · Alzheimer s & Dementia · doi:10.1002/alz.71685
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Serotonergic Signaling Pathways that Suppress Amyloid Beta in Mouse Models of AD
Fisher, J. R. (2014) · Open Scholarship Institutional Repository (Washington University in St. Louis) · doi:10.7936/k74f1nr2
Metadata
- 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
- Published
- 2001
- Volume
- 17
- Issue
- 2
- Pages
- 101-118
- ISSN
- 0895-8696 (ISSN-L)
- 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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