Decreased Oligodendrocyte Nuclear Diameter in Alzheimer's Disease and Lewy Body Dementia
Open accessAbstract
To better understand the pathogenesis of dementia, it is important to understand histopathologic changes in neurodegenerative diseases because they might highlight key aspects of the degenerative process. In this study, the nuclear diameter of neurons and oligodendrocytes in selected temporal lobe areas were determined in autopsy tissue sections from patients with Alzheimer's disease (AD), Lewy body dementia (LBD) and controls. Our morphometric studies targeted neurons in the CA4 region of the pyramidal cell layer of the hippocampus, neurons in the granular layer of the dentate gyrus and oligodendrocytes in parahippocampal white matter. Mean neuronal nuclear diameters were not different among the studied groups. However, our studies revealed a statistically significant reduction of mean oligodendrocyte nuclear diameter in AD and LBD relative to controls. The reduction of the mean nucleus diameter of oligodendrocytes in LBD was independent of the presence of associated AD pathology in LBD. These findings for the first time identify decreased oligodendrocyte nucleus diameter as a morphologic feature of AD and LBD and may lead to a better understanding of the role of oligodendrocytes in AD and LBD pathogenesis.
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AD pathology in the white matter includes loss of myelin and a decrease in oligodendrocyte proteins.
“AD pathology in the white matter includes the loss of myelin and a decrease in oligodendrocyte proteins [62–68].”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [65]
The Discussion (page not available in our copy) describes myelin loss in AD white matter, citing a prior study, and the paper reports smaller oligodendrocyte nuclei in AD. It does not report a decrease in oligodendrocyte proteins; nuclear diameter is not a protein measurement. (LLM, conf=0.88)
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White matter changes in Alzheimer’s disease: A focus on myelin and oligodendrocytes
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- Authors
- Gagyi, E., Kormos, B., Castellanos, K. J., Valyi‐Nagy, K., Korneff, D., LoPresti, P., Woltjer, R., & Valyi‐Nagy, T.
- Affiliations
- University of Illinois Chicago (US)
- Oregon Health & Science University (US)
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2012-04-12
- Volume
- 22
- Issue
- 6
- Pages
- 803-810
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC4181948
- OpenAlex
- W2103289155
- Cited by
- 38
- References
- 4
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 3 · 2023: 6 · 2022: 3 · 2021: 4 · 2020: 3 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 2
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Rosztoczy Foundation
- National Institute on Aging (P30AG008017)
- 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 with Lewy bodies, neurodegeneration, dementia pathogenesis, histopathology
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Cell Nucleus, Female, Humans, Male, Oligodendroglia, Lewy Body Disease
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