Dynamic changes in myelin aberrations and oligodendrocyte generation in chronic amyloidosis in mice and men
Open accessAbstract
Myelin loss is frequently observed in human Alzheimer's disease (AD) and may constitute to AD‐related cognitive decline. A potential source to repair myelin defects are the oligodendrocyte progenitor cells (OPCs) present in an adult brain. However, until now, little is known about the reaction of these cells toward amyloid plaque deposition neither in human AD patients nor in the appropriate mouse models. Therefore, we analyzed cells of the oligodendrocyte lineage in a mouse model with chronic plaque deposition (APPPS1 mice) and samples from human patients. In APPPS1 mice defects in myelin integrity and myelin amount were prevalent at 6 months of age but normalized to control levels in 9‐month‐old mice. Concomitantly, we observed an increase in the proliferation and differentiation of OPCs in the APPPS1 mice at this specific time window (6–8 months) implying that improvements in myelin aberrations may result from repair mechanisms mediated by OPCs. However, while we observed a higher number of cells of the oligodendrocyte lineage (Olig2+ cells) in APPPS1 mice, OLIG2+ cells were decreased in number in postmortem human AD cortex. Our data demonstrate that oligodendrocyte progenitors specifically react to amyloid plaque deposition in an AD‐related mouse model as well as in human AD pathology, although with distinct outcomes. Strikingly, possible repair mechanisms from newly generated oligodendrocytes are evident in APPPS1 mice, whereas a similar reaction of oligodendrocyte progenitors seems to be strongly limited in final stages of human AD pathology. © 2012 Wiley Periodicals, Inc.
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Nearly all studies of oligodendrocytes and myelin in amyloid mouse models of AD have focused on the effect of amyloid plaques and Aβ on oligodendrocytes and myelin, partially describing secondary demyelination or hypomyelination.
“Nearly all have focused on the effect of amyloid plaques and Aβ on oligodendrocytes and myelin, partially describing secondary demyelination or hypomyelination.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [43]
The Introduction (p. 6) says prior analyses of myelin integrity mainly used the 3xTg AD mouse model, and the paper reports focal demyelination around plaques in APPPS1 mice (p. 11). It does not establish that nearly all earlier studies focused on plaques and Aβ or characterized the changes as secondary demyelination or hypomyelination. The Discussion (p. 16) also notes that myelin abnormalities in 3xTg mice were observed before plaques became visible. (LLM, conf=0.81)
Experimental — accuracy not yet measuredOnly a few studies have experimentally investigated oligodendrocytes and myelin in amyloid mouse models of AD.
“Only a few studies have experimentally investigated oligodendrocytes and myelin in amyloid mouse models of AD20,21,41–43.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [43]
Studies in AD transgenic mouse models show defects in myelin integrity.
“studies in AD transgenic mouse models show defects in myelin integrity [70, 71].”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [71]
Analysis of human post-mortem brain tissue suggests an age-related reduction in myelin repair capacity associated with AD pathogenesis.
“analysis of human post-mortem brain tissue suggests an age-related reduction in myelin repair capacity associated with AD pathogenesis [71].”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [71]
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References 62 · Cited by 219
Research works printed but not linked: 1
- Peters A, Moss MB, Sethares C. 2000. Effects of aging on myelinated nerve fibers in monkey primary visual cortex. Journal of Comparative Neurology 419(3): 364-76.
- Authors
- Behrendt, G., Baer, K., Buffo, A., Curtis, M. A., Faull, R. L., Rees, M. I., Götz, M., & Dimou, L.
- Affiliations
- Physiologisches Institut (DE)
- Swansea University (GB)
- Neuroscience Institute Cavalieri Ottolenghi (IT)
- University of Auckland (NZ)
- Corresponding author
- Dimou, Leda
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2012-10-22
- Volume
- 61
- Issue
- 2
- Pages
- 273-286
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2005950079
- Cited by
- 219
- References
- 62
- Citations by year
- 2026: 12 · 2025: 24 · 2024: 22 · 2023: 30 · 2022: 22 · 2021: 17 · 2020: 24 · 2019: 13 · 2018: 14 · 2017: 9 · 2016: 10 · 2015: 10 · 2014: 6 · 2013: 6
- FWCI
- 2.37
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Funders
- National Institute for Social Care and Health Research
- Neurological Foundation of New Zealand
- Deutsche Forschungsgemeinschaft (SFB 870, SFB 596)
- Health Research Council of New Zealand
- Graduate School of Systemic Neurosciences
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, demyelination, oligodendrocyte precursor cells, oligodendrocyte lineage, amyloid plaques, APP/PS1 mice, remyelination, Olig2, oligodendrocyte differentiation, myelin integrity
- MeSH terms
- Oligodendrocyte Transcription Factor 2, Adult, Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Amyloidosis, Animals, Brain, Cell Differentiation, Disease Models, Animal, Female, Gene Expression Regulation, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Middle Aged, Myelin Sheath, Nerve Tissue Proteins, Oligodendroglia, Postmortem Changes, Amyloid beta-Protein Precursor, Nonlinear Dynamics, Cell Proliferation, Mice, Basic Helix-Loop-Helix Proteins, Presenilin-1
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