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Cited by 66Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Myelin in Alzheimer’s disease: culprit or bystander?

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Maitre, Michel, Jeltsch-David, Hélène, Okechukwu, Nwife Getrude, Klein, Christian, Patte-Mensah, Christine, Mensah-Nyagan, Ayikoe-Guy·2023·Acta Neuropathologica Communications
DOI 10.1186/s40478-023-01554-5PMC PMC10067200
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Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder with neuronal and synaptic losses due to the accumulation of toxic amyloid β (Αβ) peptide oligomers, plaques, and tangles containing tau (tubulin-associated unit) protein. While familial AD is caused by specific mutations, the sporadic disease is more common and appears to result from a complex chronic brain neuroinflammation with mitochondriopathies, inducing free radicals’ accumulation. In aged brain, mutations in DNA and several unfolded proteins participate in a chronic amyloidosis response with a toxic effect on myelin sheath and axons, leading to cognitive deficits and dementia. Αβ peptides are the most frequent form of toxic amyloid oligomers. Accumulations of misfolded proteins during several years alters different metabolic mechanisms, induce chronic inflammatory and immune responses with toxic consequences on neuronal cells. Myelin composition and architecture may appear to be an early target for the toxic activity of Aβ peptides and others hydrophobic misfolded proteins. In this work, we describe the possible role of early myelin alterations in the genesis of neuronal alterations and the onset of symptomatology. We propose that some pathophysiological and clinical forms of the disease may arise from structural and metabolic disorders in the processes of myelination/demyelination of brain regions where the accumulation of non-functional toxic proteins is important. In these forms, the primacy of the deleterious role of amyloid peptides would be a matter of questioning and the initiating role of neuropathology would be primarily the fact of dysmyelination.

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  • Previous studies have shown that the lipids that were or tended to be decreased in PLCG2 KO mice (cerebrosides, sulfatides and plasmalogens) have been also reported to be decreased early in AD.

    “Notably, previous studies have shown that the lipids that were or tended to be decreased in PLCG2 KO mice (cerebrosides, sulfatides and plasmalogens) have been also reported to be decreased early in AD (39–41).”

    From Multi-omics analyses reveal novel effects of PLCγ2 deficiency in the mouse brain (2023) · cites this paper as [41]

    The section “Looking for myelin components in biological fluids” reports reduced cerebroside and sulfatide in AD brains and says these lipids are altered long before tau deposits. Our copy does not report an early decrease in plasmalogens, so it supports only two of the three lipids attributed to this source. It also does not address the citing authors’ PLCG2 KO mouse results. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Maitre, M., Jeltsch-David, H., Okechukwu, N. G., Klein, C., Patte-Mensah, C., & Mensah-Nyagan, A.-G.
Affiliations
Inserm (FR)
ORCID
Venue
Acta Neuropathologica Communications
Publisher
Springer Science and Business Media LLC
Published
2023-03-31
Volume
11
Issue
1
Pages
56-56
ISSN
2051-5960 (ISSN-L)
DOI
10.1186/s40478-023-01554-5
PMC
PMC10067200
OpenAlex
W4362470031
Cited by
66
References
29
Citations by year
2026: 17 · 2025: 22 · 2024: 20 · 2023: 7
FWCI
2.35
Type
journal article
Language
en
Open access
Licence
Locations
  • Acta Neuropathologica Communications (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Inserm Transfert (Inserm Transfert)
  • Université de Strasbourg (Université de Strasbourg)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, myelin, amyloid-beta, tau protein, neuroinflammation, myelination, demyelination, axonal injury, protein misfolding, mitochondrial dysfunction, free radicals, cognitive impairment, dementia
MeSH terms
Aged, Alzheimer Disease, Axons, Humans, Myelin Sheath, Neurons, Amyloid beta-Peptides

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