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Demyelination in Vascular Dementia: Focus on Oligodendrocytes, Microglia, and Their Interaction
Ying Liu, Li J, Yan Zhao, Yuxiao Zheng, Jialin Cheng, Chuxin Zhang, Xin Lan, Jinhua Han et al.. Current Neuropharmacology, 2026-05-05
Topic: Brain proteins, microglia and lab models
Vascular dementia (VaD), a primary cognitive disorder caused by cerebrovascular pathology, features significant white matter damage from chronic cerebral hypoperfusion strongly correlated with cognitive decline. Myelin integrity disruption represents a core pathological foundation in VaD, with dysfunctional oligodendrocytes (OLs) and microglia (MG) forming a critical pathogenic nexus. OLs govern myelin formation and maintenance while MGs modulate myelination through cerebral microenvironment regulation. In the central nervous system, precise communication and synergistic interaction between cells are the basis for maintaining homeostasis and cognitive function. The complement system, cytokine network, and extracellular vesicles together form its core communication axis. The complement system is at the forefront of the rapid innate immune response, cytokines dynamically regulate the initiation and resolution of inflammation, as carriers of functional molecules between cells, extracellular vesicles target and deliver information of bioactive molecules, upgrading intercellular communication to an active and programmed network regulation system. The three work together to maintain the homeostasis of the neural microenvironment. Their dysregulation can lead to uncontrolled neuroinflammation and tissue damage, which is the core pathological link in diseases such as VaD. This review examines the interplay between OLs and MG in VaD demyelination, detailing their complex communication networks via the complement system (including C1q, C3, C5 fragments), key cytokines (TNF-α, IL-1β, IL-4, IL-10), and extracellular vesicle signaling. Notably, these pathways exhibit bidirectionality: moderate activation promotes repair mechanisms, whereas excessive responses exacerbate injury. Future research should elucidate the spatiotemporal dynamics of OLs-MG interactions and identify precise therapeutic targets to restore cellular equilibrium, thereby informing novel VaD intervention strategies.
Key findings
- Vascular dementia (VaD), a primary cognitive disorder caused by cerebrovascular pathology, features significant white matter damage from chronic cerebral hypoperfusion strongly correlated with cognitive decline.
Why it matters
This review discusses how damage to myelin and interactions between oligodendrocytes and microglia contribute to vascular dementia. It outlines mechanisms and possible communication pathways but reports no treatment tested in patients.
Study details
- Evidence strengthLow
How this study scored 30/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current Neuropharmacology) |
| Journal's citation record | 1 / 4 | Current Neuropharmacology: journal h-index 141 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 1 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.5 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 2 / 6 | Cited 2.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Xueqian Wang: h-index 13 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Beijing University of Chinese Medicine: institution h-index 298 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 42099154) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 30 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Liu, Y., Li, J., Zhao, Y., Zheng, Y., Cheng, J., Zhang, C., et al. (2026). Demyelination in Vascular Dementia: Focus on Oligodendrocytes, Microglia, and Their Interaction. Current Neuropharmacology. https://doi.org/10.2174/011570159x445971260216112740
Vancouver
Liu Y, Li J, Zhao Y, Zheng Y, Cheng J, Zhang C, et al. Demyelination in Vascular Dementia: Focus on Oligodendrocytes, Microglia, and Their Interaction. Current Neuropharmacology. 2026. doi:10.2174/011570159x445971260216112740. PMID: 42099154.
BibTeX
@article{liu2026-42099154,
author = {Liu, Ying and Li, J. and Zhao, Yan and Zheng, Yuxiao and Cheng, Jialin and Zhang, Chuxin and Lan, Xin and Han, Jinhua and others},
title = {{Demyelination in Vascular Dementia: Focus on Oligodendrocytes, Microglia, and Their Interaction}},
journal = {Current Neuropharmacology},
year = {2026},
doi = {10.2174/011570159x445971260216112740},
pmid = {42099154},
url = {https://doi.org/10.2174/011570159x445971260216112740}
}