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Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia
Xudong Zhang, Yuhao Xu, Hai Hu, Zhenhua Liao, Changli Lou, Xiang Zou. Molecular Brain, 2025-07-07
Topic: Brain proteins, microglia and lab models
We identified 218 m6A sites significantly associated with the three diseases, highlighting 3,430 associations between m6A sites and gene expression. Functional enrichment analysis revealed key pathways, including base excision repair and chemokine-mediated signaling. MR analysis identified causal relationships, such as NBL1 in epilepsy, TPGS2 in ischemic stroke, and SERINC2 in VaD. PPI analysis revealed interactions involving critical proteins like PARP1, MCL1, and CD40, underscoring their role in neuroinflammation and apoptosis. Our findings elucidate the genetic and epigenetic roles of m6A in epilepsy, ischemic stroke, and VaD, uncovering potential mechanisms by which m6A modulates gene and protein expression to influence disease outcomes. These insights highlight m6A as a promising biomarker and therapeutic target for neurological diseases.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Zhang, X., Xu, Y., Hu, H., Liao, Z., Lou, C., & Zou, X. (2025). Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia. Molecular Brain. https://doi.org/10.1186/s13041-025-01228-4
Vancouver
Zhang X, Xu Y, Hu H, Liao Z, Lou C, Zou X. Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia. Molecular Brain. 2025. doi:10.1186/s13041-025-01228-4. PMID: 40624693.
BibTeX
@article{zhang2025-40624693,
author = {Zhang, Xudong and Xu, Yuhao and Hu, Hai and Liao, Zhenhua and Lou, Changli and Zou, Xiang},
title = {{Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia}},
journal = {Molecular Brain},
year = {2025},
doi = {10.1186/s13041-025-01228-4},
pmid = {40624693},
url = {https://doi.org/10.1186/s13041-025-01228-4}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- We identified 218 m6A sites significantly associated with the three diseases, highlighting 3,430 associations between m6A sites and gene expression.
- Functional enrichment analysis revealed key pathways, including base excision repair and chemokine-mediated signaling.
- MR analysis identified causal relationships, such as NBL1 in epilepsy, TPGS2 in ischemic stroke, and SERINC2 in VaD.
- PPI analysis revealed interactions involving critical proteins like PARP1, MCL1, and CD40, underscoring their role in neuroinflammation and apoptosis.
- Our findings elucidate the genetic and epigenetic roles of m6A in epilepsy, ischemic stroke, and VaD, uncovering potential mechanisms by which m6A modulates gene and protein expression to influence disease outcomes.
Why it matters
This multi-omics analysis identified m6A sites and gene associations linked to epilepsy, ischemic stroke and vascular dementia, including causal relationships for specific genes. It highlights m6A as a possible biomarker and therapeutic target, but the work is at the level of genetic and epigenetic mechanisms, not a treatment.
Study details
- Evidence strengthLow
How this study scored 34/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 33 of the 96 points we could judge it on, which is 34 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular Brain) |
| Journal's citation record | 1 / 4 | Molecular Brain: journal h-index 99 (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 | 4 / 5 | 2025 — within 3 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 3 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 1 / 6 | Cited 0.8× 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 | 1 / 4 | Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | 1 / 3 | Fudan University: institution h-index 954 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40624693) |
| Free to read | 2 / 2 | Free to read |
| Points | 33 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 33 of the 96 points we could judge it on is 34 out of 100. |
| Total | 34 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13041-025-01228-4
- PubMed: 40624693
- Original source →
- Free full text: Molecular Brain →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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