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IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR
Xing Fan, Hao Wang, Cuiping Guo, Shijia Huang, Liye Xia, Zheng Zhou, Ran Tao, Mingzhe Li et al.. Alzheimer's research & therapy, 2025-09-30
Topic: Disease mechanisms in lab and animal studies
In the present study, we demonstrate that Interferon Regulatory Factor-1 (IRF-1), which is deficient in the brain of individuals with Alzheimer's disease (AD), negatively regulates the O-GlcNAcylation levels of GluN1 through transcriptional regulation of the human OGA gene. Furthermore, IRF-1 may influence trafficking of NMDARs, thereby affecting dendritic spine density and synaptic plasticity, and ultimately improving the learning and memory of 3xTg-AD mice. Our results indicate that IRF1 can improve the cognitive function of 3xTg-AD mice by regulating the O-GlcNAcylation of GluN1, offering evidence that IRF-1 could serve as a novel therapeutic target for treating synaptic dysfunction in Alzheimer's diseases.
Key findings
- In the present study, we demonstrate that Interferon Regulatory Factor-1 (IRF-1), which is deficient in the brain of individuals with Alzheimer's disease (AD), negatively regulates the O-GlcNAcylation levels of GluN1 through transcriptional regulation of the human OGA gene.
- Furthermore, IRF-1 may influence trafficking of NMDARs, thereby affecting dendritic spine density and synaptic plasticity, and ultimately improving the learning and memory of 3xTg-AD mice.
- Our results indicate that IRF1 can improve the cognitive function of 3xTg-AD mice by regulating the O-GlcNAcylation of GluN1, offering evidence that IRF-1 could serve as a novel therapeutic target for treating synaptic dysfunction in Alzheimer's diseases.
Study details
- Evidence strengthLow
How this study scored 43/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 24 of the 56 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Alzheimer's research & therapy) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41029886) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 24 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Fan, X., Wang, H., Guo, C., Huang, S., Xia, L., Zhou, Z., et al. (2025). IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR. Alzheimer's research & therapy. https://doi.org/10.1186/s13195-025-01857-w
Vancouver
Fan X, Wang H, Guo C, Huang S, Xia L, Zhou Z, et al. IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR. Alzheimer's research & therapy. 2025. doi:10.1186/s13195-025-01857-w. PMID: 41029886.
BibTeX
@article{fan2025-41029886,
author = {Fan, Xing and Wang, Hao and Guo, Cuiping and Huang, Shijia and Xia, Liye and Zhou, Zheng and Tao, Ran and Li, Mingzhe and others},
title = {{IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR}},
journal = {Alzheimer's research \& therapy},
year = {2025},
doi = {10.1186/s13195-025-01857-w},
pmid = {41029886},
url = {https://doi.org/10.1186/s13195-025-01857-w}
}
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