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Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease
Roy ER, Wang B, Wan YW, Chiu G, Cole A, Yin Z, Propson NE, Xu Y et al.. The Journal of clinical investigation, 2020-04-01
Topic: Amyloid, tau and blood-test diagnosis
Type I interferon (IFN) is a key cytokine that curbs viral infection and cell malignancy. Previously, we demonstrated a potent IFN immunogenicity of nucleic acid-containing (NA-containing) amyloid fibrils in the periphery. Here, we investigated whether IFN is associated with β-amyloidosis inside the brain and contributes to neuropathology.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Roy, E. R., Wang, B., Wan, Y. W., Chiu, G., Cole, A., Yin, Z., et al. (2020). Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease. The Journal of clinical investigation. https://doi.org/10.1172/jci133737
Vancouver
Roy ER, Wang B, Wan YW, Chiu G, Cole A, Yin Z, et al. Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease. The Journal of clinical investigation. 2020. doi:10.1172/jci133737. PMID: 31917687.
BibTeX
@article{roy2020-31917687,
author = {Roy, E. R. and Wang, B. and Wan, Y. W. and Chiu, G. and Cole, A. and Yin, Z. and Propson, N. E. and Xu, Y. and others},
title = {{Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease}},
journal = {The Journal of clinical investigation},
year = {2020},
doi = {10.1172/jci133737},
pmid = {31917687},
url = {https://doi.org/10.1172/jci133737}
}
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.
Key findings
- Previously, we demonstrated a potent IFN immunogenicity of nucleic acid-containing (NA-containing) amyloid fibrils in the periphery.
- Here, we investigated whether IFN is associated with β-amyloidosis inside the brain and contributes to neuropathology.
- An IFN-stimulated gene (ISG) signature was detected in the brains of multiple murine Alzheimer disease (AD) models, a phenomenon also observed in WT mouse brain challenged with generic NA-containing amyloid fibrils.
- In vitro, microglia innately responded to NA-containing amyloid fibrils.
Why it matters
This study found a type I interferon-stimulated gene signature in the brains of multiple mouse models of Alzheimer's disease and in normal mouse brain challenged with amyloid fibrils, and reports that this response drives neuroinflammation and synapse loss. It is largely animal and in-vitro work and reports no treatment, cure or prevention for people.
Study details
- Evidence strengthLow
How this study scored 56/100
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 (The Journal of clinical investigation) |
| Journal's citation record | 4 / 4 | Journal of Clinical Investigation: journal h-index 706 (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 | 2 / 5 | 2020 — within 10 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 | 6 / 7 | Cited 558 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 69.8 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 5 / 6 | Cited 21.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 12 other studies in this library |
| Still being cited | 4 / 4 | Cited 296 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Wei Cao: h-index 37 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 8 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31917687) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 56 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1172/jci133737
- PubMed: 31917687
- Original source →
- Free full text: Journal of Clinical Investigation →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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