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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Vascular contributions

Topic: Brain proteins, microglia and lab models

variants) was not associated with small vessel stroke (odds ratio [OR], 1.02 [95% CI, 0.95-1.10]), magnetic resonance imaging-confirmed lacunar stroke (OR, 0.95, [95% CI, 0.81-1.11]), nonlobar intracerebral hemorrhage (OR, 1.04 [95% CI, 0.72-1.50]), or vascular dementia (OR, 1.09 [95% CI, 0.95-1.25]). Similarly, we found no significant association with cSVD imaging biomarkers or pathology-defined arteriolosclerosis. As expected, genetically downregulated IL-6 signaling was associated with lower odds of large artery stroke (OR, 0.79 [95% CI, 0.74-0.84]) and carotid plaque (OR, 0.88 [95% CI, 0.83-0.94]). Results were consistent across sensitivity analyses and when using the rs2228145 missense variant to proxy IL-6 signaling downregulation. Unlike atherosclerotic traits, genetically proxied IL-6 signaling downregulation is not associated with clinical, imaging, or pathological manifestations of arteriolosclerotic cSVD. These genetic findings suggest that targeting IL-6 signaling is unlikely to yield effects on cSVD prevention comparable with those expected for atherosclerotic disease.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Tchuisseu‐Kwangoua, L. A., Omarov, M., Shatunov, A., Markus, H. S., Tatuene, J. K., & Georgakis, M. K. (2025). Genetic Downregulation of Interleukin‐6 Signaling and Arteriolosclerotic Cerebral Small Vessel Disease: A Drug Target Mendelian Randomization Analysis. Journal of the American Heart Association. https://doi.org/10.1161/jaha.124.041814

Vancouver

Tchuisseu‐Kwangoua LA, Omarov M, Shatunov A, Markus HS, Tatuene JK, Georgakis MK. Genetic Downregulation of Interleukin‐6 Signaling and Arteriolosclerotic Cerebral Small Vessel Disease: A Drug Target Mendelian Randomization Analysis. Journal of the American Heart Association. 2025. doi:10.1161/jaha.124.041814. PMID: 41182006.

BibTeX

@article{tchuisseukwangoua2025-41182006,
  author  = {Tchuisseu‐Kwangoua, Larissa Ange and Omarov, Murad and Shatunov, Aleksey and Markus, Hugh Stephen and Tatuene, Joseph Kamtchum and Georgakis, Marios K.},
  title   = {{Genetic Downregulation of Interleukin‐6 Signaling and Arteriolosclerotic Cerebral Small Vessel Disease: A Drug Target Mendelian Randomization Analysis}},
  journal = {Journal of the American Heart Association},
  year    = {2025},
  doi     = {10.1161/jaha.124.041814},
  pmid    = {41182006},
  url     = {https://doi.org/10.1161/jaha.124.041814}
}

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Key findings

variants) was not associated with small vessel stroke (odds ratio [OR], 1.02 [95% CI, 0.95-1.10]), magnetic resonance imaging-confirmed lacunar stroke (OR, 0.95, [95% CI, 0.81-1.11]), nonlobar intracerebral hemorrhage (OR, 1.04 [95% CI, 0.72-1.50]), or vascular dementia (OR, 1.09 [95% CI, 0.95-1.25]).
Similarly, we found no significant association with cSVD imaging biomarkers or pathology-defined arteriolosclerosis.
As expected, genetically downregulated IL-6 signaling was associated with lower odds of large artery stroke (OR, 0.79 [95% CI, 0.74-0.84]) and carotid plaque (OR, 0.88 [95% CI, 0.83-0.94]).
Results were consistent across sensitivity analyses and when using the rs2228145 missense variant to proxy IL-6 signaling downregulation.
Unlike atherosclerotic traits, genetically proxied IL-6 signaling downregulation is not associated with clinical, imaging, or pathological manifestations of arteriolosclerotic cSVD.

Why it matters

This genetic analysis found that downregulating interleukin-6 signaling was not associated with small vessel stroke, lacunar stroke, brain hemorrhage, vascular dementia, or small vessel disease markers. The authors conclude that targeting IL-6 signaling is unlikely to prevent this type of small vessel disease.

Study details

Evidence strengthLow

How this study scored 41/100

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.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of the American Heart Association)
Journal's citation record	2 / 4	Journal of the American Heart Association: journal h-index 200 (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	2 / 6	Cited 1.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	1 / 6	Cited by 1 other studies in this library
Still being cited	1 / 4	Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Marios K. Georgakis: h-index 48 (OpenAlex, whole career)
Institution's track record	3 / 3	Broad Institute: institution h-index 2,541 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 7 institution(s) in 4 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 41182006)
Free to read	2 / 2	Free to read
Total	41 / 100	—

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