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61/100

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Inflammation and the immune system

Topic: Brain proteins, microglia and lab models

Plain-language summary

Pathological hallmarks of Alzheimer's disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia. Here, we report that activation of cyclic GMP-AMP synthase (cGAS) diminishes cognitive resilience by decreasing the neuronal transcriptional network of myocyte enhancer factor 2c (MEF2C) through type I interferon (IFN-I) signaling. Pathogenic tau activates cGAS and IFN-I responses in microglia, in part mediated by cytosolic leakage of mitochondrial DNA.

What this study adds

Evidence grade: Low

In mice with tauopathy, removing the Cgas gene reduced the microglial interferon response and preserved synapses and plasticity. This is animal research, so it does not yet show any treatment or prevention benefit in people.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

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

APA 7th

Udeochu, J. C., Amin, S., Huang, Y., Fan, L., Torres, E. R. S., Carling, G. K., et al. (2023). Tau activation of microglial cGAS-IFN reduces MEF2C-mediated cognitive resilience. Nature neuroscience. https://doi.org/10.1038/s41593-023-01315-6

Vancouver

Udeochu JC, Amin S, Huang Y, Fan L, Torres ERS, Carling GK, et al. Tau activation of microglial cGAS-IFN reduces MEF2C-mediated cognitive resilience. Nature neuroscience. 2023. doi:10.1038/s41593-023-01315-6. PMID: 37095396.

BibTeX

@article{udeochu2023-37095396,
  author  = {Udeochu, J. C. and Amin, S. and Huang, Y. and Fan, L. and Torres, E. R. S. and Carling, G. K. and Liu, B. and McGurran, H. and others},
  title   = {{Tau activation of microglial cGAS-IFN reduces MEF2C-mediated cognitive resilience}},
  journal = {Nature neuroscience},
  year    = {2023},
  doi     = {10.1038/s41593-023-01315-6},
  pmid    = {37095396},
  url     = {https://doi.org/10.1038/s41593-023-01315-6}
}

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.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

Here, we report that activation of cyclic GMP-AMP synthase (cGAS) diminishes cognitive resilience by decreasing the neuronal transcriptional network of myocyte enhancer factor 2c (MEF2C) through type I interferon (IFN-I) signaling.
Pathogenic tau activates cGAS and IFN-I responses in microglia, in part mediated by cytosolic leakage of mitochondrial DNA.
Genetic ablation of Cgas in mice with tauopathy diminished the microglial IFN-I response, preserved synapse integrity and plasticity and protected against cognitive impairment without affecting the pathogenic tau load. cGAS ablation increased, while activation of IFN-I decreased, the neuronal MEF2C expression network linked to cognitive resilience in AD.
Pharmacological inhibition of cGAS in mice with tauopathy enhanced the neuronal MEF2C transcriptional network and restored synaptic integrity, plasticity and memory, supporting the therapeutic potential of targeting the cGAS-IFN-MEF2C axis to improve resilience against AD-related pathological insults.

Why it matters

Study details

Evidence strengthLow

How this study scored 61/100

Published in a leading specialty 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	9 / 10	Tier 2 — leading specialty journal (Nature neuroscience)
Journal's citation record	4 / 4	Nature Neuroscience: journal h-index 593 (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	3 / 5	2023 — within 6 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	5 / 7	Cited 289 times (OpenAlex, 2026-10-10)
Citations per year	5 / 5	57.8 citations a year over 5 year(s) since 2023
Impact for its field and year	6 / 6	Cited 42.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 8 other studies in this library
Still being cited	4 / 4	Cited 264 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Li Gan: h-index 71 (OpenAlex, whole career)
Institution's track record	3 / 3	Massachusetts Institute of Technology: institution h-index 2,557 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 6 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 37095396)
Free to read	2 / 2	Free to read
Total	61 / 100	—

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