ArticleCell death discovery2026
Transcriptome analysis of the prefrontal cortex identifies inflammatory genes associated with cognitive impairment in a model of multiple sclerosis.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Type-I IFNs in EAE drive synaptic transcriptional responses in neurons and astrocytes in the brain.bioRxiv : the preprint server for biology · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Cognitive impairment (CI) is a hallmark of multiple sclerosis (MS). Despite its relevance, however, knowledge of the key steps involved in its pathogenesis remains incomplete. Consequently, predictive biomarkers and actionable therapeutic options to counteract CI in MS patients are not available. To identify changes associated with CI in MS, we performed transcriptomic analyses of the prefrontal cortex (PFC), a cortical region relevant for cognition, in the experimental autoimmune encephalomyelitis (EAE) mouse model. Our analyses highlighted the strong upregulation of inflammatory pathways in the PFC of EAE mice. Clustering of the top differentially expressed genes (DEGs) in the PFC identified a low (EAE-L) and a high (EAE-H) inflammation subgroup. Notably, enhanced inflammation in the EAE PFC caused increased changes in expression levels of MS-associated genes with relevance for CI. Cell Type-Specific Expression Analysis (CSEA) and morphological analyses indicated that, while EAE-L mice showed only microglia activation, EAEH mice also displayed the involvement of astrocytes, consistent with a more advanced stage of disease. Moreover, neuronal genes were only downregulated in the EAE-H PFC. Analysis of cognitive performance in pre-symptomatic EAE mice revealed that high expression of genes associated with the antigen presentation and the complement pathways was associated with CI. Moreover, expression of C1q complement proteins was increased in the cerebrospinal fluid of MS patients affected by CI. These findings indicate that inflammation in the PFC during EAE is associated with CI and identify a subset of inflammatory genes that may represent early markers and risk factors for functional PFC impairment and loss of cognitive performance in MS patients.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.