ArticleMolecular biology reports2025
Toll-like receptor 3 (TLR 3) polymorphisms predisposition to schizophrenia and bipolar disorder.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The association of the TLR3 SNP rs3775291 with schizophrenia is influenced by age.Frontiers in genetics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundToll-like receptor 3 (TLR 3) abnormal inflammatory response was described as one of the possible mechanisms implicated in the pathophysiology of schizophrenia (SCZ) and bipolar disorder (BD). However, the genetic predisposition of TLR 3 to these disorders' onset is still unclear. Therefore, the predisposition of TLR 3 functional variants L412F (rs3775291) and F459L (rs3775290) was examined in both disorders. METHODS AND
resultsIn a case-control study, 260 controls, 260 SCZ, and 130 BD patients were recruited and genotyped by PCR-RFLP. Genotypes, alleles, and haplotypes frequencies were compared between controls and patients based on clinical features. Statistical analyses were adjusted by gender and age and validated by Bonferroni correction. In the dominant model, our results showed significantly higher L412F AA + GA frequency in controls compared to BD patients (p
conclusionsThe present study suggests that L412F could be a protective genetic factor from BD onset. However, F459L could be a genetic risk factor for the paranoid subtype and a potential genetic predictor of SCZ negative symptoms treatment improvement.
Indexed as
Identifiers
41264056What 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.