ArticleItalian journal of pediatrics2025
Identifying potential drug targets for tourette syndrome: a Mendelian randomization study based on druggable genes.
Article in Italian journal of pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTourette syndrome (TS) is a chronic neurodevelopmental disorder with childhood onset characterized by multiple motor tics and at least one vocal tic, with symptoms persisting for over one year. Its exact etiology remains unclear. Identifying novel therapeutic targets for TS is critically important.
methodsWe utilized cis-expression quantitative trait loci (cis-eQTLs) of druggable genes obtained from the eQTLGen Consortium and genome-wide association study (GWAS) data for TS from the Psychiatric Genomics Consortium as the outcome to simulate the effects of pharmacological interventions on TS via Mendelian randomization (MR). Colocalization analyses were then conducted to validate the findings. To further corroborate these results, we investigated the role of DNA methylation in mediating the relationship between druggable gene expression and TS.
resultsThe expression of seven druggable genes was significantly associated with TS susceptibility (FDR < 0.05). TS susceptibility and three key genes (RET, CAPNS1, and LAMA5) were likely to share a causal variant. Further DNA methylation analysis identified seven critical methylation sites (cg02605258, cg02907768, cg06026331, cg09831553, cg12382846, cg19674797, and cg20752878), which indirectly influence TS development by regulating LAMA5 gene expression.
conclusionLAMA5 is the most promising potential drug target for mitigating TS risk. Our study not only reveals potential therapeutic targets but also provides directions for future TS drug development.
Indexed as
Identifiers
What Socratic 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 Socratic graph.