ArticleMolecular psychiatry2024
Sex dimorphism controls dysbindin-related cognitive dysfunctions in mice and humans with the contribution of COMT.
Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Investigating the mechanisms of PhIP-induced colorectal cancer through network toxicology, machine learning, and molecular dynamics simulation.Translational cancer research · 2026Article
- Genetic Risk and Resilience for Schizophrenia Stratified by Perinatal Gene Expression Predict Adult Cognitive Performance.bioRxiv : the preprint server for biology · 2026Article
- Exact box-counting and temporal sampling algorithms for fractal dimension estimation with applications to animal behavior analysis.Results in engineering · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Cognitive dysfunctions are core-enduring symptoms of schizophrenia, with important sex-related differences. Genetic variants of the DTBPN1 gene associated with reduced dysbindin-1 protein (Dys) expression negatively impact cognitive functions in schizophrenia through a functional epistatic interaction with Catechol-O-methyltransferase (COMT). Dys is involved in the trafficking of dopaminergic receptors, crucial for prefrontal cortex (PFC) signaling regulation. Moreover, dopamine signaling is modulated by estrogens via inhibition of COMT expression. We hypothesized a sex dimorphism in Dys-related cognitive functions dependent on COMT and estrogen levels. Our multidisciplinary approach combined behavioral-molecular findings on genetically modified mice, human postmortem Dys expression data, and in vivo fMRI during a working memory task performance. We found cognitive impairments in male mice related to genetic variants characterized by reduced Dys protein expression (p
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