ArticleMolecular psychiatry2026
Cadherin 11 regulates presynaptic vesicle trafficking and neuronal activity in autism-related brain circuit.
Article in Molecular psychiatry, 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.
- Targeting C/EBPβ/ Calbindin 1 pathway bolsters the neural resilience to tau pathology and improves tau-impaired episodic memory.Molecular psychiatry · 2026Article
- miR-205a mediated suppression of CDH11 disrupts Wnt/β-catenin signaling and impairs chondrocyte differentiation.Cell death discovery · 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
8 authors.
Funding
Abstract
The molecular etiology of numerous risk genes for autism spectrum disorder (ASD), including Cadherin 11 (CDH11), remains elusive. We investigated the role of CDH11 in the development of ASD-related behaviors using gene-deficient mice. CDH11 is enriched at synapses in glutamatergic neurons of the anterior cingulate cortex (ACC), which project to the dorsal striatum, nucleus accumbens, and the basolateral amygdala. Developmental ablation of Cdh11 in these neurons led to increased self-grooming, reduced sociability, and decreased neuronal activity in the ACC. Chemogenetic inhibition of ACC glutamatergic neurons recapitulates the over-grooming phenotype, while activation of these neurons mitigates self-grooming in Cdh11-deficient mice. Moreover, targeted expression of CDH11 in the ACC of these mice significantly attenuated their over-grooming behaviors. Proteomics of ACC synaptosomes and CDH11 interactomes revealed that CDH11 participates in synaptic vesicle trafficking, as evidenced by a reduction in presynaptic vesicle density at excitatory synapses in Cdh11-deficient mice. These findings highlight an important role of CDH11 in the development of ASD-related brain circuits and provide insights into the molecular basis of repetitive behaviors in ASD.
Indexed as
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.