SynthesisMolecular psychiatry2018
The protocadherin 17 gene affects cognition, personality, amygdala structure and function, synapse development and risk of major mood disorders.
Synthesis in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 3 of them syntheses that pooled it.
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Who cites it
52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 73 citations in OpenAlex.
- An epigenome-wide association study of early-onset major depression in monozygotic twins.Translational psychiatry · 2020Pooled it
- The Gene Encoding Protocadherin 9 (PCDH9), a Novel Risk Factor for Major Depressive Disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Pooled it
- Common variants at 2q11.2, 8q21.3, and 11q13.2 are associated with major mood disorders.Translational psychiatry · 2017Pooled it
- δ2-Protocadherins organize parallel indirect basal ganglia circuits.Science advances · 2026Article
- Standardized chronic restraint stress protocols reveal dynamic evolution of behavioral adaptations in male mice: implications for translational neuroscience.Molecular psychiatry · 2026Article
- Complementary δ2-protocadherin expression delineates parallel basal ganglia circuits in primates.iScience · 2026Article
- Canalization of neural dynamics by δ-protocadherins in the developing zebrafish optic tectum.PLoS genetics · 2026Article
- DNA methylation signatures of treatment response in medication-overuse headache.The journal of headache and pain · 2026Observational
- Analysis of Genomic and Transcriptomic Data Revealed Key Genes and Processes in the Development of Major Depressive Disorder.International journal of molecular sciences · 2025Article
- Epilepsy Associated Gene,Genes · 2025Article
- Differential relationships among homocysteine levels, cognitive deficits, and low-frequency fluctuation in brain activity in bipolar disorder with suicidal ideation.BMC psychiatry · 2025Article
- Neurobiological Relationships Between Neurodevelopmental Disorders and Mood Disorders.Brain sciences · 2025Review
- Canalization of circuit assembly by δ-protocadherins in the zebrafish optic tectum.bioRxiv : the preprint server for biology · 2025Article
- The Interaction Between Family Functioning and thePsychology research and behavior management · 2025Article
- PCDH17 restricts dendritic spine morphogenesis by regulating ROCK2-dependent control of the actin cytoskeleton, modulating emotional behavior.Zoological research · 2024Article
- Multi-ancestry genome-wide association study of major depression aids locus discovery, fine mapping, gene prioritization and causal inference.Nature genetics · 2024Article
- Alterations in electroencephalographic functional connectivity in individuals with major depressive disorder: a resting-state electroencephalogram study.Frontiers in neuroscience · 2024Article
- Identification of novel loci associated with starch content in maize kernels by a genome-wide association study using an enlarged SNP panel.Molecular breeding : new strategies in plant improvement · 2023Article
- Development and cadherin-mediated control of prefrontal corticostriatal projections in mice.iScience · 2023Article
- The Big Five as Predictors of Cognitive Function in Individuals with Bipolar Disorder.Brain sciences · 2023Article
Corrections and comments
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Authors and funding
38 authors at 15 institutions in 10 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major mood disorders, which primarily include bipolar disorder and major depressive disorder, are the leading cause of disability worldwide and pose a major challenge in identifying robust risk genes. Here, we present data from independent large-scale clinical data sets (including 29 557 cases and 32 056 controls) revealing brain expressed protocadherin 17 (PCDH17) as a susceptibility gene for major mood disorders. Single-nucleotide polymorphisms (SNPs) spanning the PCDH17 region are significantly associated with major mood disorders; subjects carrying the risk allele showed impaired cognitive abilities, increased vulnerable personality features, decreased amygdala volume and altered amygdala function as compared with non-carriers. The risk allele predicted higher transcriptional levels of PCDH17 mRNA in postmortem brain samples, which is consistent with increased gene expression in patients with bipolar disorder compared with healthy subjects. Further, overexpression of PCDH17 in primary cortical neurons revealed significantly decreased spine density and abnormal dendritic morphology compared with control groups, which again is consistent with the clinical observations of reduced numbers of dendritic spines in the brains of patients with major mood disorders. Given that synaptic spines are dynamic structures which regulate neuronal plasticity and have crucial roles in myriad brain functions, this study reveals a potential underlying biological mechanism of a novel risk gene for major mood disorders involved in synaptic function and related intermediate phenotypes.
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