ArticleTranslational psychiatry2017
The CACNA1C risk allele rs1006737 is associated with age-related prefrontal cortical thinning in bipolar I disorder.
Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 52 citations in OpenAlex.
- Network localization of genetic risk for schizophrenia and bipolar disorder.Psychological medicine · 2025Article
- Immediate and sustained effects of acupuncture on the default mode network.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2025Article
- Cacna1c deficiency in forebrain glutamatergic neurons alters behavior and hippocampal plasticity in female mice.Translational psychiatry · 2024Article
- The genetic association between bipolar disorder and dementia: a qualitative review.Frontiers in psychiatry · 2024Review
- Morphological abnormalities in youth with bipolar disorder and their relationship to clinical characteristics.Journal of affective disorders · 2023Article
- Prediction of the Duration to Next Admission for an Acute Affective Episode in Patients with Bipolar I Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023Article
- Cortical morphological heterogeneity of schizophrenia and its relationship with glutamatergic receptor variations.European psychiatry : the journal of the Association of European Psychiatrists · 2023Article
- Antihypertensive drugs and brain function: mechanisms underlying therapeutically beneficial and harmful neuropsychiatric effects.Cardiovascular research · 2023Review
- The association of genetic variation in CACNA1C with resting-state functional connectivity in youth bipolar disorder.International journal of bipolar disorders · 2023Article
- Phenotypes, mechanisms and therapeutics: insights from bipolar disorder GWAS findings.Molecular psychiatry · 2022Review
- Cocaine- and stress-primed reinstatement of drug-associated memories elicit differential behavioral and frontostriatal circuit activity patterns via recruitment of L-type CaMolecular psychiatry · 2020Article
- Psychiatric neuroimaging research in Brazil: historical overview, current challenges, and future opportunities.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2020Article
- Article
- Age-related atrophy of cortical thickness and genetic effect of ANK3 gene in first episode MDD patients.NeuroImage. Clinical · 2020Article
- Genetic Associations between Voltage-Gated Calcium Channels and Psychiatric Disorders.International journal of molecular sciences · 2019Review
- Review
- Dendritic structural plasticity and neuropsychiatric disease.Nature reviews. Neuroscience · 2018Review
- Design of FRET Probes for SNP RS1006737, Related to Mood Disorder.Clinical practice and epidemiology in mental health : CP & EMH · 2018Article
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium channels control the inflow of calcium ions into cells and are involved in diverse cellular functions. The CACNA1C gene polymorphism rs1006737 A allele has been strongly associated with increased risk for bipolar disorder (BD) and with modulation of brain morphology. The medial prefrontal cortex (mPFC) has been widely associated with mood regulation in BD, but the role of this CACNA1C polymorphism in mPFC morphology and brain aging has yet to be elucidated. One hundred seventeen euthymic BD type I subjects were genotyped for CACNA1C rs1006737 and underwent 3 T three-dimensional structural magnetic resonance imaging scans to determine cortical thickness of mPFC components (superior frontal cortex (sFC), medial orbitofrontal cortex (mOFC), caudal anterior cingulate cortex (cACC) and rostral anterior cingulate cortex (rACC)). Carriers of the CACNA1C allele A exhibited greater left mOFC thickness compared to non-carriers. Moreover, CACNA1C A carriers showed age-related cortical thinning of the left cACC, whereas among A non-carriers there was not an effect of age on left cACC cortical thinning. In the sFC, mOFC and rACC (left or right), a negative correlation was observed between age and cortical thickness, regardless of CACNA1C rs1006737 A status. Further studies investigating the direct link between cortical thickness, calcium channel function, apoptosis mechanism and their underlying relationship with aging-associated cognitive decline in BD are warranted.
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