ArticleBrain and behavior2014
Candidate gene associations with mood disorder, cognitive vulnerability, and fronto-limbic volumes.
Article in Brain and behavior, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.
- A Systematic Review of Candidate Genes for Major Depression.Medicina (Kaunas, Lithuania) · 2022Pooled it
- Peripheral blood brain-derived neurotrophic factor in bipolar disorder: a comprehensive systematic review and meta-analysis.Molecular psychiatry · 2016Pooled it
- Can an Investigation of a Single Gene be Effective in Differentiating Certain Features of the Bipolar Disorder Profile?Clinical practice and epidemiology in mental health : CP & EMH · 2021Article
- Analysis of KCNH2 and CACNA1C schizophrenia risk genes on EEG functional network modulation during an auditory odd-ball task.European archives of psychiatry and clinical neuroscience · 2020Article
- Article
- Predictors of Functional Outcome in Patients With Bipolar Disorder: Effects of Cognitive Psychoeducational Group Therapy After 12 Months.Frontiers in psychiatry · 2020Article
- Design of FRET Probes for SNP RS1006737, Related to Mood Disorder.Clinical practice and epidemiology in mental health : CP & EMH · 2018Article
- Cognitive Characterization of Schizophrenia Risk Variants Involved in Synaptic Transmission: Evidence of CACNA1C's Role in Working Memory.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Role of CACNA1C gene polymorphisms and protein expressions in the pathogenesis of schizophrenia: a case-control study in a Chinese population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Article
- The CACNA1C risk allele rs1006737 is associated with age-related prefrontal cortical thinning in bipolar I disorder.Translational psychiatry · 2017Article
- Integrative Bayesian analysis of neuroimaging-genetic data with application to cocaine dependence.NeuroImage · 2016Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundFour of the most consistently replicated variants associated with mood disorder occur in genes important for synaptic function: ANK3 (rs10994336), BDNF (rs6265), CACNA1C (rs1006737), and DGKH (rs1170191).
aimsThe present study examined associations between these candidates, mood disorder diagnoses, cognition, and fronto-limbic regions implicated in affect regulation. METHODS AND MATERIALS: Participants included 128 individuals with bipolar disorder (33% male, Mean age = 38.5), 48 with major depressive disorder (29% male, Mean age = 40.4), and 149 healthy controls (35% male, Mean age = 36.5). Genotypes were determined by 5'-fluorogenic exonuclease assays (TaqMan®). Fronto-limbic volumes were obtained from high resolution brain images using Freesurfer. Chi-square analyses, bivariate correlations, and mediational models examined relationships between genetic variants, mood diagnoses, cognitive measures, and brain volumes.
resultsCarriers of the minor BDNF and ANK3 alleles showed nonsignificant trends toward protective association in controls relative to mood disorder patients (P = 0.047). CACNA1C minor allele carriers had larger bilateral caudate, insula, globus pallidus, frontal pole, and nucleus accumbens volumes (smallest r = 0.13, P = 0.043), and increased IQ (r = 0.18, P < 0.001). CACNA1C associations with brain volumes and IQ were independent; larger fronto-limbic volumes did not mediate increased IQ. Other candidate variants were not significantly associated with diagnoses, cognition, or fronto-limbic volumes. DISCUSSION AND
conclusionsCACNA1C may be associated with biological systems altered in mood disorder. Increases in fronto-limbic volumes and cognitive ability associated with CACNA1C minor allele genotypes are congruent with findings in healthy samples and may be a marker for increased risk for neuropsychiatric phenotypes. Even larger multimodal studies are needed to quantify the magnitude and specificity of genetic-imaging-cognition-symptom relationships.
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