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Association of ATP6V1B2 rs1106634 with lifetime risk of depression and hippocampal neurocognitive deficits: possible novel mechanisms in the etiopathology of depression.

ABSTRACT: Current understanding and treatment of depression is limited to the monoaminergic theory with little knowledge of the involvement of other cellular processes. Genome-wide association studies, however, implicate several novel single-nucleotide polymorphisms with weak but replicable effects and unclarified mechanisms. We investigated the effect of rs1106634 of the ATPV1B2 gene encoding the vacuolar H+ATPase on lifetime and current depression and the possible mediating role of neuroticism by logistic and linear regression in a white European general sample of 2226 subjects. Association of rs1106634 with performance on frontal (Stockings of Cambridge (SOC)) and hippocampal-dependent (paired associates learning (PAL)) cognitive tasks was investigated in multivariate general linear models in a smaller subsample. The ATP6V1B2 rs1106634 A allele had a significant effect on lifetime but not on current depression. The effect of the A allele on lifetime depression was not mediated by neuroticism. The A allele influenced performance on the PAL but not on the SOC test. We conclude that the effects of variation in the vacuolar ATPase may point to a new molecular mechanism that influences the long-term development of depression. This mechanism may involve dysfunction specifically in hippocampal circuitry and cognitive impairment that characterizes recurrent and chronic depression.

SUBMITTER: Gonda X

PROVIDER: S-EPMC5314132 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

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Association of ATP6V1B2 rs1106634 with lifetime risk of depression and hippocampal neurocognitive deficits: possible novel mechanisms in the etiopathology of depression.

Gonda X X Eszlari N N Anderson I M IM Deakin J F W JF Bagdy G G Juhasz G G

Translational psychiatry 20161108 11

Current understanding and treatment of depression is limited to the monoaminergic theory with little knowledge of the involvement of other cellular processes. Genome-wide association studies, however, implicate several novel single-nucleotide polymorphisms with weak but replicable effects and unclarified mechanisms. We investigated the effect of rs1106634 of the ATPV1B2 gene encoding the vacuolar H+ATPase on lifetime and current depression and the possible mediating role of neuroticism by logist ...[more]

PMID: 27824360

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Project description:ImportanceNeurocognitive deficits (NCD) have been observed in noncentral nervous system cancers, yet short- and long-term neurocognitive data on patients treated for head and neck cancer (HNC) are lacking.ObjectiveTo assess objective neurocognitive function before and after definitive radiation therapy for HNC.Design, setting, and participantsIn a prospective, longitudinal study, neurocognitive function and self-reported symptoms were assessed in 80 patients with histologically proven HNC requiring definitive chemoradiotherapy or radiotherapy and in 40 healthy controls 4 times (baseline, 6, 12, and 24 months after baseline) prior to commencing treatment at Princess Margaret Cancer Centre, Toronto, Canada.Main outcomes and measuresNeurocognitive test scores were converted to age-corrected z scores (mean, 0; standard deviation, 1) and reported as mean scores, standardized regression-based scores, and frequencies of impairments in intellectual capacity, concentration, memory, executive function, processing speed, and motor dexterity. Multivariable analysis was used to identify factors associated with NCD 2 years after treatment.ResultsEighty patients and 40 healthy controls enrolled. Analyses revealed significant differences between patient and control mean performance in some domains, with patient deficits increasing over time: intellectual capacity (Cohen d, effect sizes [95% CIs] of -0.46 [-0.64 to 0.30], -0.51 [-0.72 to -0.30], and -0.70 [-0.92 to -0.49] for time points 6, 12, and 24 months, respectively); concentration/short-term attention span (-0.19 [-0.37 to 0.00], -0.38 [-0.55 to -0.21], -0.54 [-0.71 to -0.37]); verbal memory (-0.16 [-0.33 to 0.02], -0.38 [-0.64 to -0.12], -0.53 [-0.74 to -0.32]); executive function (-0.14 [-0.27 to 0.00], -0.34 [-0.52 to -0.16], -0.43 [-0.64 to -0.22]), and global cognitive function composite (-0.38 [-0.55 to -0.22], -0.75 [-0.92 to -0.58], -1.06 [-1.26 to -0.86]). There was an increased rate of impaired global neurocognitive functioning among patients (38%) at 24 months compared with controls (0%). Neurocognitive deficits were not associated with baseline cytokines.Conclusions and relevanceHead and neck cancer survivors have neurocognitive sequelae up to 2 years after definitive chemoradiotherapy or radiation treatment. Patients and health care teams should know about such potential risks. Further research is warranted in search of strategies to avoid, reduce, and compensate for declines.

Dataset Information

Association of ATP6V1B2 rs1106634 with lifetime risk of depression and hippocampal neurocognitive deficits: possible novel mechanisms in the etiopathology of depression.

Publications

Association of ATP6V1B2 rs1106634 with lifetime risk of depression and hippocampal neurocognitive deficits: possible novel mechanisms in the etiopathology of depression.

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