Brain-derived neurotrophic factor Val66Met polymorphism affects cortical thickness of rostral anterior cingulate in patients with major depressive disorder

Shen, Zonglin; Lü, Yi; Jiang, Hong-Yan; Ye, Jing; Zhou, Cong; He, Mengxin; Li, Na; Xu, Xiufeng; Cheng, Yuqi

doi:10.1097/wnr.0000000000001528

Cited by 6 publications

(5 citation statements)

References 48 publications

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“…To test our hypotheses, the general linear model in SPSS was performed to analyze differences in subcortical volumes, with age, sex, education level, and ICV included as covariates. Multiple comparisons were corrected using the least significant difference method, and the significance threshold was set at P < 0.05 [37,38]. Two-tailed Pearson partial correlations were conducted to examine the relationships between abnormal subcortical volumes and clinical characteristics in the MD group, with age, sex, education level, and ICV controlled as covariates.…”

Section: Discussionmentioning

confidence: 99%

Atrophy of bilateral nucleus accumbens in melancholic depression

Chu

Yuan

et al. 2023

NeuroReport

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Evidence from previous literature suggests that the nucleus accumbens (NAc), hippocampus, and amygdala play critical roles in the reward circuit. Meanwhile, it was also suggested that abnormalities in the reward circuit might be closely associated with the symptom of anhedonia of depression. However, few studies have investigated the structural alterations of the NAc, hippocampus, and amygdala in depression with anhedonia as the main clinical manifestation. Thus, the current study aimed to explore the structural changes of the subcortical regions among melancholic depression (MD) patients, especially in the NAc, hippocampus, and amygdala, to provide a theoretical basis for understanding the pathological mechanisms of MD. Seventy-two MD patients, 74 nonmelancholic depression (NMD) patients, and 81 healthy controls (HCs) matched for sex, age, and years of education were included in the study. All participants underwent T1-weighted MRI scans. Subcortical structure segmentation was performed using the FreeSurfer software. MD and NMD patients had reduced left hippocampal volume compared with HCs. Meanwhile, only MD patients had reduced bilateral NAc volumes. Moreover, correlation analyses showed correlations between left NAc volume and late insomnia and lassitude in MD patients. The reduced hippocampal volume may be related to the pathogenesis of major depressive disorder (MDD), and the reduced volume of the NAc may be the unique neural mechanism of MD. The findings of the current study suggest that future studies should investigate the different pathogenic mechanisms of different subtypes of MDD further to contribute to the development of individualized diagnostic and treatment protocols.

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Section: Discussionmentioning

confidence: 99%

Atrophy of bilateral nucleus accumbens in melancholic depression

Chu

Yuan

et al. 2023

NeuroReport

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“…Cortical volume may also explain the genotype-related MEP changes that occur after NIBS. Neuroimaging studies reported that the cortical volume varied in some cortical regions between the genotype groups (Yang et al, 2012 ; Jasińska et al, 2017 ; Shen et al, 2020 ). When the interaction of cortical volume with the NIBS effect was considered, the volume of the sensorimotor cortex positively predicted the NIBS effect on MEP changes (Conde et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

“…When the interaction of cortical volume with the NIBS effect was considered, the volume of the sensorimotor cortex positively predicted the NIBS effect on MEP changes (Conde et al, 2012 ). However, this hypothesis lacks reliable information, because the different cortical volumes did not correspond to the same regions (Yang et al, 2012 ; Jasińska et al, 2017 ; Shen et al, 2020 ), and some studies failed to show the genotype-related cortical volume changes (Kim et al, 2015 ; McKay et al, 2019 ). Moreover, one study showed that the M1 volume in the Met/Met group was larger than that in the other groups (Jasińska et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Do Brain-Derived Neurotrophic Factor Genetic Polymorphisms Modulate the Efficacy of Motor Cortex Plasticity Induced by Non-invasive Brain Stimulation? A Systematic Review

Sasaki

Kojima

Onishi

2021

Front. Hum. Neurosci.

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Techniques of non-invasive brain stimulation (NIBS) of the human primary motor cortex (M1) are widely used in basic and clinical research to induce neural plasticity. The induction of neural plasticity in the M1 may improve motor performance ability in healthy individuals and patients with motor deficit caused by brain disorders. However, several recent studies revealed that various NIBS techniques yield high interindividual variability in the response, and that the brain-derived neurotrophic factor (BDNF) genotype (i.e., Val/Val and Met carrier types) may be a factor contributing to this variability. Here, we conducted a systematic review of all published studies that investigated the effects of the BDNF genotype on various forms of NIBS techniques applied to the human M1. The motor-evoked potential (MEP) amplitudes elicited by single-pulse transcranial magnetic stimulation (TMS), which can evaluate M1 excitability, were investigated as the main outcome. A total of 1,827 articles were identified, of which 17 (facilitatory NIBS protocol, 27 data) and 10 (inhibitory NIBS protocol, 14 data) were included in this review. More than two-thirds of the data (70.4–78.6%) on both NIBS protocols did not show a significant genotype effect of NIBS on MEP changes. Conversely, most of the remaining data revealed that the Val/Val type is likely to yield a greater MEP response after NIBS than the Met carrier type in both NIBS protocols (21.4–25.9%). Finally, to aid future investigation, we discuss the potential effect of the BDNF genotype based on mechanisms and methodological issues.

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“…Symptom severity and illness duration did not exhibit significant correlations with cortical thickness. These findings suggest that the presence of the Met allele may be a vulnerability factor for cortical thickness loss in the left rACC among MDD patients [ 76 ].…”

Section: Polymorphismmentioning

confidence: 99%

“…Additionally, the study demonstrated that among Val/Val individuals, the relationship between neglect and depression was mediated by emotion-focused coping styles and reduced perceived control, while this mediation was not observed in Met carriers [75]. Shen et al (2020) investigated the cortical thickness in MDD patients and found that individuals carrying the Met allele showed thinner cortical thickness in the left rostral anterior cingulate (rACC) compared to healthy controls carrying the same allele. Symptom severity and illness duration did not exhibit significant correlations with cortical thickness.…”

Section: Snp Rs6265 and Depressionmentioning

confidence: 99%

Associations of BDNF/BDNF-AS SNPs with Depression, Schizophrenia, and Bipolar Disorder

Shkundin,

Halaris

2023

JPM

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Brain-Derived Neurotrophic Factor (BDNF) is crucial for various aspects of neuronal development and function, including synaptic plasticity, neurotransmitter release, and supporting neuronal differentiation, growth, and survival. It is involved in the formation and preservation of dopaminergic, serotonergic, GABAergic, and cholinergic neurons, facilitating efficient stimulus transmission within the synaptic system and contributing to learning, memory, and overall cognition. Furthermore, BDNF demonstrates involvement in neuroinflammation and showcases neuroprotective effects. In contrast, BDNF antisense RNA (BDNF-AS) is linked to the regulation and control of BDNF, facilitating its suppression and contributing to neurotoxicity, apoptosis, and decreased cell viability. This review article aims to comprehensively overview the significance of single nucleotide polymorphisms (SNPs) in BDNF/BDNF-AS genes within psychiatric conditions, with a specific focus on their associations with depression, schizophrenia, and bipolar disorder. The independent influence of each BDNF/BDNF-AS gene variation, as well as the interplay between SNPs and their linkage disequilibrium, environmental factors, including early-life experiences, and interactions with other genes, lead to alterations in brain architecture and function, shaping vulnerability to mental health disorders. The potential translational applications of BDNF/BDNF-AS polymorphism knowledge can revolutionize personalized medicine, predict disease susceptibility, treatment outcomes, and guide the selection of interventions tailored to individual patients.

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Brain-derived neurotrophic factor Val66Met polymorphism affects cortical thickness of rostral anterior cingulate in patients with major depressive disorder

Cited by 6 publications

References 48 publications

Atrophy of bilateral nucleus accumbens in melancholic depression

Atrophy of bilateral nucleus accumbens in melancholic depression

Do Brain-Derived Neurotrophic Factor Genetic Polymorphisms Modulate the Efficacy of Motor Cortex Plasticity Induced by Non-invasive Brain Stimulation? A Systematic Review

Associations of BDNF/BDNF-AS SNPs with Depression, Schizophrenia, and Bipolar Disorder

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