Anxiety and Polymorphism Val66Met of BDNF gene – Predictors of Depression Severity in Ischemic Heart Disease

Ve, Golimbet; Ba, Volel'; FIu, Kopylov; Av, Dolzhikov; Коровайцева, Г. И.; Sv, Kasparov; Mi, Isaeva

doi:10.18565/cardio.2015.1.9-13

Cited by 4 publications

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“…[ 8 , 9 ] On the other hand, the brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors and it is concentrated in brain regions such as hippocampus and amygdala. [ 10 , 11 ] Therefore, the BDNF gene has been involved in the pathophysiology of anxiety disorders. [ 12 , 13 ]…”

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confidence: 99%

Association between BDNF Val66Met polymorphism and generalized anxiety disorder and clinical characteristics in a Mexican population

et al. 2019

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The aim of the present case–control study was to explore the association between BDNF Val66Met (rs6265) polymorphism and generalized anxiety disorder in Mexican individuals, and whether this polymorphism plays a role in the symptomatology of anxiety.A total of 212 subjects were included in the study. Around 75 patients with generalized anxiety disorder were diagnosed by psychiatrists based on the DSM-IV instrument and 137 unrelated subjects psychiatrically healthy were used as comparison group. The subclinical symptomatology in patients was assessed with the State-Trait Anxiety Inventory. BDNF rs6265 genotypes were analyzed using the polymerase chain reaction end-point method.The association between BDNF Val66Met with the risk for generalized anxiety disorder was evaluated using 4 inheritance models. The present study showed that carrying the Met allele confers increased risk for the presence of generalized anxiety disorder (χ2 = 4.7, P = .03; OR (95%) 1.96 (1.05–3.56)) when patients with generalized anxiety disorder were compared with the comparison group.Our results provide evidence of an association between the Val66Met polymorphism of the BDNF gene and generalized anxiety disorder in a Mexican population. However, no association was observed between this polymorphism and the symptomatology of anxiety.

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Section: Introductionmentioning

confidence: 99%

Association between BDNF Val66Met polymorphism and generalized anxiety disorder and clinical characteristics in a Mexican population

et al. 2019

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“…These protective proteins, for instance BDNF (Brain Derived Neurotrophic Factor), protect and support brain cell structure and function. It has been strikingly implicated in the genesis of depressive disorders [41][42][43][44][45][46][47][48]. The neurothrophin BDNF is a molecule extremely sensible to stress, and its expression or production is reduced in key brain regions of animal model of depression [49][50][51] and also in the blood of depressed patients [52][53][54].…”

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A Brief Review on Epigenetic Aspects involved in Depression

Conti¹,

Silva-Conforti²

2016

Biol Med (Aligarh)

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It is known that external environmental or internal physiologic factors interact with an individual's genetic constitution to determine risk for depression throughout life. This can be possible through epigenetic mechanisms that lead to changes in gene expression -with transgenerational abilities -that do not involve a change in the DNA sequence. Here we briefly summarize the link between depressive disorders and epigenetics, considering stressful events as important triggers for these modifications. The increasing knowledge in this issue is relevant for updating and expanding comprehension in the molecular basis of this mood disorder. Keywords Epigenetic aspects involved in depressionGrowing evidences support the hypothesis that epigenetics is a key mechanism through which environmental exposures interact with our genetic constitution and this interaction is able to cause depression throughout life. The term epigenetics ("epi" means above in Greek) is used to denote transgenerational transmission of traits without a change in the nucleotide sequence of DNA [1][2][3][4]. It had emerged as a mechanism initiated by environmental cues and cellular events mediated by various cellular mechanisms that originate phenotypes during the development. However, recently, it has been postulated that these cellular modifications can be converted into alterations in chromatin structure -non related with DNA sequence alteration -that finally lead to expression or suppression of altered gene programs [5].While the genome defines the potential genetic information, the epigenome defines which genes are actually expressed. This regulation over the gene expression without altering the sequence of the DNA is possible by epigenetic modifications including microRNAs (small RNA molecules that can negatively control their target gene expression posttranscriptionally), covalent modifications of histone proteins, mechanisms controlling higher order chromatin organization and DNA methylation. Among numerous epigenetic processes, DNA methylation is one of the major mechanisms studied in the context of early life adversities as a potential via to explain the long-term effects on gene transcription [3]. It is a stable mark that is important for diverse cellular processes [6]. Methyl group is added to the C5 position catalyzed by DNA methyltransferases (DNMTs) [7]. Considering all cytosines in the human genome, about 3% is methylated and proper cytosine methylation is required for cell differentiation, genetic imprinting and suppression of repetitive elements. In the central nervous system, DNA methylation is a physiological process, relevant for normal brain development, differentiation and maintenance of function [8,9]. Indeed, during development, pluripotent stem cells undergo division and differentiate into different cell types that ultimately become different organs and tissues with specific patterns of gene expression [10].Epigenetics refers to how both the external environment and internal physiologic environment can interact wit...

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Edaravone reduces depression severity in patients with symptomatic intracranial stenosis and is associated with the serum expression of sex hormones

et al. 2020

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Objective: To investigate the effect of edaravone on depression relief in symptomatic patients with intracranial stenosis and its relationship with the expression of sex hormones. Methods: We recruited 112 patients with symptomatic intracranial arterial stenosis from Renmin Hospital, Wuhan University, between October 2014 and October 2017. All patients were divided into the traditional or experimental (traditional treatment + intravenous infusion of edaravone 30 mg twice a day for 14 days) treatment groups. The general clinical data were collected, and neurological functional recovery using the Modified Rankin Scale (mRS) and National Institute of Health stroke scale (NIHSS) scores were recorded. Symptom Checklist 90 (SCL-90) was used to assess the general psychological changes of the patient, followed by the 24 Hamilton Depression Scale (HAMD) to examine the incidence of post-stroke depression (PSD). This divided the patients into the mild, moderate, and severe depression groups. Next, we measured the serum protein expression of the sex hormones estradiol (E2), testosterone (T), follicle stimulating hormone (FSH), prolactin (PRL), and luteinizing hormone (LH). Results: The mRS and NIHSS scores were significantly lower in the experimental group than in the control group (P < .05). There was no significant difference in SCL90 score before intervention (P > .05); the scores were significantly lower in the experimental group after intervention (P < .05). There was a significant difference in SCL-90 and HAMD scores between groups before treatment (P < .05), with significantly lower scores in the experimental group post-treatment (P < .05). The incidence of depression was significantly reduced in the experimental group post-treatment. Furthermore, the expression of E2 and FSH was significantly higher (P < .01) and lower (P < .001), respectively, in women than in men in the experimental group post-treatment. Interestingly, the expression of T was significantly lower in men in the experimental group post-treatment (P < .001). Conclusion: Edaravone significantly improved the clinical efficacy of stent implantation in intracranial artery stenosis treatment by alleviating depression and reducing the incidence of PSD.

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Anxiety and Polymorphism Val66Met of BDNF gene – Predictors of Depression Severity in Ischemic Heart Disease

Cited by 4 publications

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Association between BDNF Val66Met polymorphism and generalized anxiety disorder and clinical characteristics in a Mexican population

Association between BDNF Val66Met polymorphism and generalized anxiety disorder and clinical characteristics in a Mexican population

A Brief Review on Epigenetic Aspects involved in Depression

Edaravone reduces depression severity in patients with symptomatic intracranial stenosis and is associated with the serum expression of sex hormones

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