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1.
BDNF与抑郁症的研究现状及进展 总被引：2，自引：0，他引：2
脑源性神经营养因子(brain-derived neurothrophic factor,BDNF)在中枢和外周均广泛存在,基于对其神经再生和修复功能的普遍认识,越来越多的研究开始关注BDNF在抑郁发生过程中对神经可塑性的影响以及BDNF在抗抑郁药物治疗中发挥的作用.本文综述了BDNF与抑郁症关系的基础性研究成果,以及近两年的相关研究趋势,更多的关于BDNF与其前体(precursor of brain derived neurothrophic factor,proBDNF)以及BDNF与其它神经递质在神经网络中的相互作用的研究需要被深入开展. 相似文献
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科学家最近发现一种在抑郁症发展过程中起关键作用的蛋白质,这一发现为抑郁症的治疗提供了新思路,并有可能因此而阐明该病的发病机制。 相似文献
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抑郁症是一种高患病率、高致残率及高自杀率的严重精神疾患。在过去10年中,抗抑郁药物研究取得了突飞猛进的进展。然而,在临床上仍约有20%的抑郁症患者最终成为难治性抑郁症病例。难治性抑郁症是一种情感障碍,目前尚无较好的治疗策略。现对有关难治性抑郁症的病因学现状进行文献回顾与总结,了解难治性抑郁症的发病机制,便于从临床治疗角度早期识别该类患者,尽可能及早地给予积极的抗抑郁治疗,以提高临床缓解率。 相似文献
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张延霞张桂青 《现代生物医学进展》2011,11(6):1194-1196
抑郁症是一种高患病率、高致残率及高自杀率的严重精神疾患。在过去10年中,抗抑郁药物研究取得了突飞猛进的进展。然而,在临床上仍约有20%的抑郁症患者最终成为难治性抑郁症病例。难治性抑郁症是一种情感障碍,目前尚无较好的治疗策略。现对有关难治性抑郁症的病因学现状进行文献回顾与总结,了解难治性抑郁症的发病机制,便于从临床治疗角度早期识别该类患者,尽可能及早地给予积极的抗抑郁治疗,以提高临床缓解率。 相似文献
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抑郁症是一种由多因素相互作用引起的复杂的精神疾病。其患病率达15%,带来的负担占全球疾病负担的12.3%,且有很高的致残、致死率,严重危及到人类的健康。抑郁症的病因并不清楚,一般认为是社会、环境、个体三方面因素相互作用的结果。肠道微生物作为人体最大、最直接的外环境,在抑郁症形成中的作用已明确,但具体机制仍不清楚。近年来,随着肠道微生态研究的兴起以及关于“抗抑郁药安全且有效”的说法被提出,肠道菌群失调在抑郁症的发生和发展中的作用越来越受到重视,“微生物—肠—脑轴”被提出,本文就肠道菌群失调致抑郁症可能的发病机制及微生态治疗作一综述。 相似文献
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目的:探讨天麻素对慢性不可预见应激(CUS)大鼠抑郁样行为的改善作用及对海马脑源性神经营养因子(BDNF)及胶质原纤维酸性蛋白(GDNF)表达的影响。方法:将64只SD大鼠随机分为对照组(Sham),Sham+天麻素低、中、高剂量组,模型组(CUS),模型(CUS)+天麻素低、中、高剂量组,每组8只。对照组每天腹腔注射生理盐水(1 m L/kg),连续14天;Sham+天麻素低、中、高剂量组每天腹腔注射不同剂量的天麻素(50、100或者200 mg/kg),连续14天;模型组接受CUS造模,并且在造模结束后每天腹腔注射生理盐水(1 m L/kg),连续14天;模型+天麻素低、中、高剂量组在CUS造模结束后每天腹腔注射不同剂量的天麻素(50、100或者200 mg/kg),持续14天。随后,通过糖水偏好实验和强迫游泳实验检测各组大鼠的抑郁样行为,在行为学检测结束后处死大鼠,通过Elisa检测海马GFAP和BDNF的表达情况。结果:(1)慢性不可预见应激(CUS)可以导致明显的抑郁样行为,包括糖水偏好减少(P0.05)和强迫游泳不动时间增加(P0.01),CUS组大鼠海马GFAP和BDNF水平下降(P0.01)。(2)一定剂量(100和200 mg/Kg)天麻素干预可以缓解CUS大鼠的抑郁行为,CUS与CUS+GAS(M)组(P0.05)以及CUS与CUS+GAS(H)组之间(P0.01)存在显著性差异。(3)中高剂量的天麻素可以恢复CUS大鼠海马的BDNF和GDNF水平,CUS与CUS+GAS(M)组(P0.05)以及CUS与CUS+GAS(H)组之间(P0.05)的BDNF和GDNF水平存在显著性差异。结论:天麻素可以缓解CUS模型大鼠抑郁样行为,恢复CUS模型大鼠海马的BDNF和GDNF水平。 相似文献
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陈爱萍;王惠芹;陈乃宏 《生命科学》2025,(3):250-260
抑郁症是一种复杂的精神障碍,其发病机制尚未完全阐明。近年来,HPA轴(下丘脑-垂体-肾上腺轴)功能紊乱及基因水平变异在抑郁症中的关键作用引起了广泛关注。本文系统综述了HPA轴相关的三种主要激素,CRH、ACTH和GC,在抑郁症中的异常变化及其病理机制。这些异常包括神经递质失调、神经营养因子功能障碍、神经炎症反应及肠道菌群紊乱等。未来研究应重点探索这些激素的具体作用机制及基因多态性与抑郁症的关系,以期为抑郁症的个性化治疗和新药开发提供理论基础。 相似文献
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摘要 目的：探讨舒眠胶囊联合阿戈美拉汀片对抑郁症伴失眠患者多导睡眠图特征和血清5-羟色胺（5-HT）、胶质细胞源性神经营养因子（GDNF）、脑源性神经营养因子（BDNF）的影响。方法：采用随机数字表法将94例抑郁症伴失眠患者分为研究组（接受阿戈美拉汀片、舒眠胶囊联合治疗）、对照组（接受阿戈美拉汀片治疗）,各为47例。对比两组汉密顿抑郁量表-17（HAMD-17）、匹兹堡睡眠质量指数（PSQI）、疲劳量表（FS-14）量表评分、5-HT、BDNF、GDNF、多导睡眠监测（PSG）相关指标[总睡眠时间（TST）、睡眠效率（SE）、非快速眼动睡眠1、2、3期（NREM1、NREM2、NREM3）]。结果：与对照组治疗后相比,研究组HAMD-17、PSQI、FS-14评分相对更低（P<0.05）。与对照组治疗后相比,研究组5-HT、BDNF、GDNF相对更高（P<0.05）。与对照组治疗后相比,研究组TST、SE、NREM1、NREM2、NREM3相对更高（P<0.05）。结论：抑郁症伴失眠患者经阿戈美拉汀片和舒眠胶囊联合治疗,失眠和抑郁症状得到显著改善,可能与改善血清5-HT、BDNF、GDNF水平有关。 相似文献
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抑郁症是当今社会较多发的严重影响人类生活质量的疾病,迄今为止,抑郁症病因与发病机制还不完全明确,在过去的很多年,单胺类神经递质假说一直处在相对重要的位置,然而,近年越来越多的临床证据表明,单胺类递质假说并不能完全解释抑郁症的发病机制与其所起到的治疗作用,是否还有另一种机制参与其中呢?近期大量实验研究表明谷氨酸能系统在抑郁症的发病及治疗中扮演了重要的角色,本文就谷氨酸能系统在抑郁症的发病及治疗中发挥的疗效作用综述如下。 相似文献
11.
Cole J Weinberger DR Mattay VS Cheng X Toga AW Thompson PM Powell-Smith G Cohen-Woods S Simmons A McGuffin P Fu CH 《Genes, Brain & Behavior》2011,10(7):756-764
Neuroimaging research implicates the hippocampus in the aetiology of major depressive disorder (MDD). Imaging genetics studies have investigated the influence of the serotonin transporter-linked polymorphic region (5HTTLPR) and brain-derived neurotrophic factor (BDNF) Val66Met polymorphism on the hippocampus in healthy individuals and patients with depression (MDD). However, conflicting results have led to inconclusive evidence about the effect of 5HTTLPR or BDNF on hippocampal volume (HCV). We hypothesized that analysis methods based on three-dimensional (3D) hippocampal shape mapping could offer improved sensitivity to clarify these effects. Magnetic resonance imaging data were collected in parallel samples of 111 healthy individuals and 84 MDD patients. Manual hippocampal segmentation was conducted and the resulting data used to investigate the influence of 5HTTLPR and BDNF Val66Met genotypes on HCV and 3D shape within each sample. Hippocampal volume normalized by intracranial volume (ICV) showed no significant difference between 5HTTLPR S allele carriers and L/L homozygotes or between BDNF Met allele carriers and Val/Val homozygotes in the group of healthy individuals. Moreover, there was no significant difference in normalized HCV between 5HTTLPR diallelic and triallelic classifications or between the BDNF Val66Met genotypes in MDD patients, although there was a relationship between BDNF Val66Met and ICV. Shape analysis detected dispersed between-group differences, but these effects did not survive multiple testing correction. In this study, there was no evidence of a genetic effect for 5HTTLPR or BDNF Val66Met on hippocampal morphology in either healthy individuals or MDD patients despite the relatively large sample sizes and sensitive methodology. 相似文献
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The brain-derived neurotrophic factor (BDNF) Val(66) Met allelic variation is linked to both the occurrence of mood disorders and antidepressant response. These findings are not universally observed, and the mechanism by which this variation results in increased risk for mood disorders is unclear. One possible explanation is an epistatic relationship with other neurotransmitter genes associated with depression risk, such as the serotonin-transporter-linked promotor region (5-HTTLPR). Further, it is unclear how the coexistence of the BDNF Met and 5-HTTLPR S variants affects the function of the affective and cognitive control systems. To address this question, we conducted a functional magnetic resonance imaging (fMRI) study in 38 older adults (20 healthy and 18 remitted from major depressive disorder). Subjects performed an emotional oddball task during the fMRI scan and provided blood samples for genotyping. Our analyses examined the relationship between genotypes and brain activation to sad distractors and attentional targets. We found that 5-HTTLPR S allele carriers exhibited stronger activation in the amygdala in response to sad distractors, whereas BDNF Met carriers exhibited increased activation to sad stimuli but decreased activation to attentional targets in the dorsolateral prefrontal and dorsomedial prefrontal cortices. In addition, subjects with both the S allele and Met allele genes exhibited increased activation to sad stimuli in the subgenual cingulate and posterior cingulate. Our results indicate that the Met allele alone or in combination with 5-HTTLPR S allele may increase reactivity to sad stimuli, which might represent a neural mechanism underlying increased depression vulnerability. 相似文献
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This study examined whether polymorphisms in the serotonin transporter (SLC6A4, 5-HTTLPR) and brain-derived neurotropic factor (BDNF Val66Met, rs6265) genes moderate the relationship between life stress and rumination. Participants were a large homogenous group of healthy, unmedicated, never depressed individuals with few current symptoms of depression (N = 273). Results indicate that individuals with two short (S) alleles of the 5-HTTLPR polymorphism or two Met alleles of the BDNF Val66Met polymorphism ruminate more under conditions of life stress, compared to the other genotypes. Moreover, the accumulation of risk alleles (i.e. S and Met alleles) across genes is associated with significantly greater rumination in the context of life stress. These results suggest that both 5-HTTLPR and BDNF Val66Met moderate the relationship between life stress and rumination. These findings support the notion that variation in these genes is associated with biological sensitivity to the negative effects of stress. 相似文献
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F. Benedetti I. Bollettini S. Poletti C. Locatelli C. Lorenzi A. Pirovano E. Smeraldi C. Colombo 《Genes, Brain & Behavior》2015,14(3):238-250
Bipolar disorder (BD) is associated with signs of widespread disruption of white matter (WM) integrity. A polymorphism in the promoter of the serotonin transporter (5‐HTTLPR) influenced functional cortico‐limbic connectivity in healthy subjects and course of illness in BD, with the short (s) allele being associated with lower functional connectivity, and with earlier onset of illness and poor response to treatment. We tested the effects of 5‐HTTLPR on diffusion tensor imaging (DTI) measures of WM microstructure in 140 inpatients, affected by a major depressive episode in course of BD, of Italian descent. We used whole brain tract‐based spatial statistics in the WM skeleton with threshold‐free cluster enhancement of DTI measures of WM microstructure: axial, radial and mean diffusivity and fractional anisotropy. Compared with l/l homozygotes, 5‐HTTLPR*s carriers showed significantly increased radial and mean diffusivity in several brain WM tracts, including corpus callosum, cingulum bundle, uncinate fasciculus, corona radiata, thalamic radiation, inferior and superior longitudinal fasciculus and inferior fronto‐occipital fasciculus. An increase of mean and radial diffusivity, perpendicular to the main axis of the WM tract, is thought to signify increased space between fibers, thus suggesting demyelination or dysmyelination, or loss of bundle coherence. The effects of 5‐HTTLPR on the anomalous emotional processing in BD might be mediated by changes of WM microstructure in key WM tracts contributing to the functional integrity of the brain. 相似文献
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Henry R. Kranzler Stephen Armeli Howard Tennen Jonathan Covault 《Addiction biology》2013,18(6):1024-1031
We previously reported moderating effects of age of onset of alcohol dependence (AD) and a functional polymorphism (5‐HTTLPR) in the gene encoding the serotonin transporter protein in a sample of 134 individuals participating in a 12‐week, placebo‐controlled trial of sertraline. To understand more fully the effects seen in that study, we examined moderation by negative moods reported each evening, with nighttime drinking intensity (i.e. the number of standard drinks consumed at night) as the dependent variable. We found a daily anxiety × age of onset × 5‐HTTLPR polymorphism × medication interaction, which reflected a daily anxiety × medication group effect for early‐onset individuals homozygous for the high‐expression (L′) allele, but not others. Specifically, on days characterized by relatively high levels of anxiety, early‐onset L′ homozygotes receiving placebo reduced their drinking intensity significantly. In contrast, early‐onset L′ homozygotes treated with sertraline non‐significantly increased their drinking intensity. These findings implicate anxiety as a key moderator of the observed pharmacogenetic effects. These findings have important implications because of the high prevalence of AD and the frequency with which SSRIs are prescribed to treat the disorders. 相似文献
16.
《Addiction biology》2017,22(4):1081-1089
There is substantial evidence for the assumption that particularly heavy cannabis usett is associated with a variety of psychopathologic conditions. Little is known about the relationship between cannabis and anxiety. Prior studies have concluded that cannabis use alone is not sufficient for the development of long‐term anxiety, and it has been suggested that cannabis is simply a risk factor that operates in conjunction with other risk factors. One such risk factor may be an individuals' genetic vulnerability. The present study examines the relationship between cannabis use and symptoms of anxiety by taking a developmental molecular‐genetic perspective with a focus on a polymorphism involved in the regulation of serotonin. Specifically, we concentrated on changes in cannabis use and symptoms of anxiety over time and differences herein for individuals with and without the short allele of the 5‐HTTLPR genotype. Data were from 1424 adolescents over a period of 5 years. We used different statistical analyses to test co‐development of cannabis use and symptoms of anxiety throughout adolescence and the possible role of the 5‐HTTLPR genotype in this process. Results from different analyses showed that cannabis use is associated with an increase in symptoms of anxiety, but only in carriers of the short allele of the 5‐HTTLPR genotype, not in non‐carriers. The findings of the present study show first evidence that the links between cannabis use and symptoms of anxiety are conditional on the individuals' genetic make‐up. 相似文献
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Dennis L. Thombs Ryan J. O'Mara Wei Hou Alexander C. Wagenaar Hui‐Jia Dong Michele L. Merves Bruce A. Goldberger Robert M. Weiler Virginia J. Dodd John D. Clapp 《Addiction biology》2011,16(1):133-141
The serotonin transporter promoter polymorphism (5‐HTTLPR) has been linked to a number of human behavioral traits and disorders. The variants of 5‐HTTLPR are commonly reported in three forms, L/L, S/L and S/S, with the latter most often associated with emotional distress and/or behavioral dysfunction. Missing from the research literature are investigations that assess event‐level associations between 5‐HTTLPR genotype and specific incidents of risk behavior in natural drinking settings. This study reports associations between 5‐HTTLPR, alcohol intoxication and intention to drive among young adult patrons exiting on‐premise drinking establishments (i.e. bars) at night. Self‐report measures, breath alcohol concentration (BrAC) readings and saliva samples for DNA analysis were collected from 477 bar patrons. Analyses were performed on 225 patrons likely to be near their peak intoxication level for the night. Results from a linear regression revealed that the 5‐HTTLPR genotype was associated with exiting patron BrAC, after adjusting for random and fixed effects of other variables. An interaction effect involving 5‐HTTLPR and bar‐sponsored drink specials also had an independent association with BrAC, suggesting that selection of price‐discounted alcoholic beverages increased intoxication in patrons with an L allele. In addition, results from logistic regression indicated that patrons with the S/S genotype were three times more likely to intend to drive a motor vehicle (after drinking on the night of study participation) compared with those with the L/L genotype. The 5‐HTTLPR genotype may play an important role in the etiology of problems associated with on‐premise drinking establishments. 相似文献
18.
Holmboe K Nemoda Z Fearon RM Sasvari-Szekely M Johnson MH 《Genes, Brain & Behavior》2011,10(5):513-522
Existing studies of the effect on infant temperament of the 48 base pair variable number of tandem repeats polymorphism in exon 3 of the dopamine D4 receptor gene, DRD4 VNTR, and the serotonin transporter-linked polymorphic region, 5-HTTLPR, have provided contradictory results, and age seems to be an important factor. The present study investigated the effect of these two polymorphisms on the stability of infant temperament between 4 and 9 months of age. Furthermore, the effect of a recently discovered single nucleotide polymorphism which modulates the 5-HTTLPR (rs25531) was investigated in relation to infant temperament. The study sample consisted of 90 infants, who were assessed by parental report at the two ages under consideration using the Revised Infant Behavior Questionnaire. It was found that infants carrying the 7-repeat allele of the DRD4 VNTR had higher levels of Negative Affect. Furthermore, there was an interaction between DRD4 VNTR and 5-HTTLPR genotype such that infants with the DRD4 VNTR 7-repeat allele and the highest expressing 5-HTTLPR genotype (L(A) L(A) ) had the highest level of Negative Affect. These effects were largely driven by scores on the Falling Reactivity scale. Genetic effects were stable across age. The results emphasize the need for developmental studies of genetic effects on temperament. 相似文献
19.
摘要 目的：探讨帕利哌酮治疗伴有精神病性症状的抑郁发作患者的疗效分析及对神经功能及血清脑源性神经营养因子（BDNF）的影响。方法：选取本院2021年1月到2021年10月收治的100例伴有精神病性症状的抑郁发作患者作为研究对象,随机将其分为观察组（n=50）和对照组（n=50）。对照组采用常规药物为伴有精神病性症状的抑郁发作患者进行治疗,观察组在对照组的基础上采用帕利哌酮为伴有精神病性症状的抑郁发作患者进行治疗,对比两组患者治疗前、治疗后2周、治疗后6周的汉密尔顿焦虑量表（HAMD）评分、汉密尔顿抑郁量表（HAMA）评分、精神经功能缺损程度、血清BDNE、神经病评定量表（BPRS）评分、社会功能缺陷筛选量表（SDSS）评分、日常生活能力量表（ADL）评分以及不良反应发生率。结果：治疗前两组患者的HAMA评分和HAMD评分对比无明显差异（P>0.05）,治疗后2周、6周评分均降低,且观察组较对照组低（P＜0.05）;治疗前两组患者的NIHSS评分和血清BDNE水平对比无明显差异（P>0.05）,治疗后2周、6周两组患者的NIHSS评分均低,且相较于观察组,对照组较高（P＜0.05）,但血清BDNE水平均升高,且观察组较对照组高（P＜0.05）;治疗前两组患者的BPRS、SDSS、ADL评分对比明显差异（P＞0.05）。治疗后2周、6周两组患者的BPRS、SDSS皆降低,并且观察组低于对照组（P＜0.05）,但两组患者的ADL评分均升高并且观察组高于对照组（P＜0.05）;观察组患者的不良反应总发生率与对照组比较无差异（P>0.05）。结论：将帕利哌酮应用于伴有精神病性症状的抑郁发作患者当中,可改善患者的焦虑、抑郁以及神经功能缺损情况,提高血清BDNE水平,并降低神经病性和社会功能缺陷情况,提高患者日常生活能力,值得临床借鉴。 相似文献
20.
目的:探讨拉莫三嗪和丙戊酸钠治疗癫痫合并抑郁障碍的疗效,为其临床治疗提供依据。方法:选择2011年2月~2015年2月在我院接受治疗的癫痫合并抑郁障碍患者60例,根据随机数字表法将患者分为观察组(30例)和对照组(30例),观察组给予拉莫三嗪治疗,对照组给予丙戊酸钠治疗,于治疗前、治疗后8周末和16周末采用HAMD-17和MADRS量表进行评分,并比较两组患者的临床疗效和不良反应。结果:治疗8周末和16周末两组患者的HAMD-17和MADRS量表评分较治疗前均降低,且观察组降低幅度大于对照组,差异均有统计学意义(P0.05)。治疗16周末观察组患者的总有效率为86.67%显著高于对照组的63.33%,差异有统计学意义(P0.05)。两组患者的不良反应主要为皮疹、嗜睡、恶心呕吐等,发生率低,差异无统计学意义(P0.05)。结论:拉莫三嗪和丙戊酸钠均可改善抑郁状态,但拉莫三嗪的疗效优于丙戊酸钠,且不会增加患者不良反应,值得临床推广应用。 相似文献