抑郁症患者血清脑源性神经营养因子水平及其相关因素

目的 探讨抑郁症患者血清脑源性神经营养因子水平及其相关因素,为防治抑郁症提供重要依据.方法 采用酶联免疫吸附法和汉密尔顿抑郁量表分别测定40例抑郁症患者(患者组)的血清BDNF水平和抑郁严重程度,并与49名正常者(对照组)进行对比分析.结果 患者组治疗前血清BDNF水平明显降低,与对照组比较差异有统计学意义(P＜0.01).患者组治疗8周末血清BDNF水平明显升高,HAMD总分明显降低,与治疗前比较差异有统计学意义(P＜0.05).患者组治疗前后血清BDNF水平与性别及年龄均呈负相关,差异具有统计学意义(P＜0.05),与受教育程度、病程及HAMD总分比较无统计学意义(P＞0.05).结论 抑郁症患者存在血清BDNF水平的下降,抗抑郁治疗可改善抑郁症状,并显著提高血清BDNF水平.     

抑郁症自杀未遂患者血清脑源性神经营养因子水平的变化

目的探讨血清脑源性神经营养因子（BDNF）水平与抑郁症患者自杀行为的关系。方法采用酶联免疫分析实验测定抑郁症自杀未遂患者（36例）、无自杀行为患者（55例）及36名正常对照血清BDNF水平,对抑郁症患者以汉密尔顿抑郁量表（HAMD）评定抑郁症状,以自杀意念自评量表（SIOSS）评定自杀意念的强烈程度。结果抑郁症患者组血清BDNF水平低于正常对照组（P〈0．01）。自杀未遂组血清BDNF水平低于无自杀组及正常对照组（P〈0．01）。自杀未遂组HAMD总分和SIOSS总分高于无自杀组。抑郁症患者血清BDNF水平与SIOSS总分呈负相关。结论抑郁症患者存在血清BDNF降低,BDNF水平可能是自杀倾向行为的生物学标志。     

脑源性神经营养因子与抑郁症

神经营养因子是神经元网络形成和可塑性的重要调节因子,以脑源性神经营养因子(BDNF)最受关注。抗抑郁治疗通过提高BDNF表达来促进神经元可塑性,从而取得疗效。本文从临床前研究、临床研究和基因多态性等方面对BDNF与抑郁症作一综述。     

脑源性神经营养因子和抑郁症

抑郁症是以显著而持久的情绪低落或心境改变为主要特征的一组精神疾病。其高发病率、致死率、高疾病负担已引起社会各界的关注。然而,由于其发病机制的不详,患者很难获得完全治愈的机会。近年来,国内外研究者发现脑源性神经营养因子可能参与抑郁症的发病和治疗过程。脑源性神经营养因子(Brain-derived neurotrophic factor,BD-NF)在中枢神经系统及周围神经系统的多种神经元均有分布,尤以海马和皮层含量最高。其基因定位于11p13,酪氨酸激酶受体B(tyrosine kinase receptor,TrkB)是其特异性受体,当BDNF与TrkB结合时,受体分子二聚化,其多…     

抑郁症患者自杀行为与血清脑源性神经营养因子水平的关系

目的:探讨血清脑源性神经营养因子(BDNF)水平与抑郁症患者自杀行为之间的关系.方法:采用酶联吸附反应方法对有自杀行为的21例抑郁症患者(自杀组)、无自杀行为的52例抑郁症患者(非自杀组)以及80例正常人(对照组)血清的BDNF进行检测,应用汉密尔顿抑郁量表(HAMD)对抑郁症患者的抑郁症状进行评定. 结果:抑郁症患者...     

抑郁症患者应用无抽搐电休克治疗对患者血清脑源性神经营养因子的影响

目的分析抑郁症患者应用无抽搐电休克治疗对患者血清脑源性神经营养因子的影响。方法将160例抑郁症患者按照入院先后顺序依次编号,采用数字随机表法分组,单号为研究组,双号为对照组。对照组采用艾司西酞普兰治疗;研究组采用艾司西酞普兰联合无抽搐电休克治疗。结果治疗前,2组患者BDNF水平比较无显著差异(P0.05);治疗后,2组患者均出现明显升高,与治疗前比较差异有统计学意义(P0.05);但研究组优于对照组(P0.05)。研究组治疗有效率为92.50%(74/80)与对照组82.50%(66/80)比较差异有统计学意义(P0.05)。同时2组患者治疗前后HAMD、HAMA及CGI、认知功能均得到明显改善(P0.05)。此外,2组患者均未发生性功能障碍等不良反应。结论采用无抽搐电休克治疗抑郁症,有效改善患者抑郁、焦虑及认知功能,提高患者BDNF水平,对患者性功能无影响,是一种安全有效的治疗方式,值得推广应用。     

脑源性神经营养因子与抑郁症的研究进展

海马结构和功能的改变涉及抑郁症的病理生理学过程，海马脑源性神经营养因子表达下调与海马结构和功能的改变密切相关，促进细胞凋亡可能参与慢性应激损伤海马。抗抑郁剂通过调节脑源性神经营养因子的表达逆转海马损伤而发挥治疗作用。     

难治性抑郁症患者血清脑源性神经营养因子动态分析

目的 通过对难治性抑郁症(TRD)患者不同阶段血清脑源性神经营养因子(BDNF)水平的动态监测,探讨TRD与BDNF的关系.方法 26例TRD患者分别在治疗前、急性治疗期、巩固期、维持期四个阶段进行汉密尔顿抑郁量表(HAMD)评定,用酶联免疫吸附法(ELISA)测定其血清BDNF含量.并于治疗前与非难治性抑郁症(TNRD)患者及正常体检者各30例进行对照.结果 治疗前,TRD组与TNRD组HAMD评分均较正常组显著升高(P＜0.01);血清BDNF水平则较正常组显著降低(P＜0.01),其中TRD组比TNRD组下降更明显(P＜0.01),相关性分析表明血清BDNF水平与HAMD评分呈明显负相关(r=-0.667,P＜0.01);治疗后,TRD巩固期和维持期血清BDNF水平较治疗前和急性治疗期均有明显升高(P＜0.01),同时HAMD评分也较治疗前和急性治疗期减少(P＜0.01),其中维持期减少更为明显(P＜0.01).结论 血清BDNF水平低下可能是TRD的病理机制之一,有效的抗抑郁药物治疗机制之一可能是通过提高BDNF水平而起作用的,BDNF可以作为反映TRD疗效的生物学指标.     

抑郁症治疗前后执行功能及其与血清脑源性神经营养因子水平的关系

目的 探讨抑郁症患者执行功能、血清脑源性神经营养因子(BDNF)水平治疗前后的动态变化及其与抑郁严重程度三者之间的关系.方法 采用威斯康星卡片分类试验(WCST)和汉密尔顿抑郁量表(HAMD)分别评定77例抑郁症患者抗抑郁药物治疗4周前后及74名正常对照组的执行功能和抑郁严重程度;采用酶联免疫吸附法(ELISA)测定受试者血清BDNF水平.结果 与对照组比较,患者组治疗前WCST的总应答数、持续性错误数、随机错误数均增加,完成分类数减少,血清BDNF水平降低[(36.34±15.16)ng/mL vs(23.09±12.13)ng/mL],上述差异均有统计学意义(P＜0.01),而4周治疗后两组间的上述指标的差异均无统计学意义(P＞0.05).与治疗前比较,患者组治疗后完成分类数增加、血清BDNF水平[(37.37±21.04)ng/mL]升高,总应答数、持续错误数、随机错误数减少和HAMD总分降低,上述差异均有统计学意义(P＜0.01).治疗前后血清BDNF水平与相应HAMD总分值均呈负相关(r=-0.28,P=0.01;r=-0.28,P=0.01),而治疗前WCST 5个指标及其治疗后变化值分别与相应血清BDNF水平、HAMD总分值及疗后变化值均无相关(P＞0.05).结论 抑郁症患者存在执行功能受损和血清BDNF水平的下降,后者与抑郁严重程度密切相关,且抗抑郁治疗后执行功能和抑郁症状均改善,血清BDNF水平升高.     

抑郁症血清胶质源性神经营养因子与生活事件

目的:研究抑郁症患者血清胶质源性神经营养因子(GDNF)水平变化及其与生活事件之间的关系. 方法:76例未经药物治疗的抑郁症患者(患者组),采用生活事件量表(LES)和汉密尔顿抑郁量表(HAMD)进行评定.用酶联吸附反应方法对患者进行血清GDNF检测,并与50名正常人(对照组)进行对照比较. 结果:患者组血清GDNF水平平均为(343.3±201.3)pg/ml,显著低于对照组的GDNF水平平均(749.9±300.4)pg/ml(t=8.41,P<0.001).以LES评分200分为界,将抑郁症患者分为高应激状态(n=23例)和低应激状态(n=53例),高应激状态患者的血清GDNF水平平均为(244.3±144.1)pg/ml,显著低于低应激状态患者的平均(386.2±208.5)pg/ml(t=2.97,P<0.001).LES总分和血清GDNF水平之间呈显著负相关(r=-0.291,P<0.05). 结论:抑郁症患者可能存在GDNF水平下降,应激对血清GDNF水平可能有调节作用.     

抑郁症首次发病患者情绪加工特征及抗抑郁剂治疗前后的变化

目的 探讨首次发病(以下简称首发)抑郁症情绪加工特征及抗抑郁剂治疗前后变化与症状改善的关联作用.方法 17例抑郁症首发患者治疗前后及22名对照者完成情绪词识别任务.患者组抗抑郁剂治疗9周,以汉密尔顿抑郁量表(17项,HAMD)评估疗效.结果 (1)患者组治疗有效率为88%,HAMD总分减分率75%.(2)情绪词识别任务:抑郁症组治疗前后正性词遗漏数[分别为(7.4±6.9)个和(4.1±5.3)个]均大于负性词遗漏数[分别为(3.2±3.3)个和(1.8±2.7)个;P＜0.05),治疗后正性词遗漏数小于治疗前(P=0.002),与对照组[(3.0±2.6)个]差异无统计学意义(P=0.44);治疗前后负性词遗漏数[分别为(3.2±3.3)个和(1.8±2.7)个]与对照组[(2.1±2.4)个],以及正负性词错判数与对照组差异均无统计学意义(P＞0.05);正性词平均反应时治疗后[(514±68)ms]短于治疗前[(550±75)ms;P=0.036],负性词平均反应时治疗前后[分别为(540±80)ms和(521±61)ms]差异无统计学意义(P=0.16).(3)治疗前正性词遗漏数与抑郁症状和负性思维评分正相关(r=0.36～0.50,P＜0.05).(4)治疗前后正、负性词遗漏数变化对HAMD分数变化有不同预测作用(r_( chang) ~2=0.45,P=0.002).结论首发抑郁症患者可能存在正性情绪加工缺陷,治疗后可恢复至正常水平;以负性情绪加工占优势的认知结构不因抑郁症状缓解而改变;正负性情绪加工变化与症状改善可能有不同的关联作用.     

晚发性抑郁症患者血浆脑源性神经营养因子水平与认知功能

目的 探讨晚发性抑郁症患者血浆脑源性神经营养因子(BDNF)水平与抑郁症发病及认知功能之间的关系.方法 采用酶联免疫吸附法测定34例未经治疗的晚发性抑郁症患者(患者组)和32名正常对照(对照组)血浆BDNF水平;对患者组及对照组进行17项汉密尔顿抑郁量表( HAMD17)评估及神经心理学测试;对患者组的血浆BDNF水平及HAMD17总分与认知功能进行Pearson相关分析.结果 患者组治疗前的神经认知测试成绩显著差于对照组(P＜0.01);患者组的血浆BDNF水平[(3.24±2.67) μg/L]低于对照组[(6.71±3.16)μg/L,P＜0.01].血浆BDNF水平与各项认知成绩、HAMD17总分值均无显著相关性(P＞0.05).结论 部分晚发性抑郁症患者存在认知功能广泛受损;血浆BDNF水平低下与晚发性抑郁症发病密切相关,与认知功能可能无直接相关性.     

Decreased serum BDNF levels in major depressive patients

Background

Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal plasticity. The aim of the present study was to measure serum BDNF levels in depression and to analyze the relationship between BDNF levels and severity of depression.

Methods

Thirty patients meeting the DSM-IV criteria for major depressive disorder and 40 normal control subjects were recruited for this study. Patients had not used psychotropic drugs. The severity of depression was assessed by the Hamilton Rating of Depression Scale (HAM-D). Serum BDNF levels were determined by using ELISA.

Results

HAM-D scores were 17.09 ± 4.96 in depressed patients. We determined that the serum BDNF levels of the depression patients were lower than those of the healthy control group (respectively, 1453.42 ± 144.51 pg/ml, 1632.23 ± 252.93 pg/ml, t = 3.467, p = 0.001, independent t test). No correlation was found between the patients’ serum BDNF levels and HAM-D scores (p > 0.05, Pearson correlation analysis).

Conclusions

Our results suggest that serum BDNF levels are low in depression. However it was not found association between serum BDNF levels and the severity of depression.     

学习障碍患儿血清BDNF水平的研究

目的探讨学习障碍血清脑源性神经营养因子(BDNF)水平的变化,及其与学习障碍病理基础的关系。方法患者组为22例未治疗过且不共患其他疾病的学习障碍患儿,对照组为16例年龄性别匹配正常儿童,以瑞文标准推理测验(SPM)测定智商,BDNF采用酶联夹心免疫吸附法检测。结果LD患者血清BDNF浓度为:平均(4.603±3.620)ng/ml高于对照组(1.843±0.728)ng/ml(t=3.326,P=0.003<0.01)。边缘智商组(4.523±4.618)ng/ml,与正常对照组比较差异有非常显著性(P=0.008<0.01)。结论学习障碍患儿血清BDNF浓度高于正常儿童,边缘智商者升高更明显。     

抑郁发作自杀未遂患者脑源性神经营养因子水平及其相关因素研究

目的 探讨脑源性神经营养因子(BDNF)在抑郁发作自杀未遂者中的可能作用.方法 对抑郁发作自杀未遂患者(自杀未遂组,23例)和抑郁发作无自杀行为患者(无自杀组,24例)采用汉密尔顿抑郁量表(24项,HAMD24)、Beck绝望量表(BHS)和自杀意念自评量表(SIOSS)评定抑郁严重程度、绝望程度及自杀意图的强烈程度;采用酶联免疫吸附法测定其血清BDNF浓度,并与正常对照者(对照组,30名)比较;对自杀未遂组的血清BDNF浓度与各相关因素进行Pearson相关分析.结果 (1)自杀未遂组的HAMD24[(37.8±8.7)分]、BHS[(13.0±3.8)分]及SIOSS评分[(18.1±3.9)分]均高于无自杀组[分别为(26.0±6.0)分、(7.5±4.3)分、(12.0±4.0)分;P<0.01].(2)自杀未遂组的BDNF平均浓度[(57 ±16)ng/L]低于无自杀组[(75 ±28)ng/L;P<0.05],无自杀组的BDNF平均浓度亦低于正常对照组[(111±39)ng/L;P<0.01].(3)自杀未遂组的血清BDNF浓度与抑郁发作的病程(r=-0.541)、BHS总分(r=-0.494)、SIOSS总分(r=-0.754)呈负相关(P<0.01-0.05).结论 低水平的BDNF可能是抑郁发作自杀未遂的一个危险因素.     

BDNF and COMT polymorphisms

Recent investigations in several species have suggested a role for brain-derived neurotrophic factor (BDNF) in memory, which may be mediated by the influence of BDNF on neuronal plasticity in the hippocampus. BDNF polymorphisms have also been associated with mood disorders. Catechol-O-methyltransferase (COMT) metabolizes dopamine and has been implicated in prefrontal function, another area of the brain relevant for memory. In a sample of 63 young adults with a history of childhood-onset mood disorder, we typed three BDNF polymorphisms, including the BDNF Val66Met single nucleotide polymorphism (SNP), and the COMT Val108/158Met SNP. Multivariate analysis of variance was used to test the association between BDNF and COMT markers and measures of declarative memory. Variants at the three BDNF markers and one COMT marker were not associated with declarative memory function—p-values ranged from 0.25 to 0.98. Higher IQ (F=6.18, df=4, 58, p=0.0003) and female gender (F=4.41, df=4, 58, p=0.0035) were associated with more optimal performance on the memory tasks. This study did not provide evidence supporting an association between BDNF and COMT genes and declarative memory phenotypes.     

Serum concentrations of brain-derived neurotrophic factor in patients with gender identity disorder

Gender Identity Disorder (GID) is characterized by a strong and persistent cross-gender identification that affects different aspects of behavior. Brain-derived neurotrophic factor (BDNF) plays a critical role in neurodevelopment and neuroplasticity. Altered BDNF-signaling is thought to contribute to the pathogenesis of psychiatric disordersand is related to traumatic life events. To examine serum BDNF levels, we compared one group of DSM-IV GID patients (n = 45) and one healthy control group (n = 66). Serum BDNF levels were significantly decreased in GID patients (p = 0.013). This data support the hypothesis that the reduction found in serum BDNF levels in GID patients may be related to the psychological abuse that transsexuals are exposed during their life.     

The roles of BDNF in the pathophysiology of major depression and in antidepressant treatment

Neurotrophic factors are critical regulators of the formation and plasticity of neuronal networks. Brain-derived neurotrophic factor (BDNF) is abundant in the brain and periphery, and is found in both human serum and plasma. Animal studies have demonstrated that stress reduces BDNF expression or activity in the hippocampus and that this reduction can be prevented by treatment with antidepressant drugs. A similar change in BDNF activity occurs in the brain of patients with major depression disorder (MDD). Recently, clinical studies have indicated that serum or plasma BDNF levels are decreased in untreated MDD patients. Antidepressant treatment for at least four weeks can restore the decreased BDNF function up to the normal value. Therefore, MDD is associated with impaired neuronal plasticity. Suicidal behavior can be a consequence of severe impaired neuronal plasticity in the brain. Antidepressant treatment promotes increased BDNF activity as well as several forms of neuronal plasticity, including neurogenesis, synaptogenesis and neuronal maturation. BDNF could also play an important role in the modulation of neuronal networks. Such a neuronal plastic change can positively influence mood or recover depressed mood. These alterations of BDNF levels or neuronal plasticity in MDD patients before and after antidepressant treatment can be measured through the examination of serum or plasma BDNF concentrations. BDNF levels can therefore be useful markers for clinical response or improvement of depressive symptoms, but they are not diagnostic markers of major depression.     

慢性应激诱导的抑郁大鼠海马脑源性神经营养因子蛋白和miR-16的表达

目的 研究慢性应激对大鼠行为及海马中脑源性神经营养因子（BDNF）和microRNA-16（miR-16）表达的影响.方法 在大鼠出生后1d,按窝别分为慢性应激组和对照组,各6只.慢性应激组大鼠在其出生后第1-14天每天接受6h母爱剥夺应激,然后喂养至10周龄时给予21d慢性温和应激,对照组不给予任何处理.两组大鼠均于13周龄时,采用强迫游泳、糖水偏爱和旷场试验测定大鼠的行为,采用免疫印迹法检测BDNF蛋白的表达情况,采用实时定量聚合酶链反应检测海马miR-16表达水平.结果 旷场实验中,应激组大鼠直立次数少于对照组（P＜0.05）,而爬行总路程,中央格比例和大便颗数差异均无统计学意义（P＞0.05）;强迫游泳实验中应激组大鼠的被动漂浮时间长于对照组（P＜0.05）;糖水测验中应激组大鼠的糖水偏爱率低于对照组（P＜0.05）.应激组大鼠海马BDNF蛋白表达量低于对照组（P＜0.05）;应激组大鼠海马内miR-16的表达量高于对照组（P＜0.05）.Pearson相关分析显示,两组大鼠的miR-16表达水平均与BDNF蛋白表达水平呈负相关（P＜0.05）.大鼠直立次数和糖水偏爱率分别与海马内BDNF蛋白表达量与呈正相关（P＜0.05）,与miR-16表达量呈负相关（P＜0.05）而被动漂浮时间与海马内BDNF蛋白表达量呈负相关（P＜0.05）,与miR-16表达量呈正相关（P＜0.05）.结论 慢性应激可导致大鼠抑郁样行为的出现及海马中miR-16与BDNF蛋白表达发生改变,并且大鼠的抑郁样水平与海马中miR-16和BDNF蛋白表达水平明显相关;大鼠海马中miR-16与BDNF蛋白可能参与了调节抑郁症的病理过程.