伴自杀未遂双相障碍患者的血清脑源性神经营养因子水平

目的 分析伴自杀未遂的双相障碍（BD）患者与不伴自杀未遂患者及健康人群间血清BDNF水平的差异,探讨BDNF在预防BD患者自杀中的作用.方法 采用DSM-IV轴Ⅰ障碍用临床定式检查（患者版）（SCID-I/P）对临床诊断为心境障碍的患者进行评佑.纳入111例BD患者（26例有自杀未遂史）及41例健康对照.使用汉密尔顿抑郁量表（HAMD-17）及杨氏躁狂量表（YMRS）评估患者症状严重程度;使用酶联免疫吸附测定法测定所有研究对象的血清BDNF水平.结果 伴自杀未遂的BD患者血清BDNF水平（13.8±7.4） ng/ml显著低于无自杀未遂患者（18.7±11.9） ng/ml及健康对照组（26.0±12.9）ng/ml（F=9.371,P＜0.01）;伴自杀未遂的BD患者抑郁发作次数显著多于不伴自杀未遂患者,在控制抑郁发作次数后,两组间血清BDNF水平差异消失（P=0.236）;伴自杀未遂的BD患者血清BDNF水平和抑郁发作次数有相关性的倾向（r=-0.388,P=0.068）,与HAMD-17得分呈负相关（r=-0.585,P＜0.01）.结论 本研究提示BDNF在BD及BD患者自杀未遂的病理生理机制中起重要作用;伴自杀未遂的BD患者血清BDNF水平可能与抑郁发作次数、抑郁严重程度相关;通过有效治疗来提高BDNF水平可能通过减少抑郁发作次数,降低抑郁严重程度来降低自杀风险.     

双相障碍与脑源性神经营养因子外周血mRNA和蛋白表达相关性的研究

目的 探讨脑源性神经营养因子(BDNF)外周血mRNA表达和血清蛋白水平与双相障碍、双相躁狂和双相抑郁的关系.方法 应用TaqMan探针及荧光实时定量逆转录-聚合酶链反应方法,检测并比较双相障碍组(61例)、双相躁狂组(29例)、双相抑郁组(32例)和对照组(61名)外周血白细胞BDNF基因的mRNA表达水平的差异;采用酶联免疫吸附方法测定血清BDNF浓度;应用17项汉密尔顿抑郁量表(HAMD17)和Young氏躁狂量表(YMRS)评定患者抑郁症状严重程度和躁狂症状的严重程度,采用Pearson相关分析分析BDNF基因mRNA表达水平和血清蛋白浓度与HAMD17和YMRS评分的关系.结果 (1)双相障碍组BDNF基因mRNA相对表达水平(0.0077±0.0019)较对照组(0.0096±0.0028)下降(t=-3.74,P＜0.01);双相躁狂组(0.0081±0.0023)、双相抑郁组(0.0073±0.0024)与对照组3组间BDNF基因mRNA相对表达水平的差异有统计学意义(F=7.55,P＜0.01),且双相躁狂组和双相抑郁组均低于对照组(P＜0.05或P＜0.01).(2)双相障碍组BDNF血清蛋白浓度低于对照组(t=-2.90,P＜0.01);双相躁狂组、双相抑郁组与对照组3组间BDNF血清蛋白浓度的差异有统计学意义(F=4.21,P＜0.05);双相躁狂组和双相抑郁组BDNF血清蛋白浓度均低于对照组(P均＜0.05),但双相躁狂组与双相抑郁组比较差异无统计学意义(P＞0.05).(3)双相躁狂组BDNF基因mRNA表达水平及血清蛋白浓度与YMRS评分未见相关(P＞0.05),双相抑郁组BDNF基因mRNA表达水平及血清蛋白浓度与HAMD17评分未见相关(P＞0.05).结论 双相障碍与BDNF水平下调可能相关,这种下降贯穿于躁狂相和抑郁相,而且BDNF的变化不会因双相障碍患者极性的变化而处于两极状态.     

双相障碍患者脑源性神经营养因子和白介素血清水平检测

目的：探讨脑源性神经营养因子（BDNF）和白介素-1β（IL-1β）在双相障碍患者的血清水平。方法：采用Young躁狂量表（YMRS）和汉密尔顿抑郁量表（HAMD）对102例双相障碍患者进行评定,其中双相障碍抑郁发作组31例,双相障碍躁狂发作组71例;以单相抑郁症组21例,双相障碍缓解组18例和健康正常者33名作为对照。采用酶联免疫吸附法检测血清BDNF和IL-1β水平。结果：双相障碍躁狂发作组和双相障碍抑郁发作组血清BDNF水平分别为（32.46±1.54）ng/ml和（28.75±1.62）ng/ml,IL-1β水平分别为（39.63±3.13）ng/ml和（34.84±1.87）ng/ml,均明显低于健康对照组的（45.70±5.74）ng/ml和（54.48±9.46）ng/ml（P〈0.01）;而双相障碍缓解组BDNF和IL-1β水平与健康对照组比较,差异无显著性（P〉0.05）。结论：双相障碍躁狂发作和抑郁发作与BDNF及IL-1β水平有关。     

双相Ⅰ型与双相Ⅱ型患者血清脑源性神经营养因子水平的研究

目的 探讨血清脑源性神经营养因子(BDNF)水平在双相I型(BD Ⅰ型)、双相Ⅱ型(BD Ⅱ型)患者与正常对照者间的差异.方法 对广州市3家三级甲等医院精神科临床诊断为情感性精神障碍的患者使用SCID-I/P再诊断,符合BD Ⅰ型和BD Ⅱ型诊断标准的患者为研究组,并进行YMRS及MADRS评定.对照组为经SCID-I/P排除符合DSM-Ⅳ轴Ⅰ障碍的人员.用ELISA方法测定所有研究对象的血清BDNF水平.结果 患者血清BDNF水平显著低于正常对照[(17.60±11.24)ng/ml vs(26.04±12.85)ng/ml,t=-3.953,P＜0.001)];未发现BD Ⅰ型与BD Ⅱ型患者间血清BDNF水平存在统计学差异;未发现患者血清BDNF水平与YMRS、MADRS评分问存在相关关系;合用与未合用情感稳定剂患者间血清BDNF差异无统计学意义.结论 BDNF可能作为BD的生物学标记,在BD Ⅰ型与BD Ⅱ型障碍的病理生理学上起重要作用.     

广泛性焦虑障碍治疗前后血清脑源性神经营养因子水平的变化

目的研究广泛性焦虑障碍(generalized anxiety disorder,GAD)患者血清脑源性神经营养因子(brain derived neurotrophic factor,BDNF)水平的特点及其治疗变化。方法收集GAD患者及正常对照者各40名,采用帕罗西汀片有效治疗量治疗12周,治疗前后采用汉密尔顿焦虑量表(Hamilton Anxiety Scale,HAMA)进行疗效评估,采用ELISA法测定血清BDNF的浓度并与对照组比较。结果治疗前GAD患者的血清BDNF水平[(26.03±10.52)ng/mL]低于对照组[(43.27±10.28)ng/mL],治疗后GAD患者血清BDNF水平[(35.85±11.96)ng/mL]较治疗前升高,但仍低于正常对照组,其差异均有统计学意义(P均<0.05);治疗后GAD显效患者[(39.43±12.35)ng/mL]与对照组血清BDNF水平的差异无统计学意义(P>0.05);基线时,GAD患者血清BDNF水平与HAMA量表总分、精神性焦虑因子分呈负相关(P<0.05),与躯体性焦虑因子分的相关没有统计学意义(P>0.05);治疗后,GAD患者血清BDNF水平的变化与HAMA总分、躯体性焦虑因子分、精神性焦虑因子分变化均呈负相关(P均<0.05)。结论血清BDNF水平可能是GAD的状态性指标之一。     

双相情感障碍认知功能损害与脑源性神经营养因子基因遗传学研究的进展

双相情感障碍（BD）患者存在持续的认知功能损害，这种损害可对患者的病程以及预后产 生不利影响。脑源性神经营养因子（BDNF）是神经生长因子家族的一种神经营养因子，参与神经元的发 生、存活以及突触可塑性，与 BD 患者认知功能损害密切相关。本文综述了 BDNF 表达水平、基因多态性 与 BD 认知功能损害的关系，BDNF 表观遗传学与 BD 及认知功能损害的研究，为早期识别及治疗 BD 患 者认知功能损害提供理论依据。     

脑源性神经营养因子与阿尔茨海默病的关系

脑源性神经营养因子（brain-derived neurotrophic factor,BDNF）是一种广泛分布于哺乳类动物脑中的一种蛋白。近年来的研究表明其对阿尔茨海默病（Alzheimer＇s disease,AD）的临床症状和病理改变有重要影响。此文就BNDF的基因、转录物、功能、与AD的关系、在AD时功能和表达降低的原因、及仍有待研究的问题作一综述。     

脑源性神经营养因子与精神分裂症

脑源性神经营养因子BDNF在精神分裂症发病中的作用得到了越来越广泛的关注。目前研究发现,BDNF与精神分裂症发病机制假说、分裂症动物模型的建立及分裂症治疗均存在相关性。通过综合评价该领域近年来的实验结果,对BDNF与精神分裂症的关系作一综述。     

社区轻度认知障碍患者血清脑源性神经营养因子的影响因素

正轻度认知障碍(MCI)可进展为阿尔茨海默病(AD)[1],脑源性神经营养因子(BDNF)对认知功能有保护作用,且血清BDNF水平能反映脑内水平[2]。为此本研究探讨MCI患者血清BDNF水平及其影响因素,报告如下。1对象和方法为2011年7月至2012年7月浦东新区4家社区卫生服务中心建档的194例老年MCI患者,其中47例拒绝参加,30例不符合诊断标准,共有120例符合2010年中华医学会     

脑源性神经营养因子与癫痫研究进展

癫痫发作后 ,脑内BDNF的表达升高 ,其在时间和地域分布上有一定规律 ,这与其维持神经元存活和再生的功能紧密相关 ;BDNF对癫痫动物模型的痫性发作有阻止作用 ;痫性发作后 ,BDNF的表达受到多种分子的影响     

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。     

Reduced serum levels of brain-derived neurotrophic factor in adult male patients with autism

BACKGROUND: The precise mechanisms underlying the pathophysiology of autism are currently unknown. Given the key role of brain-derived neurotrophic factor (BDNF) in brain development, we hypothesized that BDNF may play a role in the pathophysiology of autism. In this study, we studied whether serum levels of BDNF are altered in patients with autism. METHODS: We measured serum levels of BDNF in 18 adult male patients with autism and 18 age-matched healthy male control subjects. RESULTS: The serum levels of BDNF in patients with autism (25.6+/-2.15 ng/ml (mean+/-S.D.)) were significantly (z = -4.42, p < 0.001) lower than those of normal controls (61.6+/-10.9 ng/ml (mean+/-S.D.)). Nevertheless, we found no correlations between BDNF levels and clinical variables in autistic patients. CONCLUSIONS: This study suggests that reduced BDNF levels may play a role in the pathophysiology of autism.     

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.     

共患学习障碍的注意缺陷多动障碍儿童脑源性神经营养因子与5-羟色胺的关联性研究

目的 探讨脑源性神经营养因子(BDNF)与血清5-羟色胺(5-HT)在伴学习障碍(LD)的注意缺陷多动障碍(ADHD)患儿中的作用及关系. 方法 选择河南省精神卫生中心门诊及病房自2011年1月至2011年10月收治的ADHD患儿40例,其中伴LD患儿15例,不伴LD患儿25例,选择同期健康体检儿童25例作为正常对照组,比较3组受试者血清BDNF、5-HT的水平并分析ADHD伴LD组患儿血清BDNF及5-HT水平的相关性. 结果 ADHD伴LD组、ADHD不伴LD组及正常对照组BDNF水平依次降低,差异有统计学意义(P＜0.05);与ADHD伴LD组比较,ADHD不伴LD组及正常对照组5-HT水平升高,差异有统计学意义(P＜0.05);ADHD伴LD组患儿血清BDNF、5-HT水平呈负相关关系(r=-0.084,P=0.004). 结论 伴LD的ADHD患儿中存在BDNF及5-HT异常,二者可能相互作用共同参与ADHD的病理过程.     

Gender-specific association of the brain-derived neurotrophic factor gene with attention-deficit/hyperactivity disorder

Objective

Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder with a strong genetic component. Brain-derived neurotrophic factor (BDNF), which participates in the differentiation and survival of dopaminergic and noradrenergic neurons, could play a role in ADHD development. We aimed to explore the relationships between ADHD and BDNF gene polymorphism.

Methods

We conducted a case-control analysis of 202 ADHD subjects and 159 controls, performed a transmission disequilibrium test on 151 trios, and compared the results of a continuous performance test (CPT) according to the genotype of the three single nucleotide polymorphisms (rs11030101, rs6265, rs16917204) in the BDNF gene.

Results

In the case-control analysis, the AA genotype of the BDNF rs11030101 polymorphism was significantly associated with ADHD only in girls (p=0.024, odds ratio=3.00). The T-G-G haplotype was significantly less frequent (p=0.005) and A-G-G was more frequent (p=0.048) in girls with ADHD than in control girls (global p=0.027). A multivariate analysis of variance for commission errors on the CPT showed a significant main effect for the rs11030101 genotype (p=0.026) and an interaction effect of the rs11030101 genotype and gender (p=0.032) in ADHD probands.

Conclusion

These results provide preliminary evidence for a gender-specific association between BDNF and ADHD in the Korean population.     

Post-traumatic stress disorder risk and brain-derived neurotrophic factor Val66Met

Brain-derived neurotrophic factor (BDNF), which regulates neuronal survival, growth differentiation, and synapse formation, is known to be associated with depression and post-traumatic stress disorder (PTSD). However, the molecular mechanism for those mental disorders remains unknown. Studies have shown that BDNF is associated with PTSD risk and exaggerated startle reaction (a major arousal manifestation of PTSD) in United States military service members who were deployed during the wars in Iraq and Afghanistan. The frequency of the Met/Met in BDNF gene was greater among those with PTSD than those without PTSD. Among individuals who experienced fewer lifetime stressful events, the Met carriers have significantly higher total and startle scores on the PTSD Checklist than the Val/Val carriers. In addition, subjects with PTSD showed higher levels of BDNF in their peripheral blood plasma than the non-probable-PTSD controls. Increased BDNF levels and startle response were observed in both blood plasma and brain hippocampus by inescapable tail shock in rats. In this paper, we reviewed these data to discuss BDNF as a potential biomarker for PTSD risk and its possible roles in the onset of PTSD.     

Effects of paroxetine or milnacipran on serum brain-derived neurotrophic factor in depressed patients

Brain-derived neurotrophic factor (BDNF) is an important member of the neurotrophin family of growth factors, abundant in the brain and periphery. Researchers have reported that serum BDNF levels in drug-free depressed patients are lower than those of healthy controls, and have proposed that these low levels might reflect a failure of neuronal plasticity in depression. In the present study, we investigated the effects of paroxetine, an SSRI, and milnacipran, an SNRI, on serum BDNF levels in depressed patients. Serum levels of BDNF were measured by ELISA before, 4 weeks, and 8 weeks after the start of treatment with antidepressants. Forty-two patients were randomly administered paroxetine (21 cases) or milnacipran (21 cases). A negative correlation was found between serum BDNF levels and baseline Ham-D scores. The response and remission rates for each drug were not significantly different. Serum BDNF levels in responders were significantly increased 2.6- and 1.8-fold 8 weeks after treatment with paroxetine or milnacipran, respectively. These results suggest that both drugs improve the depressive state by increasing BDNF levels.     

Cognitive functions and serum levels of brain-derived neurotrophic factor in patients with major depressive disorder

Objective

We assessed major cognitive domains in major depressive disorder (MDD) compared to a healthy control group using neurocognitive tests. We hypothesized that lower serum brain-derived neurotrophic factor (BDNF) levels would be associated with poorer neurocognitive performance in patients with major depression and that these associations would be shown in healthy controls as well.

Method

Executive functions, sustaining and focusing of attention, memory functions, and verbal fluency were assessed in this study using the Trail-Making Test (TMT), Stroop Color Word Interference Test-TBAG Form (SCWT), Wisconsin Card Sorting Test (WCST), Test of Variables of Attention (TOVA), Auditory Consonant Trigram test (ACTT), Digit Span subtest of the Wechsler Memory Scale (DST), Rey Auditory Verbal Learning Test (RAVLT), and Controlled Oral Word Association Test (COWAT).

Results

The MDD group showed significantly poorer performance than the control group in cognitive functions; they also had lower levels of BDNF than the control group. However, there was no correlation between cognitive performances and BDNF levels except in the TMT, Part B.

Conclusions

The current understanding of the importance of neurocognitive assessment and related biological markers in depression is improving. Further studies with larger sample sizes evaluating neurocognitive functions with molecular analyses of BDNF levels may reveal a novel marker for predicting and monitoring neurocognitive deficits in depression.