细胞色素P450 2D6酶基因多态性与氟西汀临床效应的相关性研究

目的：研究中国人P450 2D6酶（CYP2D6）基因多态性与氟西汀临床效应之间的关系。方法：用氟西汀对108例抑郁患者（抑郁症89例，精神分裂症后抑郁7例，分裂情感性精神病抑郁型4例，强迫性神经症2例，焦虑性神经症1例，抑郁性神经症4例，分裂样精神病（伴抑郁症状）1例）进行治疗， 和汉密尔顿抑郁量表（HAMD）和治疗中需处理的副反应症状量表（TESS）评定疗效和副反应，用聚合酶链反应－限制性片段长度多态性分析法（PCR－RFLP）分析患者CYP2D6基因型。结果：（1）PCR－RFLP分析表明，在108例抑郁患者中，CYP2D6基因型为wt/wt者26例，wt/Ch者55例，Ch/Ch者26例，wt/A者1例，未发现B等位基因。CYP2D6等位基因频率分别为CYP2D6wt(50%),CYP2D6Ch(49.5%),CYP2DY6A(0.5).(2）入组时，不同基因型的患者之间HAMD基础评分的差异无显著性（P＞0．05）。经氟西汀治疗后4周和8周后，不同CYP2D6基因型患者的HAMD量表评分比治疗前 降低，差异均有非常显著性（P＝0．000）；8周后减分率达80％左右，TESS评分较低。在不同基因型的患者之间，治疗后的HAMD评分、HAMD减分率及TESS评分的差异均无显著性（P＞0．05）。患者治疗前后的HAMD评分及HAMD减分率、TEWW评分等与CYP2D6基因型及CYP2D6突变等位基因数目的相关关系均无显著性（P＞0．05）。结论：未发现中国人CYP2D6基因多态性与氟西汀临床效应之间的关联。     

抗抑郁剂联合心境稳定剂治疗双相障碍患者:1年随访

目的:观察抗抑郁剂联合心境稳定剂治疗双相障碍1年的结局,并评价不同疗效对双相抑郁结局的影响。方法:选择符合ICD-10双相障碍诊断标准患者,急性期进行8周抗抑郁剂和心境稳定剂联合治疗,痊愈和有效者进入1年维持治疗期。用24项汉密顿抑郁量表(HAMD)、Bech-Rafaelsen躁狂量表(BRMS)和临床疗效总评量表(CGI)评定疾病严重程度和疗效。结果:76例患者急性期治疗痊愈者53例,有效者23例。随访1年后,共43例(56.57%)维持痊愈,17例症状复发,总复发率22.36%。痊愈组36例(67.92%)仍保持痊愈,有效组7例(30.43%)达痊愈,两组差异有显著性(χ2=9.176,P=0.002)。痊愈组抑郁复发率低于有效组(3.77%vs.17.39%,χ2=4.091,P=0.045),两组转躁率差异无统计学意义(11.32%vs.21.74%;χ2=1.406,P=0.236)。生存分析显示痊愈组平均复发时间显著长于有效组[(10.06±2.14)个月vs.(9.00±3.67)个月;u=9.327,P=0.002]。结论:抗抑郁剂联合心境稳定剂治疗双相障碍抑郁发作患者1年后复发率低,急性期治疗痊愈者优于非痊愈者。     

儿童精神分裂症患者脑源型神经营养因子基因VaL66Met多态性与颅脑结构关系的研究

目的分析脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)基因VaL66Met多态性与儿童精神分裂症及其脑结构之间的关系。方法采用限制性片段长度多态性技术测定199例儿童精神分裂症患者与和200名健康儿童的BDNF基因VaL66Met多态性,用磁共振成像对104例患者进行检测,并采用计算机软件测量颅腔结构。结果患者组与对照组的BDNF VaL66Met基因型(A/A,A/G,G/G)和等位基因(A,G)频率的差异均无统计学意义(掊2=1.22,P>0.05;掊2=0.24,P>0.05)。BDNF基因VaL66Met不同基因型之间患者比较,左外侧裂脑沟根部宽(F=8.11,P<0.01)、右外侧裂脑沟根部宽(F=10.25,P<0.00)、顶叶脑沟宽(F=8.23,P<0.01)、右颞角宽度(F=5.13,P<0.05)差异具有统计学意义。且各基因型两两比较显示,A/A型的患者的顶叶脑沟宽(3.77±1.36)cm、右外侧裂脑沟根部宽(6.44±2.75)cm显著高于A/G型[(3.19±0.74)cm,(5.19±1.16)cm]、G/G型[(3.15±0.60)cm,(4.92±1.83)cm];A/A型的患者的左外侧裂脑沟根部宽(6.28±1.79)cm显著高于A/G型(5.11±1.56)cm;A/A型患者的右颞角宽度(5.05±1.36)cm显著高于G/G型(4.05±2.13)cm,均具有统计学意义(P<0.05)。结论儿童精神分裂症易感性与BDNF基因VaL66Met多态性无显著相关;儿童精神分裂症患者中携带BDNF基因(VaL66Met)A/A基因型的患者存在显著的脑室扩大、右颞角宽度增大。     

脑卒中后抑郁与脑源性神经营养因子基因Val66Met单核苷酸多态性的相关性研究

目的探讨脑卒中后抑郁(PSD)与脑源性神经营养因子(BDNF)基因Val66Met单核苷酸多态性(SNP)的相互关系。方法选择86例PSD患者为PSD组,68例脑卒中无PSD患者为无PSD组,另选择46名健康者为对照组。3组研究对象年龄及性别基本匹配。采用酶联免疫吸附法检测BDNF浓度和等位基因特异性聚合酶链反应(A-S PCR)技术检测BDNF基因Val66Met位点SNP的分布。结果 PSD组和无PSD组间BDNF表达差异有统计学意义(t=-2.038,P=0.043);两组间基因型频率(χ2=0.340,P=0.844)和等位基因频率(χ2=0.036,P=0.849)差异均无统计学意义。结论 BDNF表达与PSD发生相关,但BDNF基因Val66Met位点SNP与PSD未发现有相关关系。     

抑郁症患者脑源性神经营养因子Val66Met多态性与血清浓度的关系

目的探讨脑源性神经营养因子（BDNF）基因Val66Met多态性与抑郁症之同的关系以及Val66Met多态性是否影响血清BDNF浓度。方法对76例未经药物治疗的抑郁症患者和50例正常人,用限制性片段长度多态性方法分析Val66Met多态性,采用酶联吸附反应方法对血清BDNF浓度进行检测。结果（1）抑郁症患者血清BDNF浓度（24．7±12．7）ng／m1显著低于正常对照组（36．6±16．4）pg／m｜,差异有统计学意义（P〈0．01）;（2）抑郁症组和对照组之间的Val66Met多态性位点的等位基因频率和基因型分布差异无统计学意义（P〉0．05）;（3）在抑郁症组和对照组,Val／Met＋Met／Met基因型组与Val／Val基因型相比,血清BDNF浓度差异无统计学意义（P〉0．05）。结论抑郁症患者存在较低的血清BDNF水平,BDNF基因Val66Met多态性与抑郁症之间无相关性,Val66Met多态性对血清BDNF水平浓度无明显影响。     

神经源型一氧化氮合酶C276T基因多态性与抗抑郁疗效相关分析

目的探讨抑郁症患者血浆一氧化氮（NO）水平及神经源型一氧化氮合酶（nNOS）基因C276T多态性与抗抑郁剂疗效相关性。方法抑郁症患者予选择性5-羟色胺再摄取抑制剂（SSRIs）单药治疗8周,采用汉密尔顿抑郁量表（HAMD）评估患者抑郁症状严重程度;采用硝酸盐还原酶法测定正常对照组及抑郁症患者治疗前后血浆NO水平;全部受试者提取基因组DNA,并采用PCR-RFLP方法对nNOS基因C276T多态性进行基因分型。结果患者组疗前血浆NO水平为（76.8±31.6）μmol/L,显著高于疗后[（66.9±25.7）μmol/L,P=0.044]及正常对照组[（64.2±33.3）μmol/L,P=0.02],患者组疗后血浆NO水平为（66.9±25.7）μmol/L,与正常对照组（64.2±33.3）μmol/L相比差异无显著性（P=0.588）;患者组疗前HAMD评分为（24.3±4.3）分,疗后HAMD评分为（10.5±5.0）分,治疗前后HAMD减分率为（57.5±15.9）%;疗前血浆NO水平为（76.8±31.6）μmol/L,与疗前HAMD评分（24.3±4.3）分显著正相关（r=0.311,P=0.009）;nNOS基因可见两种等位基因条带C、T,组成三种基因型CC、CT、TT,携带不同基因型患者治疗前后HAMD评分和HAMD减分率差异无显著性（P〉0.05）。结论血浆NO浓度可能提示抑郁症急性发作期病情严重程度;nNOS基因C276T多态性可能不是影响抗抑郁剂治疗疗效的主要遗传因素。     

MTRR A66G、MS D919G、MTHFR C677T基因多态性与脑梗死的关系

目的 探讨MTRR A66G、MS D919G、MTHFR C677T基因多态性与脑梗死的关系。方法 选择136例脑梗死（CI）患者和70例对照，用PCR-RFLP方法分析其MTRR、MS和MTHFR基因型。结果 CI组和对照组的MTRR A66G多态性的分布差异无显著性意义（X^2=1.645，P=0．439）；CI组与对照组相比，MS D919G各基因型的频率差异无显著性意义（X^2=1．040，P=0．595）；两组的MTHFR C677T各基因型的频率差异也没有显著性意义（X^2=1．399，P=0．497）。结论 通过实验推测MTRR A66G、MS D919G、MTHFR C677T基因多态性不是CI的独立遗传危险因素。     

5-羟色胺转运体基因多态性与西酞普兰抗抑郁疗效的关系

目的探讨5-羟色胺转运体基因多态性和西酞普兰抗抑郁疗效之间的关系。方法给予99例符合美国精神障碍诊断与统计手册第四版(DSM-IV)单相抑郁诊断标准的患者西酞普兰20mg～60mg/d治疗,选取其中完成8周治疗的87例患者为研究对象。于第0、2、4、6、8周评定汉密尔顿抑郁量表24项版本(HAMD-24)。HAMD总分减分率≥50%为有效(66例),以8周时HAMD≤7分为治愈(52例)。应用聚合酶链反应技术检测5-羟色胺转运体基因5-HTTLPR及5-HTTVNTR两种多态性。结果不同疗效组间5-羟色胺转运体基因两种多态性的基因型频数分布的差异均无统计学意义(P>0.05);不同基因型组间治疗后各期HAMD总分及抑郁核心症状分的差异也均无统计学意义(P>0.05)。结论未发现5-羟色胺转运体基因多态性与西酞普兰抗抑郁疗效存在关联。     

脂肪酰胺水解酶基因rs324420多态性与抑郁障碍及抗抑郁疗效的关系

目的:探讨脂肪酰胺水解酶(FAAH)基因rs324420多态性与抑郁障碍及抗抑郁疗效的关系。方法:采用聚合酶链反应技术检测219例抑郁障碍患者(患者组)及411名健康对照者(对照组)FAAH基因rs324420多态性;患者组中98例完成8周抗抑郁药物治疗并分别于治疗前及治疗后2、4、6、8周采用17项汉密尔顿抑郁量表(HAMD-17)进行评估;治疗后HAMD≤7分为界将患者分为缓解亚组51例与非缓解亚组47例。结果:患者组与对照组FAAH基因rs324420基因型及等位基因频率差异无统计学意义。缓解亚组与非缓解亚组间rs324420基因型频率差异无统计学意义,A等位基因频率明显高于非缓解组(χ~2=4.28,P=0.039)。不同基因型患者间,AA基因型患者治疗后2、4、6、8周HAMD总分低于AC、CC型,减分率高于AC、CC型,但差异无统计学意义。结论:FAAH基因rs324420多态性可能与抗抑郁药的疗效相关,A等位基因及AA基因型携带者的抗抑郁疗效较好。     

精神分裂症伴发2型糖尿病与色氨酸羟化酶基因多态性关联研究

目的：在中国汉族精神分裂症患者中探讨色氨酸羟化酶（TPH）基因A218C（rs1800532）多态性与2型糖尿病共病的关联性。方法：采用聚合酶链反应-限制性片断长度多态（PCR-RFLP）技术在中国汉族人群中对98例伴发2型糖尿病的精神分裂症患者（伴糖尿病组）及109例单纯精神分裂症患者（不伴糖尿病组）进行TPH基因A218C的分型,并进行等位基因及基因型比较。结果：伴糖尿病组与不伴糖尿病组比较,TPH6基因A218C多态性等位基因分布（χ^2=0．00,df=1,P〉0．05）和基因型分布（χ^2=3．78,df=2,P〉0．05）均无显著差异。在男性患者中,伴糖尿病组与不伴糖尿病组基因型分布存在显著差异（χ^2=6．57,df=2,P=0．037）,而等位基因分布（χ^2=1．28,df=1,P=0．26）则无明显差异;在女性患者组中,伴糖尿病组与不伴糖尿病组基因型分布（χ^2=1．54,df=2,P=0．46）和等位基因分布（χ^2=0．02,df=1,P〉0．05）均无显著差异。结论：在中国汉族男性精神分裂症患者中TPH基因A218C多态性与患2型糖尿病存在关联,其可能是男性精神分裂症患者患2型糖尿病的易感基因。     

儿茶酚氧位甲基转移酶基因多态性与抑郁症易感性及抗抑郁药物疗效的Meta分析

目的探讨儿茶酚氧位甲基转移酶（catechol—O—methyhransferase，COMT）基因Vall58Met多态性与抑郁症发病风险及抗抑郁药物疗效的遗传相关性。方法计算机检索Med—line、Embase、Web of Science和Cochrane Library，检索时间范围从建库至2014年3月1日，收集COMT基因Val158Met多态性与抑郁症相关性的病例对照研究，以及与抗抑郁药物疗效相关性的遗传药理学研究。采用Stata12．0软件进行meta分析，合并效应值及其95％CI并对结果进行异质性检验和纳入文献发表偏倚进行评估。结果COMT纯合子Met／Met或Val／Val基因型为抑郁症的保护因素（OR=0．82，95％CL：0．75-0．91）；在抑郁症患者中，COMT纯合子Met／Met或Val／Val基因型携带者对抗抑郁症药物的治疗反应较差（反应-无反应组：OR=0．73，95％CL：0．56—0．96；缓解一无缓解组：OR：0．65，95％CL：0．48—0．66）。结论COMT基因Val158Met多态性与抑郁症及抗抑郁药物临床疗效存在显著的遗传关联性。     

The brain-derived neurotrophic factor Val66Met polymorphism is associated with reduced hippocampus perfusion in frontotemporal lobar degeneration

Brain-derived neurotrophic factor (BDNF) promotes several functions in neurons and modulates neurotransmissions, especially in hippocampal regions. Frontotemporal lobar degeneration (FTLD) has a strong genetic background, but genetic risk factors associated with sporadic disease are unknown. Hippocampal involvement is frequently observed in FTLD. The aims of this study were: i) to evaluate if BDNF genetic variations are associated with an increased risk of developing FTLD; and ii) to assess the neuroimaging profiles associated with BDNF polymorphisms. Ninety-one FTLD patients who underwent SPECT imaging and blood sampling entered the study, and clinical, cognitive, and behavioral examinations were performed. A larger group of FTLD patients (n = 194) and controls (n = 396; 162 healthy subjects and 234 Alzheimer's disease (AD) patients) underwent genetic analyses, considering BDNF polymorphisms (Val66Met, rs2049045 C/G, G11757C). A significant different distribution of G11757C genotype in FTLD (GG 53.1%, GC 42.8%, CC 4.1%) compared to controls (G/G 55.6%, G/C 34.6%, C/C 9.8%, p = 0.020) was found. No other significant differences in genotype and allele distributions were detected. The effect of BDNF polymorphisms on brain perfusion was analyzed. BDNF Val66Met A* carriers (A/A or G/A) showed a significant greater hypoperfusion parahippocampal regions as compared to G/G carriers (p < 0.005). No effect of G11757C polymorphism on brain perfusion was found. rs2049045 C/G was not considered as in linkage disequilibrium with Val66Met polymorphism. BDNF Val66Met polymorphism may play a role as a modulator of the FTLD expression and may drive a selective damage in specific brain region affected by the disease.     

弥漫性轴索损伤BDNF及其Val66Met基因多态性与认知功能的相关性研究

目的探讨弥漫性轴索损伤（DAI）（Ⅱ型）患者伤后1个月血清脑源性神经营养因子（BDNF）水平及其Val66Met基因多态性与认知功能的关系。 方法选取晋江市医院神经外科自2015年8月至2020年8月收治的106例DAI（Ⅱ型）患者为病例组,选择同期来本院体检的105名健康体检者为对照组,采用第二版洛文斯顿作业疗法认知量表（LOTCA）、蒙特利尔评估量表中文版（MoCA）分别评估对照组和病例组伤后1个月时的认知功能;采用酶联免疫吸附试验测定2组研究对象的血清BDNF水平;聚合酶链反应-限制性片段长度多态性分析BDNF Val66Met基因多态性;多元逐步回归法分析病例组整体认知功能与BDNF及BDNF Val66Met基因多态性的相关性。 结果病例组伤后1个月相同基因亚型血清BDNF浓度均低于对照组,差异有统计学意义（P<0.05）;病例组Val/Val亚型血清BDNF浓度高于Val/Met、Met/Met亚型,差异有统计学意义（P<0.05）,而Val/Met和Met/Met亚型血清BDNF浓度比较差异无统计学意义（P>0.05）。病例组患者3种基因亚型伤后1个月的LOTCA和MoCA评分均低于对照组,差异有统计学意义（P<0.05）;病例组Val/Val亚型评分高于Val/Met、Met/Met评分,差异有统计学意义（P<0.05）,而Val/Met和Met/Met亚型评分比较,差异无统计学意义（P>0.05）。DAI（Ⅱ型）整体认知水平与BDNF Val66Met基因多态性、BDNF浓度具有线性回归关系（F=11.417,P<0.001）,其具有一定的相关性（|β|=0.966、0.877;r=0.569、0.579）。 结论BDNF可影响DAI认知功能,其BDNF Val66Met基因多态性可能是影响DAI认知功能的风险因素之一。     

Brain-derived neurotrophic factor (Val66Met) genetic polymorphism is associated with substance abuse in males

Data from animal studies and from genetic scans in humans suggest that brain-derived neurotrophic factor (BDNF), a member of the neurotrophic factor family, may be involved in the mechanisms underlying substance abuse. The present study tested the hypothesis that the BDNF-gene Val66Met polymorphism is associated with substance abuse. We studied this polymorphism in 103 methamphetamine- and 200 heroin-dependent cases and 122 normal controls. We also considered the association of this polymorphism with age of onset of substance abuse in the heroin-dependent cases. Significant differences in BDNF Val66Met genotype distribution were found between subjects dependent on methamphetamine (P = 0.046) or heroin (P = 0.045) and controls, suggesting that the lower 66Met carrier frequency is associated with substance abuse. Furthermore, in the heroin-dependent group, the Val/Val homozygotes had a later onset of substance abuse compared with the Met allele carriers. The results suggest that the BDNF Val66Met polymorphism or a nearby locus may be involved in the pathogenesis of substance abuse. Our findings support previous genetic scan results showing that BDNF may contribute to substance abuse vulnerability.     

Is the Val66Met polymorphism of the brain‐derived neurotrophic factor gene associated with panic disorder? A meta‐analysis

Although emerging evidence has suggested an association between the Val66Met (rs6265) polymorphisms in brain‐derived neurotrophic factor (BDNF) gene and the panic disorder, the conclusion is inclusive given the mixed results. This meta‐analysis reviewed and analyzed the recent studies addressing the potential association between the Val66Met polymorphisms and panic disorder susceptibility. Related case–control studies were retrieved by database searching and selected according to established inclusion criteria. Six articles were identified, which explored the association between the BDNF Val66Met polymorphism and panic disorder. Statistical analyses revealed no association for the allele contrast and the dominant model. However, the recessive model showed a significant association between the BDNF Val66Met polymorphism and panic disorder (odds ratio = 1.26, 95% confidence interval = 1.04–1.52, z = 2.39, P = 0.02). Despite of some limitations, this meta‐analysis suggests that the Val66Met polymorphism of BDNF gene is a susceptibility factor for panic disorder.     

Association of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism with Parkinson's disease in a Greek population

Brain-derived neurotrophic factor (BDNF) enhances survival of dopaminergic neurons in the substantia nigra, whereas in patients with Parkinson's disease (PD), the expression of BDNF mRNA is decreased, thus making BDNF a candidate gene for PD susceptibility. The association between BDNF Val66Met polymorphism and PD has been evaluated in several studies with controversial results. Thus, we determined the distribution of BDNF Val66Met polymorphism in 184 Greek patients with sporadic PD and 113 control participants using polymerase chain reaction-restriction fragment length polymorphism, and explored the association of the polymorphism with certain clinical parameters of the disease. Our results do not support a major role for the BDNF Val66Met polymorphism in PD in the Greek population.     

抗抑郁剂疗效的预测因素分析

目的:探索影响抑郁症患者抗抑郁剂疗效的预测因素。方法:241例抑郁症患者给予抗抑郁药治疗6周,治疗前后进行汉密顿抑郁量表17项(HAMD)评分,采用减分率评定疗效。分析人口学因素、基线HAMD、明尼苏达多项人格测定(MMPI-2)、认知功能评分及脑源性神经营养因子(BDNF)、5-羟色胺转运体(5-HTTLPR)和糖皮质激素受体(GR)3种基因多态对疗效的预测。结果:基线HAMD评分(β=0.771,P0.001)、MMPI-2中偏执(Pa)分(β=-0.322,P=0.032,R2=0.451)、连线测验B评分(TMT-B)(β=-0.045,P=0.013)、汉诺塔总分(β=-0.067,P=0.026)、数字广度(倒序)分(β=-0.974,P=0.025)及GR BclI基因G-等位基因携带者(P=0.05)与抗抑郁剂HAMD减分率有关。整合模型回归分析显示,结合基线HAMD评分(β=0.894,P0.001)、MMPI-2-Pa分(β=-0.155,P=0.036)和TMT-B分(β=-0.038,P=0.034)3个预测因子可解释57.1%的变异。结论:基线HAMD评分、MMPI-2-Pa分和TMT-B分可预测抗抑郁剂的疗效。     

Meta-analysis of the BDNF Val66Met polymorphism in major depressive disorder: effects of gender and ethnicity

Brain-derived neurotrophic factor (BDNF) is a nerve growth factor that has antidepressant-like effects in animals and may be implicated in the etiology of mood-related phenotypes. However, genetic association studies of the BDNF Val66Met polymorphism (single nucleotide polymorphism rs6265) in major depressive disorder (MDD) have produced inconsistent results. We conducted a meta-analysis of studies comparing the frequency of the BDNF Val66Met-coding variant in depressed cases (MDD) and nondepressed controls. A total of 14 studies involving 2812 cases with DSM-III or -IV defined MDD and 10 843 nondepressed controls met the inclusion criteria. Analyses were stratified either by gender or ethnicity (Asian and Caucasian) because MDD is more prevalent in women and in Caucasians and because BDNF allele frequencies differ by ethnicity. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were provided for allelic analyses (Met versus Val), as well as for genotypic analyses (Met/Met and Val/Met versus Val/Val). In the total sample, the BDNF Val66Met polymorphism was not significantly associated with depression. However, the gender stratified analyses revealed significant effects in both the allelic and genotypic analyses in men (OR(MET), 95% CI; 1.27 (1.10-1.47); OR(MET/MET), 95% CI; 1.67 (1.19-2.36)). Stratification according to ethnicity did not show significant effects of the Val66Met polymorphism on MDD. Our results suggest that the BDNF Val66Met polymorphism is of greater importance in the development of MDD in men than in women. Future research into gender issues will be of interest.     

Brain-Derived Neurotrophic Factor Polymorphism Influences Response to Single-Pulse Transcranial Magnetic Stimulation at Rest

ObjectivesThe ability of noninvasive brain stimulation to modulate corticospinal excitability and plasticity is influenced by genetic predilections such as the coding for brain-derived neurotrophic factor (BDNF). Otherwise healthy individuals presenting with BDNF Val66Met (Val/Met) polymorphism are less susceptible to changes in excitability in response to repetitive transcranial magnetic stimulation (TMS) and paired associative stimulation paradigms, reflecting reduced neuroplasticity, compared to Val homozygotes (Val/Val). In the current study, we investigated whether BDNF polymorphism influences “baseline” excitability under TMS conditions that are not repetitive or plasticity-inducing. Cross-sectional BDNF levels could predict TMS response more generally because of the ongoing plasticity processes.Materials and MethodsForty-five healthy individuals (23 females; age: 25.3 ± 7.0 years) participated in the study, comprising two groups. Motor evoked potentials (MEP) were collected using single-pulse TMS paradigms at fixed stimulation intensities at 110% of the resting motor threshold in one group, and individually-derived intensities based on MEP sizes of 1 mV in the second group. Functional variant Val66Met (rs6265) was genotyped from saliva samples by a technician blinded to the identity of DNA samples.ResultsTwenty-seven participants (60.0%) were identified with Val/Val, sixteen (35.5%) with Val/Met genotype, and two with Met/Met genotype. MEP amplitudes were significantly diminished in the Val/Met than Val/Val individuals. These results held independent of the single-pulse TMS paradigm of choice (p = 0.017110% group; p = 0.035 1 mV group), age, and scalp-to-coil distances.ConclusionsThe findings should be further substantiated in larger-scale studies. If validated, intrinsic differences by BDNF polymorphism status could index response to TMS prior to implementing plasticity-inducing protocols.