精神分裂症血浆S100B蛋白测定及临床意义探讨

目的探讨精神分裂症急性期血浆S100B蛋白水平及临床意义。方法用ELISA法检测血浆S100B蛋白含量。应用阳性和阴性症状量表（PANSS）评定精神症状。结果精神分裂症60例急性期血浆S100B蛋白水平（0．063±0．054μg／1）显著高于对照组（0．019±0．009μg／1，P〈0．001）；治疗6周后血浆S100B蛋白水平（0．079±0．093μg／L）与治疗前（0．063±0．054μg／L）差异不显著（P〉0．05）；治疗后血浆S100B持续增高者PANSS阴性症状评分较高。结论S100B持续增高与精神分裂症阴性症状相关。S100B绝对浓度可作为阴性症状发生的预测因子。     

精神分裂症患者脑源性神经营养因子水平及其与临床症状的关系

目的探讨脑源性神经营养因子（BDNF）在精神分裂症病理生理机制中的可能作用。方法采用横断面病例一对照研究设计。患者组为48例精神分裂症患者，其中发病后从未治疗组31例，停止治疗组17例。正常对照组（以下简称对照组）为与患者组性别、年龄匹配的41名健康人。对患者组用阳性和阴性症状量表（PANSS）评定病情严重程度。血浆BDNF浓度用酶联免疫吸附试验测定。用多变量方差分析比较组间差异。结果从未治疗组[（4．5±2．2）μg/L]和停药组患者[（3．9±1．4）μg/L]血浆BDNF浓度均低于对照组[（6．5±2．2）μg/L]（F检验，P〈0．01）；而从未治疗组与停止治疗组的差异无统计学意义（P〉0．05）。患者组的血浆BDNF浓度与PANSS阴性症状因子分（r=-0．509；P〈0．01）及总病期呈负相关（r=-0．426；P〈0．01），与发病年龄、PANSS阳性因子分、总分的相关性均无统计学差异。结论精神分裂症患者BDNF浓度低于正常；BDNF可能是参与精神分裂症病理生理机制的一种重要物质。     

吸烟对男性精神分裂症患者临床症状的影响及可能机制

目的探讨吸烟对男性精神分裂症患者临床症状的影响及氧化应激在精神分裂症高吸烟率中的作用。方法研究共入组男性精神分裂症患者130例,根据目前的吸烟状况分吸烟组（74例）和非吸烟组（56侧）,运用阳性和阴性症状量表（PANSS）评定精神病理症状;采用分光光度法检测其血浆超氧化物岐化酶（SOD）、过氧化氢酶（CAT）活性以及丙二醛（MDA）浓度。结果（1）吸烟组PANSS阳性症状（14．5±6．3）分显著低于非吸烟组（17．5±4．9）分（P〈0．05）;吸烟组患者吸烟数量与PANSS阴性症状分显著负相关（r=-0．23,P=0．02）。（2）血浆CAT活性吸烟组（2．9±0．3）×10^3U／L显著高于非吸烟组（1．6±0．2）×10^3U／L,吸烟患者血浆SOD活性与吸烟数量显著相关（r=0．24,P=0．04）;血浆MDA浓度吸烟组（9．2±0．7）mmol／L显著低于非吸烟7组（14．4±1．7）mmol／L。结论男性精神分裂症患者的吸烟可能通过缓解氧化应激来改善部分精神病理症状。     

帕利哌酮合用艾司西酞普兰对精神分裂症患者BDNF及阴性症状的影响

目的探讨帕利哌酮舍用艾司西酞普兰对精神分裂症患者血清脑源性神经营养因子（BDNF）浓度及阴性症状的影响。方法将84例以阴性症状为主的精神分裂症患者随机分为研究组（帕利哌酮合用艾司西酞普兰）与对照组（单用帕利哌酮）,治疗12周。于治疗第0、4、8、12周监测血清BDNF浓度,同时采用阳性与阴性症状量表（PANSS）和副反应量表（TESS）评定疗效和不良反应。结果①两组有效率分别为85．7％和64．3％,经比较差异有统计学意义（χ^2=4．29;P〈O．05）;②疗后8、12周,两组BDNF浓度较治疗前升高,但研究组BDNF浓度升高较对照组明显（t=2．0814,2．4719;P〈0．05）;③两组PANSS总分和各阴性因子均较治疗前减少（P均〈0．05）,但研究组PANSS总分及各阴性因子分差异较对照组差异有统计学意义（t=2．059,2．014,P〈0．05）;④两组药物不良反应比较无显著差异。结论帕利哌酮合用艾司西酞普兰可明显提高BDNF浓度,改善精神分裂症的阴性症状。     

利培酮对精神分裂症首次发病患者血清脑源性神经营养因子水平的影响

目的：探讨利培酮对首发精神分裂症患者血清脑源性神经营养因子（BDNF）水平的影响。方法：采用酶联免疫吸附法测定40例首发精神分裂症患者（患者组）在给予利培酮治疗前和治疗8周后的血清BDNF水平,并与40名正常人（正常对照组）的血清BDNF水平进行比较。结果：治疗前患者组血清BDNF水平显著低于正常对照组（P〈0．05）,治疗8周,患者组血清BDNF水平较治疗前明显升高（P〈0．01）;与正常对照组差异无统计学意义（P〉0．05）。患者组中有阳性家族史者（8例）与阴性家族史者（32例）之间血清BDNF水平差异无统计学意义（P〉0．05）。患者组治疗前后血清BDNF水平与阳性与阴性症状量表评分（r=0．283,r=0．09;P〉0．05）无显著相关;两组血清BDNF水平与年龄（r=-0．142,r=-0．122;P〉0．05）、体质量指数（r=-0．112,r=0．039;P〉0．05）均无显著相关。结论：首发精神分裂症患者可能存在血清BDNF水平低下,利培酮治疗可提高其血清BDNF水平。     

长期治疗的慢性精神分裂症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营养因子(BDNF)浓度与长期抗精神病药治疗的慢性精神分裂症患者精神病理症状间的关系。方法检测81例慢性精神分裂症患者和45名正常人血清的BDNF浓度,比较2组及各类抗精神病药治疗的患者间血清BDNF浓度的差异;采用阳性和阴性症状量表(PANSS)评定精神病理症状,分析血清BDNF浓度与PANSS评分间的关系。结果①患者组血清BDNF浓度显著低于正常对照[(7.3±2.6)vs(9.9±4.3)ng/mL,P<0.001];②利培酮、氯氮平、典型抗精神病药3组间血清BDNF浓度差异有统计学意义(F=6.25,P<0.01),利培酮组显著低于氯氮平组[(5.1±1.7)vs(7.8±2.7)ng/mL,P<0.05];③患者组中血清BDNF浓度与PANSS阴性症状分呈负相关(r=-0.307,P=0.005)。结论长期抗精神病药物治疗的慢性精神分裂症患者血清BDNF浓度下降,利培酮治疗组显著低于氯氮平治疗组,阴性症状越明显的患者BDNF水平越低。     

氯氮平对精神分裂症血清IL-2、IL-6的影响及临床意义

目的探讨氯氮平对精神分裂症患血清白介素-2（IL-2）、白介素-6（IL-6）水平的影响及与精神症状、体型指数变化的关系。方法选择住院的符合中国精神障碍分类与诊断标准第3版精神分裂症诊断标准的病人35例，阳性与阴性症状量表（PANSS）评分≥60分，予氯氮平治疗10周，分别于治疗前及治疗第10周末采用PANSS评估精神症状，采用酶联免疫吸附法（ELIAS）测定血清IL-2、IL-6水平。同时记录体型指数（BMI）。选取健康志愿35例作对照组，样本采集与检测同患组。结果治疗前精神分裂症患组血清IL-2水平显高于对照组（t=2．93，P=0．006），IL-6水平与对照组比较无显差异（P〉0．05）；氯氮平治疗10周末血清IL-2水平比治疗前显下降（t=3．51，P=0．001）;血清IL-6水平与治疗前相比显增高（t=2．53，P〈0．05）。治疗后精神分裂症患组体型指数显高于治疗前（t=6．02，P〈0．01）。治疗前血清IL-2水平与阳性症状评分呈显正相关（r=0．36，n=35，P=0．042）。与阴性症状、一般病理性症状、PANSS总分及体型指数均无显相关性（P〉0．05）。治疗前血清IL-6水平与各组精神症状及体型指数均无显相关性（P〉0．05）。治疗后血清IL-2下降值与阳性症状减分值呈显正相关（r=0．35，n=35，P=0．042）；IL-6增加值与各组精神症状减分值及体型指数增加值均无显相关性（P〉0．05）。结论氯氮平对精神分裂症患血清IL-2、IL-6水平有显影响，其临床意义可能与精神症状的变化有关，与氯氮平引起的体型指数变化无关。     

急性发作精神分裂症患者血清前炎性因子与临床特征的关系

目的分析血清前炎性因子水平与急性发作精神分裂症患者临床特征间的关系,探索前炎性因子在疾病发生机制中可能的作用。方法共纳入急性发作的精神分裂症患者105例（患者组）,健康对照50名（对照组）。采用酶联免疫（ELISA）法检测所有研究对象血清IL-1B、IL-6和TNF—的浓度;使用阳性和阴性症状量表（PANSS）评定患者的精神病理症状。在比较患者组与对照组血清前炎性因子浓度差异的同时,分析其与患者临床特征的关系。结果（1）患者组与对照组相比,血清IL-1β[12.3（2．8,15．0）ng／L比7．9（1．3,9．9）ng／L]、TNF—α[151．6（58．9,186．8）ng／L比108．9（37．0,132．3）ng／L]的差异有统计学意义（P〈0．05）;（2）按照性别、发作次数、病程、家族史、精神病理症状对患者组进行分层,首发患者血清IL－1β、TNF－α[水平高于复发患者;病程小于5年患者血清TNF－α水平高于病程超过5年的患者;家族史阳性患者IL－6水平高于阴性患者;以阳性症状为主患者的TNF—α水平高于以阴性症状为主的患者,差异均有统计学意义（P〈0．05）;（3）患者组血清IL－1β与IL－6（r=0．49,P〈0．01）、TNF－α（r=0．30,P〈0．01）呈正相关;对照组血清IL－1β水平与IL－6（r=0．55,P〈0．01）、TNF—α（r=0．34,P=0．02）呈正相关。结论急性发作的精神分裂症患者存在免疫激活,免疫激活程度与疾病的临床特征有关;免疫异常可能在疾病发生过程中起关键作用。     

缺陷型与非缺陷型精神分裂症血清脑源性神经营养因子与社会功能关系

目的探讨缺陷型精神分裂症(deficit schizophrenia,DS)与非缺陷型精神分裂症(non-deficit schizophrenia,NDS)患者血清脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)水平与社会功能状况及其关联性。方法纳入年龄、教育程度相匹配的DS患者53例、NDS患者58例和正常对照41名,使用酶联免疫吸附法检测所有受试者血清BDNF水平,采用阳性与阴性症状量表(positive and negative symptom scale,PANSS)、住院精神病人社会功能评定量表(scale of social function in psychosis inpatients,SSPI)和社会适应量表(social-adaptive functioning evaluation,SAFE)分别评估患者的临床症状与社会功能。结果 DS组和NDS组血清BDNF水平均较对照组降低([2.9±1.8)μg/L(3.4±1.7)μg/L vs.(9.5±4.0)μg/L,均P0.01],而DS与NDS组间BDNF水平比较差异无统计学意义(P=0.37)。与NDS组相比,DS组SSPI总分和各因子分均较低(P0.01),SAFE总分、PANSS阴性症状分、一般精神病理分、总分均较高(P0.01)。相关分析显示,精神分裂症患者血清BDNF水平与SAFE分呈负相关(r=-0.20,P=0.04),与SSPI因子Ⅰ(r=0.23,P=0.01)、SSPI因子Ⅱ(r=0.22,P=0.02)呈正相关。线性回归分析示,控制年龄、病程等混杂因素,精神分裂症患者SSPI与BDNF呈正关联(β=1.05,P=0.02),SAFE与PANSS总分呈正关联(β=1.36,P0.01)。结论 DS患者社会功能受损明显,血清BDNF水平明显下降。精神分裂症患者血清BDNF与社会功能相关联。     

吸烟的首发精神分裂症患者脑源性神经营养因子与精神症状认知功能关系的对照研究

目的探讨吸烟与非吸烟首发精神分裂症患者临床症状、认知功能与BDNF的相关性。方法符合美国精神障碍诊断与统计手册第四版(DSM-Ⅳ)诊断标准的首发精神分裂症住院患者81例,其中吸烟27例,非吸烟54例。采用阳性和阴性症状量表(PANSS)、威斯康星卡片分类(WCST)、重复性神经心理测查系统(RBANS)评估精神症状和认知功能,采用酶联免疫吸附法检测血清BDNF水平。结果吸烟组PANSS总分、阴性症状分、一般精神病理症状分均高于非吸烟组(t=2.5,2.0,2.0,P均0.05),吸烟组的正确应答数显著高于非吸烟组,吸烟组错误应答数显著低于非吸烟组(t=2.02,-2.26,P均0.05)。吸烟组患者血清BDNF水平为(8.8±4.6)μg/L,非吸烟组为(9.2±4.3)μg/L,两组比较差异不显著,无统计学意义(t=0.38,υ=83,P0.05);吸烟患者BDNF与患者总病程、PANSS总分、一般精神病理症状分呈显著正相关(r=0.66,0.54,0.54,P均0.05);与RBANS词汇回忆、故事回忆、图形回忆、编码测验分值、延时记忆因子呈显著负相关(r=-0.48,-0.45,-0.45,-0.53,P均≤0.05);非吸烟患者BDNF与PANSS中阳性症状分呈显著正相关(r=0.27,P0.05)。结论吸烟精神分裂症患者BDNF水平与精神症状可能存在相关性。     

精神分裂症自杀未遂者脑源性神经营养因子研究

目的:探讨影响精神分裂症自杀未遂患者脑源性神经营养因子(BDNF)水平的相关因素。方法:采用横断面病例-对照研究设计。研究包括精神分裂症自杀未遂组20例,精神分裂症无自杀行为组28例,正常对照组30名。采用酶联免疫吸附试验法测定血清BDNF浓度。采用简明精神病评定量表(BPRS)和自杀意图自评量表(SIOSS)对患者组进行评定。比较各组BDNF水平及其与相关因素之间的关系。结果:三组间BDNF水平差异有统计学意义(F=32.395,P<0.01)。Post-hoc分析发现,精神分裂症自杀未遂组BDNF水平[(51.3±11.1)pg/ml]显著低于精神分裂症无自杀行为组[(67.7±20.8)pg/ml](P<0.05),而精神分裂症无自杀行为组BDNF水平也低于正常对照组[(111.3±39.0)pg/ml](P<0.01)。自杀未遂组的血清BDNF水平与自杀严重程度呈负相关(r=-0.836,P<0.01)。结论:精神分裂症自杀未遂患者BDNF水平低于精神分裂症无自杀行为患者和正常人群;BDNF可能是参与精神分裂症自杀病理生理机制的一种重要物质。     

Decreased levels of brain-derived neurotrophic factor in serum of chronic schizophrenic patients

Neurotrophic factors regulate neuronal development as well as synaptic plasticity, and their impairment is often implicated as a cause of schizophrenia. Among various neurotrophic molecules, brain-derived neurotrophic factor (BDNF) levels have been found to be increased in the corticolimbic regions of patients’ brains. In the present study, we assessed peripheral BDNF levels in whole blood as well as in the serum of two independent groups of schizophrenic patients (n=34 in each group) and healthy volunteers (n=35 and n=27, respectively). BDNF protein levels in fresh serum and blood of the patients and volunteers were measured using a two-site enzyme immunoassay and correlated with the number and decay of platelets. In addition to the studies of patients and volunteers, neuroleptic effects on BDNF levels were assessed by administering haloperidol to adult rats for 2 weeks or 5 months. The major findings were as follows: BDNF levels were significantly reduced in the serum of schizophrenic patients (P<0.005, Mann–Whitney U-test) but not in their whole blood. Antipsychotic dose did not correlate with serum BDNF levels. Moreover, chronic administration of haloperidol failed to decrease serum BDNF levels in adult rats. Abnormal levels of BDNF are evident not only in the brain of schizophrenic patients, but also in their peripheral blood. The BDNF reduction in serum but not in whole blood suggests a potential deficit in neurotrophic factor release in patients with schizophrenia.     

Associations of serum brain-derived neurotrophic factor with cognitive impairments and negative symptoms in schizophrenia

Brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of schizophrenia. The aim of this study was to examine the associations of serum BDNF levels with the cognition and clinical characteristics in patients with schizophrenia. Sixty-three patients with schizophrenia and 52 age- and sex-matched healthy controls were examined with neuropsychological tests. Serum BDNF levels were determined by enzyme-linked immunosorbent assay (ELISA). There were no significant differences in serum BDNF levels between normal controls and patients with schizophrenia. Serum BDNF levels of normal controls showed negative correlations with verbal working memory, but this was not the case with schizophrenic patients. Meanwhile, serum BDNF levels of schizophrenic patients showed positive correlations with the scores of the Scale for the Assessment of Negative Symptoms (SANS) and the Information subtest scores of Wechsler Adult Intelligence Scale Revised (WAIS-R). Serum BDNF levels are related with the impairment of verbal working memory and negative symptoms in patients with schizophrenia.     

Reduced serum BDNF levels in schizophrenic patients on clozapine or typical antipsychotics

Neurotrophic factors regulate neuronal development and synaptic plasticity, possibly playing a role in the pathophysiology of schizophrenia and other psychiatric disorders. Decreased brain-derived neurotrophic factor (BDNF) levels have been found in brains and in the serum of schizophrenic patients, but results are inconsistent. Also, clozapine may upregulate brain BDNF expression. In the present study, we assessed serum BDNF immunoreactivity in 44 schizophrenic patients (20 on clozapine and 24 on typical antipsychotics) and in 25 healthy volunteers. Serum BDNF levels were measured using an enzyme immunoassay. Healthy controls showed significantly higher levels of BDNF compared to the whole group of schizophrenic patients (p<0.001) as well as to the subgroups on typical antipsychotics and clozapine (p<0.001). Serum BDNF values for controls were 168.8+/-26.3pg/ml, for the clozapine group were 125.4+/-44.5pg/ml and for the group on typicals were 101.3+/-51.6pg/ml. BDNF values from patients on clozapine were non-significantly higher than values from patients on typical antipsychotics (p=0.09). Serum BDNF was strongly and positively correlated with clozapine dose (r=0.643; p=0.002) but not with other demographic characteristics. These results reinforce previous findings of reduced serum BDNF levels in schizophrenic patients and suggest a differential effect of clozapine compared to typical antipsychotics on such levels.     

Serum BDNF levels and weight gain in schizophrenic patients on long-term treatment with antipsychotics

Several lines of evidence suggest that central brain-derived neurotrophic factor (BDNF) modulates food intake, metabolism, and increases in body weight. Reports have also shown that serum BDNF is altered in schizophrenic patients treated with antipsychotics. This study aimed to determine if there was a relationship between BDNF and antipsychotic-induced weight gain in patients with chronic schizophrenia. Serum BDNF was measured in 124 schizophrenia patients chronically treated with clozapine (n = 57), risperidone (n = 23) or typical antipsychotics (n = 44) and 50 healthy control subjects. To further assess group differences in serum BDNF, additional analyses were performed in a subset of patients and controls individually matched for body mass index (BMI). BDNF levels were lower in patients with schizophrenia than normal controls. However, this difference was not present when controlling for current BMI. In the individually BMI-matched sample, no differences in serum BDNF levels were observed in schizophrenic patients compared to BMI-matched healthy controls. BDNF levels negatively correlated with BMI gain in female but not in male patients when gender was considered. Antipsychotic class exerted differential effects over BDNF levels and BMI gain. Our findings suggest that decreased BDNF levels may be associated with weight gain in female schizophrenic patients on long-term antipsychotic treatment.     

Serum BDNF levels and weight gain in schizophrenic patients on long-term treatment with antipsychotics

Several lines of evidence suggest that central brain-derived neurotrophic factor (BDNF) modulates food intake, metabolism, and increases in body weight. Reports have also shown that serum BDNF is altered in schizophrenic patients treated with antipsychotics. This study aimed to determine if there was a relationship between BDNF and antipsychotic-induced weight gain in patients with chronic schizophrenia. Serum BDNF was measured in 124 schizophrenia patients chronically treated with clozapine (n = 57), risperidone (n = 23) or typical antipsychotics (n = 44) and 50 healthy control subjects. To further assess group differences in serum BDNF, additional analyses were performed in a subset of patients and controls individually matched for body mass index (BMI). BDNF levels were lower in patients with schizophrenia than normal controls. However, this difference was not present when controlling for current BMI. In the individually BMI-matched sample, no differences in serum BDNF levels were observed in schizophrenic patients compared to BMI-matched healthy controls. BDNF levels negatively correlated with BMI gain in female but not in male patients when gender was considered. Antipsychotic class exerted differential effects over BDNF levels and BMI gain. Our findings suggest that decreased BDNF levels may be associated with weight gain in female schizophrenic patients on long-term antipsychotic treatment.     

Associations between serum brain-derived neurotrophic factor levels and clinical phenotypes in schizophrenia patients

This study investigated serum brain-derived neurotrophic factor (BDNF) protein levels in schizophrenia patients and healthy control subjects and schizophrenia patients with various clinical phenotypes. During a 1-year period, 126 schizophrenic patients and 96 healthy control subjects were recruited. Serum BDNF protein levels were measured using an ELISA Kit. Psychiatric diagnoses were made according to DSM-IV criteria. One-way analysis of variance (ANOVA) showed no significant differences in serum BDNF protein levels between schizophrenia and healthy normals. Additionally, no significant differences existed in BDNF levels between schizophrenia patients for the following variables: with/without a suicide attempt; antipsychotic drug use, family tendency and disease onset before and after 25 years old. However, patients with catatonic schizophrenia had lower serum BDNF protein levels than patients with paranoid or residual schizophrenia. These analytical results suggested that BDNF might play an important role in the clinical subtypes of schizophrenia, but it needed further investigation in future.     

Brain-derived neurotrophic factor and electroconvulsive therapy in a schizophrenic patient with treatment-resistant paranoid-hallucinatory symptoms

It has been proposed that deficits in the production and the utilization of brain-derived neurotrophic factor (BDNF) may contribute to the pathogenesis of schizophrenia. At the same time, electroconvulsive shock, an experimental model of electroconvulsive therapy (ECT), has been shown to induce an increase of BDNF protein in brains of animal models. These findings suggest that one putative mechanism of action of ECT is the regulation of BDNF and/or related neurotrophins. In this case report, a 54-year-old man with severe treatment-resistant schizophrenic symptoms was treated with ECT. To evaluate the effect of ECT on BDNF serum levels, we collected a blood sample before each ECT session. During the course of ECT treatment, the paranoid and hallucinatory symptoms gradually improved, whereas BDNF levels increased over time. In addition, there was a general improvement of its positive and negative schizophrenic symptoms and depressive state. In conclusion, this case report further validates the therapeutic efficacy of ECT in schizophrenic patients with inadequate or poor response to traditional treatments. Moreover, ECT therapeutic effect is associated with an increase in BDNF serum levels. Further studies are needed to characterize the relationship between BDNF and ECT in schizophrenic patients.     

伴发迟发性运动障碍的精神分裂症患者血清脑源性神经营养因子水平的对照研究

目的 探讨外周血清脑源性神经营养因子(brain derived neurotrophic factor,BDNF)浓度与精神分裂症伴发的迟发性运动障碍(tadrive dyskinesia,TD)的关系.方法 收集精神分裂症伴发TD患者61例、不伴发TD的患者78例,以及正常对照102名.用酶联免疫吸附法检测BDNF水平,采用不自主运动量表(abnormal involuntary movement scale,AIMS)评估TD的严重程度,阳性和阴性症状量表(positive and negative symptom scale,PANSS)评估患者精神症状.结果 TD组、非TD组和对照组的BDNF水平分别为(9.35±1.60)μg/L、(10.12±2.03)μg/L、(12.27±2.7)μg/L,3组的差异有统计学意义(F=37.8,P<0.01);两两比较显示,TD组和非TD组均低于对照组(P<0.01),而TD组又低于非TD组(P<0.05).使用典型和非典型抗精神病药物患者之间的BDNF水平差异无统计学意义(P>0.05).TD组BDNF水平与AIMS总分、年龄、总病程负相关(r分别为-0.24、-0.32、-0.22,P均小于0.05),而在非TD组BDNF水平与上述因素均无相关(P>0.05).结论 精神分裂症伴发TD患者外周BDNF浓度下降,且其水平与异常运动严重程度相关,提示BDNF可能在TD的病理生理中发挥作用.