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 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.     

Association of serum BDNF levels with hippocampal volumes in first psychotic episode drug-naive schizophrenic patients

Evidence suggests that hippocampal volumetric abnormalities are present in first-episode schizophrenia. The hippocampus contains the highest brain levels of neurotrophic factors, which are major determinants of neuronal plasticity. Brain-derived neurotrophic factor (BDNF) influences neuronal survival, differentiation, synaptogenesis, and maintenance and is also correlated with neuronal activation in the hippocampus. BDNF is also involved in the development and modulation of dopaminergic-related systems. Alterations of serum BDNF levels have been shown in a number of studies with first episode patients with schizophrenia, probably reflecting an association between BDNF and the pathogenesis of the disorder. In the present study we investigated the correlation between serum BDNF levels and hippocampal volumes in a sample of first episode drug-na?ve patients with schizophrenia (FEP) and healthy control subjects. We found that hippocampal volume (HV) was decreased in FEP patients. Corrected right HV of FEP patients were significantly smaller compared to corrected right HVs of healthy subjects. The serum BDNF levels in the sample of FEP patients was significantly reduced compared to the healthy subjects. A significant positive association was found between serum BDNF and the corrected right HV in the group of patients such that the smaller the HV, the more reduced the serum BDNF levels. (Pearson r=0.452, p=0.045). Our findings indicate that low serum BDNF levels are associated with reduction in HV at the onset of schizophrenia and may further support the theory of a neuroprogressive-neurotoxic reaction associated with the onset of psychosis.     

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.     

Interaction of BDNF with cytokines in chronic schizophrenia

Brain-derived neurotrophic factor (BDNF) interacts with cytokines. Although both BDNF and cytokines occur at abnormal levels in schizophrenia patients, their interactions have not yet been examined. We therefore compared serum BDNF, TNF-α, interleukin (IL)-2, IL-6, and IL-8 levels in 92 chronically medicated schizophrenia patients and 60 healthy controls. We correlated these serum levels within these subject groups with each other and with clinical symptoms assessed according to the Positive and Negative Syndrome Scale (PANSS). Compared to the control group, the schizophrenia patients had significantly lower BDNF and TNF-α levels, and higher IL-2, IL-6, and IL-8 levels. The patients also showed a significant positive correlation between BDNF and both IL-2 and IL-8 levels, and low BDNF and TNF-α levels together were associated with poor performance on the PANSS cognitive factor. Thus, an interaction between cytokines and neurotrophic factors may be implicated in the pathophysiology of chronic schizophrenia. In particular, the cytokine TNF-α may interact with BNDF causing cognitive impairment.     

Lifestyle modification and behavior therapy effectively reduce body weight and increase serum level of brain-derived neurotrophic factor in obese non-diabetic patients with schizophrenia

The goal of the study was to elucidate the relationship between serum circulating brain-derived neurotrophic factor (BDNF) and body weight reduction via lifestyle modification and behavior therapy in obese non-diabetic patients with chronic schizophrenia. Thirty-three obese non-diabetic subjects with schizophrenia treated with stable antipsychotic medication in a day-care unit for at least 3 months were recruited. Thirty age-, body weight-matched subjects without psychiatric disorders were enrolled as controls. All participants underwent a 10-week weight reduction program, including lifestyle modification, psychosocial treatment, behavior therapy and exercise in the day-care unit. Blood biochemistry, serum BDNF, adipokine (adiponectin), inflammatory markers (C-reactive protein, tumor necrosis factor-alpha and interleukin-6) and oral glucose tolerance test were evaluated before and after the program. Serum BDNF concentrations were significantly lower among patients with schizophrenia compared to control subjects. Serum BDNF levels were significantly increased following the weight reduction program. Elevations in serum BDNF levels were positively correlated with body weight and body mass index reduction. Altogether, our results demonstrate that a non-pharmacological weight reduction program effectively reduces body weight with significant elevation of serum BDNF levels in obese non-diabetic patients with schizophrenia.     

Low serum levels of brain-derived neurotrophic factor in patients with schizophrenia do not elevate after antipsychotic treatment

Brain-derived neurotrophic factor (BDNF) has been suggested to be involved in the etiology of schizophrenia. There is a line of evidence that disruption of neurotrophins could play a role in the etiology of schizophrenia, and antipsychotics show their effect by altering levels of neurotrophins. The aim of this study was to evaluate the effect of antipsychotics on serum BDNF levels and their relationship with the symptoms in patients with schizophrenia. Twenty-two schizophrenia patients were enrolled in the study. The control group consisted of 22 age- and sex-matched physically and mentally healthy volunteers (7 male, 15 female). Serum BDNF levels and the positive and negative syndrome scale (PANSS) scores were recorded at baseline and after 6 weeks of treatment. Serum BDNF levels were also recorded in the control group. Schizophrenia patients who failed to meet 30% improvement in PANSS score were excluded from the study. The baseline serum BDNF levels of schizophrenia patients were lower than those of controls (t = 4.56; df = 21; p < 0.001). There was no correlation between serum BDNF levels and PANSS scores in patients with schizophrenia (p > 0.05). Although PANSS (for positive symptoms p < 0.001, for negative symptoms p < 0.001) and general psychopathology (t = 20.9; df = 22; p < 0.001) scores improved significantly after 6 weeks of antipsychotic treatment; there was no change in BDNF levels in patients' serum (p > 0.05). Our results support the view that BDNF would be associated with schizophrenia. However, we could not conclude that treatment with antipsychotics alters serum BDNF levels in patients with schizophrenia.     

Reduced serum BDNF levels in patients with chronic schizophrenic disorder in relapse,who were treated with typical or atypical antipsychotics

Brain-derived neurotrophic factor signals and dopaminergic function in the brain are strongly associated, and research on BDNF in schizophrenia may enhance our insights on the pathophysiological mechanisms of this disease. In the present study we aimed to investigate the possible association between serum BDNF levels and schizophrenic relapses and the possible differential effects of treatment with typical and atypical antipsychotics on serum BDNF levels in the same group of patients. We measured serum BDNF levels in 47 patients with schizophrenia during a relapse and again 6 weeks after administration of antipsychotic treatment (14 on risperidone, 18 on haloperidol, 10 on olanzapine and five on amisulpride) and in 44 healthy volunteers. Patients with schizophrenia showed reduced serum BDNF levels in relation to healthy volunteers at study entry. No significant differences were revealed in BDNF serum levels after 6 weeks of antipsychotic treatment in the patients compared to their own levels at study entry. However, serum BDNF was significantly increased in the subgroup receiving olanzapine compared to the other antipsychotics. Our findings may indicate a differential effect of olanzapine on BDNF levels compared to haloperidol, risperidone, and amisulpride.     

Clinical effectiveness of the Kampo medicine kamishoyosan for adjunctive treatment of tardive dyskinesia in patients with schizophrenia: a 16-week open trial

The purpose of the present study was to evaluate the clinical effectiveness of kamishoyosan for antipsychotic-induced tardive dyskinesia, and to investigate the relationship between tardive dyskinesia and serum brain-derived neurotrophic factor (BDNF) levels. Sixty-nine schizophrenia patients were enrolled; of these, 49 presented with tardive dyskinesia while the remaining 20 patients showed no tardive dyskinesia. The tardive dyskinesia group was treated for 16 weeks with kamishoyosan and assessed using the abnormal involuntary movement scale. The abnormal involuntary movement scale scores in the tardive dyskinesia group were evaluated at baseline and after 4, 8, and 16 weeks of treatment. The BDNF levels of all subjects were measured at baseline in order to compare differences in serum BDNF levels between the tardive dyskinesia group and the non-tardive dyskinesia group, and to correlate the severity of tardive dyskinesia and serum BDNF in the tardive dyskinesia group. A meaningful reduction in total abnormal involuntary movement scale scores was observed in the tardive dyskinesia group treated with kamishoyosan at 4, 8, and 16 weeks of treatment (P < 0.01). No significant differences in serum BDNF levels were detected between the tardive dyskinesia group and the non-tardive dyskinesia group at baseline. Furthermore, no significant correlation was seen between the severity of tardive dyskinesia and serum BDNF levels. The present study suggests that kamishoyosan might be a promising adjunctive treatment for antipsychotic-induced tardive dyskinesia.     

Serum brain-derived neurotrophic factor levels in patients with major depression: effects of antidepressants

This study tried to investigate the relationships between serum brain-derived neurotrophic factor (BDNF) protein levels and major depressive patients and discuss the effects of antidepressants on the serum BDNF protein levels. A total of 218 participants, including 111 patients with major depression (91 women) and 107 healthy controls (65 women), were recruited in this study. Serum BDNF protein levels were measured using an ELISA kit. Psychiatric diagnoses were made according to DSM-IV criteria. Severity of major depression was assessed by the 17-item Hamilton Depression Rating Scale. Using analysis of covariance with age adjustment, there were significantly low serum BDNF protein levels in depressive patients than healthy controls in women (F=7.530, p=0.007), but not in men. Additionally, changes in serum BDNF protein levels were significantly increased in 79 patients taking antidepressants during a period of 4 weeks (t=2.116, p=0.038), especially in 61 women (t=2.542, p=0.014). Age-adjusted ANCOVA revealed no significant differences in serum BDNF protein levels between 58 responders and 21 non-responders (F=0.008, P=0.928). In responders, there were significantly increased changes in serum BDNF protein levels in 44 women (t=2.501, p=0.016), but not in 14 men (t=-0.767, p=0.457). These analytical results suggest that low serum BDNF may play an important role in depressive women and antidepressant treatment significantly increase serum BDNF. However, further studies of larger populations are necessary to confirm these results and further elucidate the effects of different classes of antidepressants on serum BDNF protein levels.     

BDNF serum and CSF concentrations in Alzheimer's disease, normal pressure hydrocephalus and healthy controls

Alzheimer's disease (AD) and normal pressure hydrocephalus (NPH) are common forms of dementia in the elderly. Recent findings have suggested an involvement of brain-derived neurotrophic factor (BDNF) in the pathogenesis of AD. BDNF is an endogenous protein involved in the maintenance of neuronal function, synaptic plasticity and structural integrity in the adult brain. BDNF serum and cerebrospinal fluid (CSF) concentrations were assessed by a sensitive ELISA in 27 AD patients in comparison to 9 NPH patients and 28 age-matched healthy controls (10 CSF samples). We found a significant decrease of BDNF serum concentration in AD (18.6ng/ml) and NPH patients (18.1ng/ml) as compared to healthy controls (21.3ng/ml; p=0.041/p=0.017). BDNF serum concentrations did not correlate with CSF levels, age or MMSE scores both in AD and NPH patients. In unconcentrated CSF samples, BDNF could be detected in AD patients in 8/27 cases (29.6%; mean of 4.6pg/ml), in NPH patients in 1/9 cases (11.1%; mean of 6.4pg/ml) and in the control subjects in 5/10 cases (50%; mean of 1.6pg/ml) with no significant differences as regards mean concentration and frequency of detectable BDNF in CSF. The decrease of BDNF serum levels in AD and NPH may reflect a lack of trophic support and thus contribute to progressive degeneration in both diseases. In contrast to serum, CSF seems to be no useful source to determine BDNF in AD or NPH because of too low concentrations. Further examinations have to follow to elucidate the potential sources and the meaning of reduced BDNF levels in the blood in AD and NPH.     

Cognitive function and serum levels of brain-derived neurotrophic factor in patients with bipolar disorder

Objectives:  Brain-derived neurotrophic factor (BDNF) is an important contributor to the pathophysiology of bipolar disorder (BD), and abnormalities in the BDNF-signaling system may be implicated in the cognitive decline observed in BD patients. We aimed to investigate serum BDNF levels in BD patients and its relation to neurocognitive function.
Methods:  We measured serum BDNF levels using an enzyme-linked immunosorbent assay method in 65 euthymic type I BD patients and 50 healthy controls, and administered a neuropsychological test battery to assess attention and mental control, perceptual-motor skills, executive functions, verbal fluency and abstraction, visuospatial attention, and memory.
Results:  We found no significant differences regarding serum BDNF levels in BD patients and healthy controls. We found significant positive associations between serum BDNF levels and illness duration, and manic and depressive episodes in female BD patients only. Serum BDNF levels were lower in patients medicated with antipsychotics and/or lithium, whereas patients on valproate and/or antidepressants showed higher serum BDNF levels. Patients performed significantly worse on 11 out of 16 neurocognitive tests as compared to controls. We found a significant positive association between serum BDNF levels and a test of verbal fluency in both BD patients and controls.
Conclusions:  Present results support the hypothesis that BDNF normalizes with mood stabilization and pharmacological treatment. Our findings in young and physically healthy patients with short illness duration and few mood episodes may explain the lack of association between serum BDNF levels and neurocognitive performance, even though cognitive performance in patients was overall significantly worse as compared to healthy controls.     

The relationship between metabolic syndrome,BDNF, and vitamin D in patients with schizophrenia

The objective of this study is to investigate the relationship between anthropometric (BMI and waist circumference), metabolic (glucose, insulin, insulin resistance, HbA1c, and lipid profile), psychopathologic (Positive and Negative Syndrome Scale, PANSS) parameters with vitamin D and serum brainderived neurotrophic factor (BDNF) levels in patients with schizophrenia. The study population consisted of 54 healthy control subjects, and 64 volunteer patients, monitored in the psychiatry outpatient clinics of Antalya Education and Research Hospital. Serum glucose, HDL, LDL, triglyceride, total cholesterol levels (spectrophotometric method), HbA1c (HPLC method), insulin, and vitamin 25(OH)D (chemiluminescence method), with HOMA-IR (numerical calculation), and serum BDNF levels (sandwich ELISA, enzymelinked immunosorbent assay) were quantitatively evaluated using respective analytical methods indicated in parentheses. Twenty-seven (42.18%) of 64 schizophrenia patients were diagnosed with MetS. In schizophrenia patients diagnosed with metabolic syndrome (MetS), PANSS-negative and -positive symptom scores were significantly higher, while serum BDNF levels were significantly lower. In patients with schizophrenia, significantly negative correlations were detected between PANSS-negative and -positive symptom scores, and BDNF (p < 0.001 and p < 0.001, respectively), and also between PANSS-negative symptom score and vitamin D (p = 0.022). Lower serum BDNF levels may be related to increases in the possible development of MetS and psychotic symptoms. Decrease in vitamin D levels in schizophrenia patients may be associated with an increase in PANSS-negative symptom scores. In schizophrenia patients with MetS, psychotic symptoms may be more severe.     

Effects of brain‐derived neurotrophic factor Val66Met polymorphism on hippocampal volume change in schizophrenia

A functional polymorphism of the brain‐derived neurotrophic factor (BDNF) gene (Val66Met) has been associated with the risk for schizophrenia and volume differences in the hippocampus. However, little is known about the association between progressive brain volume change in schizophrenia and BDNF genotype. The aim of this study was to investigate the relationship between hippocampal volume change in patients with schizophrenia and healthy control subjects and BDNF genotype. Two structural magnetic resonance imaging brain scans were acquired of 68 patients with schizophrenia and 83 healthy subjects with an interval of approximately 5 yrs. Hippocampal volume change was measured and related to BDNF genotype in patients and healthy controls. BDNF genotype was not associated with hippocampal volume change over time in patients or healthy controls, nor could we replicate earlier findings on smaller hippocampal volume in Met‐carriers. However, we did find a genotype‐by‐diagnosis interaction at baseline demonstrating smaller hippocampal volumes in patients homozygous for the Val‐allele relative to healthy Val‐homozygotes. In addition, irrespective of genotype, patients showed smaller hippocampal volumes compared with healthy controls at baseline. In summary, our results suggest that the BDNF Val66Met polymorphism is not associated with hippocampal volume change over time. Nevertheless, our findings may support the possibility that BDNF affects brain morphology differently in schizophrenia patients and healthy subjects. © 2009 Wiley‐Liss, Inc.     

帕利哌酮对精神分裂症患者临床症状、认知功能及神经营养因子的影响

目的探讨帕利哌酮对精神分裂症患者的临床症状、认知功能及神经营养因子水平的影响,为临床精神分裂症的合理用药提供参考。方法选取在天津市安定医院住院的符合《国际疾病分类(第10版)》(ICD-10)精神分裂症诊断标准的患者60例为研究组,同期选取60例健康志愿者作为对照组。研究组接受帕利哌酮治疗12周。于治疗前后采用阳性和阴性症状量表(PANSS)评定研究组临床症状;采用Stroop测验(SCWT)、数字符号编码测验(DSCT)、持续操作测验(CPT)和连线测验A(TMTA)评定对照组和研究组认知功能;采用酶联免疫吸附技术检测两组血清脑源性神经营养因子(BDNF)、神经生长因子(NGF)和神经营养因子3(NT-3)水平。结果研究组治疗前后PANSS总评分比较差异有统计学意义[(78.12±11.84)分vs.(38.45±7.24)分,Z=24.14,P0.01];治疗后,研究组认知功能指标(SCWT、CPT、DCST及TMTA时间)、BDNF、NGF及NT-3水平均较治疗前高,但仍低于对照组,差异均有统计学意义(P均0.01)。结论帕利哌酮有助于改善精神分裂症患者的临床症状和认知功能,治疗机制可能与上调血清神经营养因子水平有关。     

Combining ECT with pharmacological treatment of depressed inpatients in a naturalistic study is not associated with serum BDNF level increase

BackgroundBDNF blood levels are reduced in MDD. They can be increased with pharmacologic treatment and ECT, but it is not clear whether the combination of treatments promotes an additional increase. The present study aims to evaluate whether combined treatment promotes an increase in BDNF, restoring the level to that of non-depressed controls.MethodsNinety-nine adult inpatients were invited to participate in this naturalistic prospective cohort study between May 2011 and April 2013. Diagnosis was made by MINI, and the symptoms were evaluated at admission and at discharge by HDRS-17. Those inpatients with a diagnosis of depression were included and divided into two groups: those who underwent combined ECT and medication (31 subjects) and those who used only pharmacotherapy (68 subjects). Serum BDNF was measured in blood samples collected at admission and discharge. One hundred healthy blood donors without any psychiatric diagnosis were included as a control group.ResultsThere were no significant differences in serum BDNF levels between the combined and pharmacological groups at admission and at discharge, and no significant variation in BDNF occurred in any group during the treatment. There were no interactions between time and treatment groups nor significant time effects or treatment group effects for BDNF in the Generalized Estimating Equation Model (GEE). The control group had significantly higher serum BDNF levels in comparison with each of the treatment groups at admission and discharge (p = 0.00).ConclusionCombination of ECT with pharmacological treatment did not result in increased serum BDNF levels and did not restore levels to that of controls.     

Serum levels of brain-derived neurotrophic factor in patients with internet use disorder

Internet use disorder (IUD) is characterised by excessive internet gaming use and has temporarily been conceptualised as a behavioural addiction. Since brain-derived neurotrophic factor (BDNF) has been hypothesised to be involved in the development and maintenance of addictive disorders, we investigated BDNF expression in IUD. We measured BDNF serum levels in male patients with IUD (n=11) and individually matched healthy controls (n=10). There was no significant difference in BDNF serum levels of patients with IUD in comparison to control subjects. Serum levels of BDNF were not correlated with severity of IUD or clinical and demographic variables in our study. These preliminary findings possibly suggest a different underlying pathophysiology in IUD compared to addictive disorders. Thus, further studies are needed to clarify, whether IUD represents an addictive spectrum disorder, an impulse control disorder or finally an individual diagnostic entity that overlaps with both disease categories.     

重复经颅磁刺激对首发精神分裂症患者血清脑源性神经营养因子的影响

目的分析高频重复经颅磁刺激(rTMS)对首发精神分裂症患者血清脑源性神经营养因子(BDNF)的影响。方法选取82例以阴性症状为主的首发精神分裂症患者,使用随机数表将82例患者分为对照组41例和观察组41例,2组均使用常规药物治疗,观察组同时予以真刺激治疗,对照组予以假刺激治疗,对比2组治疗结果。结果治疗4周后观察组PANSS(阳性和阴性症状量表)总分、阴性症状评分、一般病理评分及血清BDNF浓度均优于治疗前,且优于对照组(P0.05);对照组PANSS总分、阴性症状评分、阳性症状评分、一般病理评分及血清BDNF浓度与之前相比无明显变化(P0.05)。观察组BDNF浓度变化与PANSS总分及各因子的变化无明显相关性(P0.05)。结论rTMS可显著增加首发精神分裂症患者的血清BDNF水平,但血清BDNF水平变化与其临床症状的改善无明显相关性。     

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。     

Serum brain-derived neurotrophic factors in Taiwanese patients with drug-naïve first-episode schizophrenia: Effects of antipsychotics

Objectives: Brain-derived neurotrophic factors (BDNF) are known to be related to the psychopathology of schizophrenia. However, studies focussing on drug-naïve first-episode schizophrenia are still rare.

Methods: Over a 5-year period, we investigated the serum BDNF levels in patients with first-episode drug-naïve schizophrenia and compared them to age- and sex-matched healthy controls. We also explored the association between antipsychotic doses, positive and negative syndrome scale (PANSS) scores, and serum BDNF levels before and after a 4-week antipsychotic treatment.

Results: The baseline serum BDNF levels of 34 patients were significantly lower than those of the controls (df?=?66, P?=?.001). Although the PANSS scores of 20 followed-up patients improved significantly after antipsychotic treatment, the elevation of the serum BDNF levels was not statistically significant (P?=?.386). In addition, Pearson’s correlation test showed significant correlations between pre-treatment negative scale scores and percentage changes in BDNF (P?=?.002).

Conclusions: The peripheral BDNF levels in Taiwanese patients with drug-naïve first-episode schizophrenia, compared with healthy controls, did not elevate after antipsychotic treatment, and pre-treatment negative symptoms played a pivotal role in trajectories of serum BDNF levels. Large samples will be needed in future studies to verify these results.