Study Of Brain-derived Neurotrophic Factor Research Articles

Study of Brain-derived Neurotrophic Factor in Drug-naive Patients with Schizophrenia

Abstract Background and Aim: Brain-derived neurotrophic factor (BDNF) is a widely studied neurotrophin and is said to be involved in the regulation of many neuronal processes, including neurogenesis, neuronal differentiation, maturation, and survival. Over the years, research has shown a significant variation of serum BDNF levels in schizophrenia with no widespread agreement. Herein, we report on serum BDNF levels in drug-naive patients of schizophrenia in comparison to healthy controls (HC) and correlates of BDNF levels in patients of schizophrenia. Materials and Methods: The study sample consisted of 120 participants with 60 drug-naive patients of schizophrenia and 60 HC. The blood sample of the study subjects was collected and processed serum was analyzed using an enzyme-linked immunosorbent assay kit for BDNF levels. Clinical assessment of patients was done using the Positive and Negative Syndrome Scale (PANSS) and Montreal Cognitive Assessment. Results: Serum BDNF levels were significantly lower in drug-naive patients of schizophrenia as compared to age and sex-matched HC (P – 0.024). The PANSS total score and positive subscale score were negatively correlated with serum BDNF levels which were statistically significant with P = 0.005 and P = 0.001, respectively. Conclusion: The index study found BDNF levels to be reduced in patients of schizophrenia and BDNF was found to correlate with severity of illness, especially positive symptoms. Thus, developing therapeutic strategies that can activate BDNF signaling may prove beneficial in improving the clinical outcome of schizophrenia.

Correlation study of brain-derived neurotrophic factor, EEG γ activity and cognitive function in first-episode schizophrenia

BackgroundSchizophrenia is characterised by neurotrophic, neuroelectrophysiological and cognitive dysfunction. However, there exists a paucity of research examining the association between serum brain-derived neurotrophic factor (BDNF) concentration, resting electroencephalogram (EEG) gamma activity, and cognitive impairment in individuals diagnosed with schizophrenia. MethodsIn this study, 87 first-episode schizophrenia patients and 75 healthy controls were assessed. Measurements were conducted to determine the levels of BDNF, resting EEG γ-activity at left and right frontal pole EEG electrodes respectively (FP1/FP2) leads, and cognitive function as assessed by the Measurement and Treatment Research to Improve Cognition in Schizophrenia MATRICS Consensus Cognitive Battery (MCCB). Comparisons were made between the patient group and the control group, revealing lower BDNF levels, lower T-scores for 7 MCCB cognitive items, and higher EEG γ-activity among patients when compared to controls. ResultsAccording to the correlation analysis, there were significant associations observed in the patient group. BDNF levels were found to be correlated with EEG γ activity as well as T-scores of speed of processing (SoP), verbal learning (VeL), and reasoning problem-solving (RPS). Moreover, EEG γ activity showed an association with both the total score of the Positive and Negative Syndrome Scale (PANSS) and T-score of SoP. These findings suggest a potential relationship between BDNF levels, EEG γ activity, cognitive domains, and clinical symptoms in individuals with first-episode schizophrenia. ConclusionsIn conclusion, our findings demonstrate the coexistence of neurobiochemical and electrophysiological abnormalities alongside cognitive dysfunction during the early stages of schizophrenia. These findings provide valuable insights into the mechanism of cognitive impairment in schizophrenia. By highlighting the simultaneous occurrence of these factors, our study contributes to a better understanding of the complex nature of schizophrenia and emphasizes the importance of studying its cognitive aspects.

Comparative psychopharmacology of autism and psychotic-affective disorders suggests new targets for treatment.

The first treatments showing effectiveness for some psychiatric disorders, such as lithium for bipolar disorder and chlorpromazine for schizophrenia, were discovered by accident. Currently, psychiatric drug design is seen as a scientific enterprise, limited though it remains by the complexity of brain development and function. Relatively few novel and effective drugs have, however, been developed for many years. The purpose of this article is to demonstrate how evolutionary biology can provide a useful framework for psychiatric drug development. The framework is based on a diametrical nature of autism, compared with psychotic-affective disorders (mainly schizophrenia, bipolar disorder and depression). This paradigm follows from two inferences: (i) risks and phenotypes of human psychiatric disorders derive from phenotypes that have evolved along the human lineage and (ii) biological variation is bidirectional (e.g. higher vs lower, faster vs slower, etc.), such that dysregulation of psychological traits varies in two opposite ways. In this context, the author review the evidence salient to the hypothesis that autism and psychotic-affective disorders represent diametrical disorders in terms of current, proposed and potential psychopharmacological treatments. Studies of brain-derived neurotrophic factor, the PI3K pathway, the NMDA receptor, kynurenic acid metabolism, agmatine metabolism, levels of the endocannabinoid anandamide, antidepressants, anticonvulsants, antipsychotics, and other treatments, demonstrate evidence of diametric effects in autism spectrum disorders and phenotypes compared with psychotic-affective disorders and phenotypes. These findings yield insights into treatment mechanisms and the development of new pharmacological therapies, as well as providing an explanation for the longstanding puzzle of antagonism between epilepsy and psychosis.Lay Summary: Consideration of autism and schizophrenia as caused by opposite alterations to brain development and function leads to novel suggestions for pharmacological treatments.

Study of brain-derived neurotrophic factor in the serum of patients with systemic lupus erythematosus

ObjectivesBrain-derived neurotrophic factor (BDNF) is an important mediator of neuronal development, survival, and function. It is related to the pathogenesis of several neuropsychiatric disorders. The aim of this study was to determine the relationship between serum BDNF (sBDNF) level and neuropsychiatric status in systemic lupus erythematosus (SLE) patients.Patients and methodsThis study included the following groups: group I included 35 SLE patients with neuropsychiatric systemic lupus erythematosus (NPSLE) manifestations, group II included 30 SLE patients without neuropsychiatric manifestations, group III included 15 patients with neuropsychiatric disorders due to causes other than SLE, and group IV included 15 apparently healthy volunteers. All groups were matched for age and sex. SLE disease activity was assessed using the SLE Disease Activity Index. A Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, 4th ed., Axis I was used for the assessment of psychiatric disorders, whereas neurological disorders were assessed by an expert neurologist. sBDNF was measured by the enzyme-linked immunosorbent assay.ResultsThere was a statistically significant increase (P<0.05) in the mean titer of sBDNF in group I compared with other groups (314.9±162.1, 151.1±188.2, 218.1±198.4, and 141.9±130.2 ng/ml in groups I, II, III, and IV, respectively), as well as in group III compared with groups II (P<0.05) and IV (P<0.05). The mean serum titer of BDNF was statistically significantly elevated in active NPSLE patients (320.7±156.2 ng/ml, P<0.05) compared with inactive NPSLE (210.6±141.89.6 ng/ml, P<0.05), active SLE (142.8±162.7 ng/ml, P<0.05), and inactive SLE (139.8±174.8 ng/ml, P<0.05) without neuropsychiatric manifestations.ConclusionVariation in sBDNF level between SLE patients with and without neuropsychiatric manifestations indicates that it has a particular role in NPSLE disease process. Likely, it could be used as a biological marker for determining NPSLE disease activity.

Family-based study of brain-derived neurotrophic factor ( ΒDNF) gene polymorphism in alcohol dependence

Brain-derived neurotrophic factor (BDNF) belongs to a family of proteins related to the nerve growth factor family, which are responsible for the proliferation, survival and differentiation of neurons. BDNF is thought to be involved in the pathogenesis of bipolar disorder, schizophrenia, eating disorders and addiction. We hypothesize that a functionally relevant polymorphism of the ΒDNF gene promoter may be associated with the pathogenesis of alcohol dependence.We performed an association study of 141 families with alcohol dependence. One hundred and thirty-eight healthy control subjects were matched based on ethnicity and gender. An association between the ΒDNF Val66Met gene polymorphism and alcoholism was not found.

Association study of brain-derived neurotrophic factor and apolipoprotein E polymorphisms and cognitive function in aged males without dementia

Genetic factors for inter-individual variation in cognition have been arousing great interest among researchers. Among the many associated genes, brain-derived neurotrophic factor (BDNF) and apolipoprotein E (APOE), as two of the most frequently studied, might be good prospects for cognitive genetics. Thus, the aim of this study was to investigate both the isolated and cooperative effect of BDNF and APOE on normal cognitive ageing. A homogeneous population of Chinese aged males (N=161) were genotyped for functional genetic variants of BDNF (BDNF-G196A) and APOE (APOE-epsilon4) and assessed by a comprehensive neuropsychological measurement (Cognitive Abilities Screening Instrument Chinese version; CASI C-2.0). Thereafter genotypic group differences of BDNF and APOE in CASI cognitive profiles were tested. Results from the present study suggest the possible influence of APOE on specific cognitive domains (CASI orientation and language domains; p=0.010 and 0.028, respectively), whereas there was no significant role of BDNF, either solely or with APOE, in cognition in the elderly. Our findings suggest a possible association between APOE-epsilon4 and specific cognitive domains in the aged male, whereas the functional genetic variant of BDNF (BDNF-G196A) played no significant role in normal cognitive ageing.

Immunohistochemical study of brain-derived neurotrophic factor and its receptor, TrkB, in the hippocampal formation of schizophrenic brains

Recently, the pathogenesis of schizophrenia has been investigated from the perspective of neurodevelopmental dysfunction theory. On the other hand, it has been indicated that neurotrophic factors, such as nerve growth factors, brain-derived neurotrophic factor (BDNF), and neurotrophin-3, are significantly involved in the development and functional differences of central nervous system (CNS). Some reports proposed that the dysfunction of these factors could explain the pathogenesis of schizophrenia possibly. In this study, the authors investigated immunohistochemically the distribution and/or morphology of BDNF and TrkB, its peculiar receptor, in the hippocampal formation of schizophrenic brain. As a result, BDNF-positive pyramidal cells in the CA2 and neurons in the CA3 and the field of the CA4 were intensely stained compared to those of normal control. Staining of TrkB-positive neurons showed a signet-ring like shape in the hippocampus of normal control brains. Such figures were not observed on staining of those neurons from schizophrenic brains. In the control cases, TrkB-immunopositive varicose fibers were frequently seen. Those observed differences between schizophrenic and normal cases may indicate the existence of dysfunction of BDNF and TrkB in schizophrenic brain, and this dysfunction may be one of the factors involved in the pathogenesis of schizophrenia.