Brain-derived Neurotrophic Factor In Patients Research Articles

Growth Factor Gene Therapy for Alzheimer's Disease.

Nervous system growth factors are natural proteins of the brain that influence neuronal survival and function throughout life, from embryonic development to old age. In animal models of Alzheimer's disease (AD), the growth factor brain derived neurotrophic factor (BDNF) prevents neuronal death, activates neuronal function, builds new synapses and improves learning and memory. Accordingly, we are determining whether gene delivery of BDNF in patients with AD will slow disease progression and improve memory. In a previous clinical trial of nerve growth factor (NGF) gene therapy in AD patients (NCT00017940, June 2001), we learned that growth factors can unequivocally elicit classic trophic responses from degenerating neurons in AD. Experience gained from the earlier NGF gene therapy trial is guiding our effort to optimize gene delivery of BDNF in our present clinical program (NCT05040217, June 2021).

Cardiovascular and kidney diseases are positively associated with neuroinflammation and reduced brain-derived neurotrophic factor in patients with severe COVID-19

Even though respiratory dysfunctions are the primary symptom associated with SARS-CoV-2 infection, cerebrovascular events, and neurological symptoms are described in many patients. However, the connection between the neuroimmune profile and the lung's inflammatory condition during COVID-19 and its association with the neurological symptoms reported by COVID-19 patients still needs further exploration. The present study characterizes the SARS-CoV-2 infectivity profile in postmortem nervous and lung tissue samples of patients who died due to severe COVID-19, and the pro-inflammatory factors present in both nervous and lung tissue samples, via a proteomic profiling array. Additionally, Brain-Derived Neurotrophic Factor (BDNF) levels and intracellular pathways related to neuroplasticity/neuroprotection were assessed in the samples. Out of the 16 samples analyzed, all samples but 1 were positive for the viral genome (genes E or N2, but only 3.9% presented E and N2) in the olfactory brain pathway. The E or N2 gene were also detected in all lung samples, with 43.7% of the samples being positive for the E and N2 genes. In the E/N2 positive brain samples, the Spike protein of SARS-CoV-2 co-localized with TUJ-1+ (neuron-specific class III beta-tubulin) and GFAP+ (glial fibrillary acidic protein) astrocytes. IL-6, but not IL-10, expression was markedly higher in most nervous tissue samples compared to the lung specimens. While intracellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), macrophage migration inhibitory factor (MIF), and plasminogen activator inhibitor 1 (PAI-1) were increased in lung samples from SARS-Cov-2 patients, only MIF and IL-18 were detected in nervous tissue samples. Correlation analysis suggested that high levels of IL-6 are followed by increased levels of IL-10 in the brain, but not in lung samples. Our analysis also demonstrated that the presence of comorbidities, such as cardiovascular disease, hypertension, and hypothyroidism, is associated with neuroinflammation, while chronic kidney conditions predict the presence of neurological symptoms, which correlate with lower levels of BDNF in the brain samples. Our results corroborate the hypothesis that a pro-inflammatory state might further impair neural homeostasis and induce brain abnormalities found in COVID-19 patients.

Shugan Jieyu capsule effects on peripheral blood micro-124, micro-132, and brain-derived neurotrophic factor in patients with mild to moderate depression

BACKGROUND To assess the effectiveness of Shugan Jieyu capsules on peripheral blood miR-124, miR-132, and brain-derived neurotrophic factor (BDNF) levels in patients with mild to moderate depression following coronary artery intervention [percutaneous coronary intervention (PCI)] for coronary heart disease. AIM To evaluate the therapeutic efficacy of Shugan Jieyu capsules and their effects on the peripheral blood levels of miR-124, miR-132, and BDNF in patients with mild to moderate depression following PCI for coronary heart disease. METHODS Patients with mild-to-moderate depression of the liver-qi stagnation type after PCI for coronary heart disease at the 305th Hospital of the People’s Liberation Army were enrolled from June 2022 to November 2023 and randomly assigned to two groups: Experimental (treated with Shugan Jieyu capsules) and control (treated with escitalopram oxalate tablets). This study compared the antidepressant effects of these treatments using 17-item Hamilton Rating Scale for Depression (HAMD-17) scores, metabolic equivalents, low-density lipoprotein cholesterol, BDNF, high-sensitivity C-reactive protein levels, miR-124 and miR-132 levels, distribution of immune-related lymphocyte subsets, and traditional Chinese medicine syndrome scores before and after 6 weeks of treatment. RESULTS No significant difference was observed in any index between the two groups before treatment (P > 0.05). After treatment, the total efficacy rates were 93.33% and 90.00% in the experimental and control groups, respectively. Experimental group had significantly lower scores for the main and secondary syndromes compared to the control group (P < 0.05). No significant difference was observed in the metabolic equivalents between the two groups before and after treatment (P > 0.05). The levels of low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and miR-132 were significantly lower, whereas those of miR-124, BDNF, CD3+T lymphocytes, CD3+CD4+T helper lymphocytes, and CD3+CD4+/CD3+CD8+ cells were significantly higher in the experimental group compared to the control group (P < 0.05). The incidence of adverse reactions during experimental group was significantly lower than that in control group (P < 0.05). CONCLUSION Shugan Jieyu capsules have good efficacy in patients with mild-to-moderate depression after PCI, and its mechanism may contribute to the regulation of miR-124, miR-132, BDNF levels, and lymphoid immune cells.

Cognitive functions and the brain-derived neurotrophic factor in patients with mild autonomous cortisol secretion.

The impact of abnormal cortisol secretion on cognitive functions in patients with mild autonomous cortisol secretion (MACS) remains uncertain. To assess cognitive functions, determine serum brain-derived neurotrophic factor (BDNF) concentration in patients with MACS, and investigate the association between cognitive subdomains and BDNF. We prospectively recruited 84 participants-28 patients with MACS, 28 patients with nonfunctional adrenal adenoma (NFAA), and 28 control subjects matched for age, gender, body mass index (BMI), visceral adiposity, and educational level. The serum BDNF concentration of participants was measured. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition-focused interviews and Montreal Cognitive Assessments (MoCA) were carried out by an experienced psychiatrist. Patients with MACS had a higher serum BDNF concentration than the NFAA (P = .001), while that of patients with NFAA was lower than the controls (P = .044). Linear regression analysis revealed BMI and morning cortisol after overnight 1 mg dexamethasone (DST) were mostly associated with BDNF (P < .05). No significant difference was found in MoCA scores between MACS and NFAA groups (P = .967), whereas those were lower than the control group (P = .004). When the cognitive subdomains were examined separately, MACS group performed higher memory score than NFAA (P = .045), but lower language scores than both the NFAA (P = .024) and control groups (P < .001). In the whole group, BDNF concentration was positively correlated with memory score (r = 0.337, P = .002), whereas DST was negatively correlated with language score (r = -0.355, P = .008). Low-grade hypercortisolism is associated with elevated BDNF concentrations, which may be a protective factor for memory function in patients with MACS relative to those with NFAA.

Investigating the role of TGF-β and BDNF in cancer-related depression: a primary cross-sectional study.

Cancer-related depression is a well-documented condition that significantly impacts long-term quality of life. Brain-derived neurotrophic factor (BDNF), a neurotrophin essential for neurogenesis and neuronal plasticity, has been implicated in various neuropsychological disorders including depression associated with cancer. Cytokines, on the other hand, play a crucial role in regulating depression, potentially by influencing BDNF expression. Transforming growth factor-β (TGF-β), a key immune regulator within the tumor microenvironment, has been found to elevate BDNF levels, establishing a link between peripheral immune responses and depression. The study aims to investigate the correlation of TGF-β and BDNF in cancer-related depression. This study involved a cohort of 153 gynecological patients, including 61 patients with gynecological cancer and 92 patients without cancer. Depression levels were assessed using the subscale of Hospital Anxiety and Depression Scale (HADS-D), and TGF-β and BDNF plasma levels were measured using enzyme-linked immunosorbent assay (ELISA). The study revealed elevated plasma TGF-β levels in patients with cancer (32.24 ± 22.93 ng/ml) compared to those without cancer (25.24 ± 19.72 ng/ml) (P = 0.046). Additionally, reduced levels of BDNF were observed in patients presenting depression symptoms (44.96 ± 41.06 pg/ml) compared to those without depression (133.5 ± 176.7 pg/ml) (P = 0.036). Importantly, a significant correlation between TGF-β and BDNF was found in patients without cancer but with depression (correlation coefficient = 0.893, **P < 0.01). Interestingly, cancer appeared to influence the association between TGF-β and BDNF in patients with depression, as evidenced by a significant difference in the correlation of TGF-β and BDNF between cancer and non-cancer groups (P = 0.041). These findings underscore the active involvement of TGF-β and BDNF crosstalk in the context of cancer-related depression.

A prognostic neural epigenetic signature in high-grade glioma

Neural–tumor interactions drive glioma growth as evidenced in preclinical models, but clinical validation is limited. We present an epigenetically defined neural signature of glioblastoma that independently predicts patients’ survival. We use reference signatures of neural cells to deconvolve tumor DNA and classify samples into low- or high-neural tumors. High-neural glioblastomas exhibit hypomethylated CpG sites and upregulation of genes associated with synaptic integration. Single-cell transcriptomic analysis reveals a high abundance of malignant stemcell-like cells in high-neural glioblastoma, primarily of the neural lineage. These cells are further classified as neural-progenitor-cell-like, astrocyte-like and oligodendrocyte-progenitor-like, alongside oligodendrocytes and excitatory neurons. In line with these findings, high-neural glioblastoma cells engender neuron-to-glioma synapse formation in vitro and in vivo and show an unfavorable survival after xenografting. In patients, a high-neural signature is associated with decreased overall and progression-free survival. High-neural tumors also exhibit increased functional connectivity in magnetencephalography and resting-state magnet resonance imaging and can be detected via DNA analytes and brain-derived neurotrophic factor in patients’ plasma. The prognostic importance of the neural signature was further validated in patients diagnosed with diffuse midline glioma. Our study presents an epigenetically defined malignant neural signature in high-grade gliomas that is prognostically relevant. High-neural gliomas likely require a maximized surgical resection approach for improved outcomes.

NeuroGenetics of Alzheimer’s Disease: Cross-Linking BDNF Brain-Derived Neurotrophic Factor in the Genetic Nexus of Type II Diabetes and Dementia

Background: Alzheimer’s disease and dementia are commonly associated with aging, particularly in the context of Type II Diabetes Mellitus (Type II DM), which is known to exacerbate micro and macrovascular complications that affect cognitive functions. The Brain-Derived Neurotrophic Factor (BDNF) gene has been implicated in the neurodegenerative processes that underscore these conditions. Objective: This study aimed to investigate the expression of the BDNF gene in diabetic patients with dementia and analyze its correlation with cognitive impairment, to establish BDNF as a potential biomarker for early detection and therapeutic targeting. Methods: A cohort of 102 patients with diabetic dementia and 32 healthy controls was enrolled. EDTA blood samples were collected and processed to measure BDNF serum levels using a Chemiluminescent Immunoassay (CLIA). Genomic DNA was isolated, and its integrity was confirmed via UV spectrophotometry and gel electrophoresis. The bisulfite DNA modification and Methylation-Specific PCR were conducted to analyze BDNF gene expression, followed by quantitative real-time PCR. Cognitive function was assessed using Mini-Mental State Examination (MMSE). Results: The study revealed a significant decrease in BDNF serum levels in diabetic dementia patients (12.6 ng/mL) compared to healthy controls (34.8 ng/mL), with MMSE scores averaging at 13.2 and 24.6, respectively. BDNF gene expression showed a 4.1-fold decrease in the dementia group. Statistical analysis indicated that these differences were significant (p&lt;0.05). Conclusion: The reduced expression of BDNF in patients with diabetic dementia confirms its potential as a biomarker for cognitive impairment. Early detection and intervention strategies that modulate BDNF could ameliorate the impact of dementia in the context of diabetes.

The relevance of BDNF for neuroprotection and neuroplasticity in multiple sclerosis.

Neuroplasticity as a mechanism to overcome central nervous system injury resulting from different neurological diseases has gained increasing attention in recent years. However, deficiency of these repair mechanisms leads to the accumulation of neuronal damage and therefore long-term disability. To date, the mechanisms by which remyelination occurs and why the extent of remyelination differs interindividually between multiple sclerosis patients regardless of the disease course are unclear. A member of the neurotrophins family, the brain-derived neurotrophic factor (BDNF) has received particular attention in this context as it is thought to play a central role in remyelination and thus neuroplasticity, neuroprotection, and memory. To analyse the current literature regarding BDNF in different areas of multiple sclerosis and to provide an overview of the current state of knowledge in this field. To date, studies assessing the role of BDNF in patients with multiple sclerosis remain inconclusive. However, there is emerging evidence for a beneficial effect of BDNF in multiple sclerosis, as studies reporting positive effects on clinical as well as MRI characteristics outweighed studies assuming detrimental effects of BDNF. Furthermore, studies regarding the Val66Met polymorphism have not conclusively determined whether this is a protective or harmful factor in multiple sclerosis, but again most studies hypothesized a protective effect through modulation of BDNF secretion and anti-inflammatory effects with different effects in healthy controls and patients with multiple sclerosis, possibly due to the pro-inflammatory milieu in patients with multiple sclerosis. Further studies with larger cohorts and longitudinal follow-ups are needed to improve our understanding of the effects of BDNF in the central nervous system, especially in the context of multiple sclerosis.

Abnormal Serum BDNF and p-mTOR in MDD in Adolescents with Childhood Trauma.

Adolescents with major depressive (MDD) episodes associated with childhood trauma have a poorer response to treatment and a higher risk of suicide. The underlying etiology is unclear. Brain-derived neurotrophic factor (BDNF) could improve depressive symptoms by down-regulating mammalian target of rapamycin (mTOR) signaling pathways, which was involved in adverse environmental stimuli during neurodevelopment. BDNF and mTOR have not been reported simultaneously in adolescents with major depressive episodes associated with childhood trauma. Childhood Trauma Questionnaire-Short Form (CTQ-SF), Children's Depression Inventory (CDI) and Children's Depression Rating Scale-Revised (CDRS-R) were used to evaluate the recruited adolescents with major depression episodes. Serum BDNF and p-mTOR levels were measured by ELISA in 31 adolescents with major depression episodes with childhood trauma and 18 matched healthy control. The serum levels of BDNF were significantly lower (p<0.001); and the serum levels of p-mTOR were high (p=0.003) in the adolescents with the first episode of major depressive episode accompanied by childhood trauma. Of the 31 adolescents with major depressive episodes, 17 had suicide or self-injury. Compared with the healthy control group, the serum levels of BDNF in patients with suicide or self-injury were lower than those without suicide or self-injury(p<0.001); the serum levels of p-mTOR were higher than those without suicide or self-injury (p=0.01). While in patients without suicide or self-injury, only serum p-mTOR was significantly higher than that in healthy group (p=0.028).BDNF was negatively correlated with CDRS-R (r=-0.427, p=0.006), p-mTOR was positively correlated with CDI (r=0.364, p=0.048). According to Receiver Operating Characteristic Curve (ROC), the combination of serum BDNF and p-mTOR levels have better diagnostic value. Neurotrophic and signaling pathways, involving BDNF and p-mTOR, may play a role in adolescent MDD with a history of childhood trauma, especially patients with suicide and self-injury tendencies.

Levels of brain-derived neurotrophic factor (BDNF) among patients with COVID-19: a systematic review and meta-analysis.

Many individuals have been suffering from consistent neurological and neuropsychiatric manifestations even after the remission of coronavirus disease (COVID-19). Brain-derived neurotrophic factor (BDNF) is a protein involved in the regulation of several processes, including neuroplasticity, neurogenesis, and neuronal differentiation, and has been linked to a range of neurological and psychiatric disorders. In this study, we aimed to synthesize the available evidence on the profile of BDNF in COVID-19. A comprehensive search was done in the Web of Science core collection, Scopus, and MEDLINE (PubMed), and Embase to identify relevant studies reporting the level of BDNF in patients with COVID-19 or those suffering from long COVID. We used the NEWCASTLE-OTTAWA tool for quality assessment. We pooled the effect sizes of individual studies using the random effect model for our meta-analysis. Fifteen articles were included in the systematic review. The sample sizes ranged from 16 to 183 participants. Six studies compared the level of BDNF in COVID-19 patients with healthy controls. The pooled estimate of the standardized mean difference in BDNF level between patients with COVID-19 and healthy individuals was - 0.84 (95% CI - 1.49 to - 0.18, p = 0.01, I2 = 81%) indicating a significantly lower BDNF level in patients with COVID-19. Seven studies assessed BDNF in different severity statuses of patients with COVID-19. The pooled estimate of the standardized mean difference in BDNF level was - 0.53 (95% CI - 0.85 to - 0.21, p = 0.001, I2 = 46%), indicating a significantly lower BDNF level in patients with more severe COVID-19. Three studies evaluated BDNF levels in COVID-19 patients through different follow-up periods. Only one study assessed the BDNF levels in long COVID patients. Sensitivity analyses did not alter the significance of the association. In this study, we showed a significant dysregulation of BDNF following COVID-19 infection. These findings may support the pathogenesis behind the long-lasting effects of this disease among infected patients. PROSPERO: CRD42023413536.

Female Pattern Hair Loss and Negative Psychological Impact: Possible Role of Brain-derived Neurotrophic Factor (BDNF).

Female Pattern Hair Loss (FPHL) is considered the most common type of hair loss in females. Women with FPHL may suffer from psychological distress and defective social functioning. Patients with psychiatric and neurodegenerative disorders almost have a deficient brain and blood brain-derived neurotrophic factor levels (BDNF). This serum BDNF level may act as a diagnostic marker for negative psychological impact in FPHL patients. Evaluate the levels of serum BDNF in patients with FPHL and correlate its level to the severity of alopecia and the degree of psychological impact. Forty-six female patients with FPHL and 41 healthy age-matched female volunteers as a control were included in the study. Patients filled out a Dermatology Life Quality Index questionnaire. Both patients and controls filled Beck Depression Inventory, Beck Anxiety Inventory, and Perceived Stress Scale (PSS) questionnaires. Serum levels of BDNF were measured for all the participants using the ELISA technique. Patients with FPHL had significantly lower levels of BDNF and significantly higher Beck depression inventory score and PSS questionnaire scores. There is a significant negative correlation between serum levels of BDNF and Beck Depression Inventory, Beck Anxiety Inventory, and PSS questionnaire scores. Patients with FPHL are at a high risk to develop chronic stress and depression. The serum level of BDNF is a good predictor for the assessment of chronic stress and depression in FPHL patients.

Preliminary study on changes in BDNF in patients with depression after percutaneous coronary intervention

IntroductionDepression and coronary artery disease (CAD) are often comorbid conditions. The presence of depression significantly interferes with the recovery after CAD therapy intervention, such as percutaneous coronary intervention (PCI), one of the most common medical procedures in developed countries. Brain derived neurotrophic factor (BDNF) has a major role in angiogenesis and neuromodulation. Its levels were previously shown to be reduced in patients with depression, and latest studies indicate similar in patients with CAD. However, the correlation of BDNF levels and depression after CAD treatment is unknown.ObjectivesThe aim of this preliminary study is to assess the changes in BDNF levels in patients with depressive symptoms during a six-month period upon PCI.MethodsAntidepressant-free participants that underwent PCI with stent placement due to myocardial infarction or angina pectoris were enrolled in the study. Depressive symptoms were evaluated at baseline using the Beck’s Depression Inventory II (BDI-II) with a cut-off score ≥20 indicating moderate depression. Serum BDNF levels were measured from blood samples drawn a day after (baseline) and six-months upon a successful PCI without complications. The t-test for dependent samples was used with marked significant differences at p&lt;0,05.ResultsAltogether, 76 participants were included in the study, of which 25 finished a six-month follow-up. Participants with BDI-II≥20 at baseline had higher serum BDNF levels in the second measurement (M=23,12, SD=6,20; M=32,02, SD=12,26, respectively). No significant difference was found in serum BDNF levels in measurements between participants with and without depressive symptoms (t=0,33, p=0,74; t=-1,40, p=0,18, respectively). Statistically significant difference was found between serum BDNF in the first and second measurement in the overall sample (t=-2,28, p=0,03) and in participants with baseline moderate depressive symptoms (t=-2,46, p= 0,03), but not in those without (t=-0,59, p=0,57).ConclusionsSerum BDNF levels in participants with baseline moderate depressive symptoms increased after a six-month period upon successful PCI treatment, whereas that trend was not observed in participants without depressive symptoms. This highlights the potential synergistic role of BDNF in comorbid depression and CAD.Disclosure of InterestNone Declared

Serum Level of Brain-Derived Neurotrophic Factor in Patients with Relapsing Remitting Multiple Sclerosis: A Potential Biomarker for Disease Activity

Serum Level of Brain-Derived Neurotrophic Factor in Patients with Relapsing Remitting Multiple Sclerosis: A Potential Biomarker for Disease Activity

Somatization is associated with altered serum levels of vitamin D, serotonin, and brain-derived neurotrophic factor in patients with predominant diarrhea irritable bowel syndrome.

Patients with irritable bowel syndrome (IBS) often show psychological disorders, including somatization, usually driven by an altered gut-brain axis. These changes are also accompanied by modifications in the circulating levels of vitamin D (VD) and neurotransmitters such as serotonin (5-HT) and brain-derived neurotrophic factor (BDNF). The present study aimed to evaluate the relationship between gastrointestinal (GI) symptoms and circulating levels of VD, 5-HT, and BDNF in IBS patients with diarrhea (IBS-D) categorized according to somatization. Fifty-three IBS-D patients were recruited and profiled for GI symptoms by validated questionnaires. The fasting serum concentrations of VD, 5-HT, and BDNF were assessed. The health of the intestinal barrier, minimal inflammation, and dysbiosis was also evaluated. Thirty patients showed high somatization scores, IBS-D(S+), and 23 low somatization scores, IBS-D(S-). IBS-D(S+) patients reported higher "Abdominal pain" and the "Abdominal pain duration in days" scores, lower serum VD levels and increased 5-HT and BDNF concentrations than IBS-D(S-). Besides, in IBS-D(S+) patients, the GI symptoms correlated with 5HT, BDNF, and VD concentrations. These parameters were associated with impaired small intestinal permeability and increased inflammation markers. These data support the multifactorial IBS pathogenesis in which organic and psychological factors interact. An active role by VD, 5-HT, and BDNF in affecting the clinical and biochemical profiles in IBS-D(S+) patients may be conceivable. Therefore, the routine VD estimation and the assay of circulating levels of 5-HT and BDNF could be considered a new approach for managing these patients.

Correlation between Vitamin D, homocysteine and brain-derived neurotrophic factor levels in patients with ischemic stroke.

Ischemic stroke risk increase is in relation to low serum vitamin D levels in some studies; however, the uncertainty about its relationship to serum homocysteine and brain-derived neurotrophic factor (BDNF) concentration remains. The aim of this study is to investigate the correlation between vitamin D, homocysteine and BDNF levels in patients with acute stroke. A total of 126 patients admitted to the emergency department with stroke and 64 healthy controls were included in this study. All patients received 150,000 U of vitamin D as part of a stroke treatment protocol during hospitalization. The patients were divided into two groups: the blood samples of the patients in the group-I (n=54) were taken at the time of admission to the hospital, and the samples of the patients in the group-II (n=72) were taken 24 hours after admission. Serum vitamin D, homocysteine, BDNF and routine biochemical analyses were performed from these samples. Compared to healthy controls, stroke patients had lower serum vitamin D (p<0.0001) and BDNF (p<0.0001) levels, and higher homocysteine levels (p<0.0001). It was found that the homocysteine level was constant and the BDNF level increased (p=0.01) 24 hours after the 150,000 U vitamin D supplementation. Furthermore, there was a negative significant correlation between vitamin D levels, homocysteine and BDNF in patients who had experienced a stroke. Vitamin D supplementation was used as a therapeutic agent in patients with acute ischemic stroke that affects homocysteine and BDNF levels. In this study, it was demonstrated for the first time that there is a correlation between serum vitamin D levels and BDNF levels in patients who have experienced a stroke.

Effect of Exercise Rehabilitation Training on Cognitive Function and Serum Level of Brain-derived Neurotrophic Factor in Patients with Chronic Schizophrenia

Effect of Exercise Rehabilitation Training on Cognitive Function and Serum Level of Brain-derived Neurotrophic Factor in Patients with Chronic Schizophrenia

Peripheral Blood Levels of Brain-Derived Neurotrophic Factor in Patients with First Episode Psychosis: A Systematic Review and Meta-Analysis.

Background: Peripheral blood level of brain-derived neurotrophic factor (BDNF) may be used as a diagnostic and/or prognostic marker for schizophrenia. Previous studies were inconsistent. A systematic review was conducted to examine whether BDNF level is different in patients with first episode psychosis (FEP) compared to health controls (HC) and whether it changes after treatment. Methods: Literature search was done in PubMed, Web of Science, and Google Scholar following standard procedures. Hedges’ g was used as the measure of effect size (ES), which was pooled with random effects model. Publication bias and moderator effects were examined. Results: Search yielded 29 studies with a total sample size of 2912. First meta-analysis included 27 studies with FEP vs. HC comparison. Pooled ES was −0.63, p < 0.001, indicating that BDNF level was lower in FEP than in HC. Studies were heterogeneous, and moderator analysis showed that studies of younger patient, higher symptom severity, and more drug naïve had larger ES. Second meta-analysis examined change in BDNF levels before and after antipsychotic treatment in eight studies. A pooled ES of −0.003 (p = 0.96) showed no change in peripheral BDNF level after treatment. Conclusion: Peripheral BDNF level was decreased in FEP compared to HC, but it did not change after treatment.

Effects of Transient Electrical Acupuncture Stimulation Combined With Rehabilitation Training on Hemorheology, Neurological Function and BDNF in Patients With Cerebral Infarction.

ObjectiveTo explore the effects of transient electric acupuncture stimulation combined with rehabilitation training on hemorheology, neurological function and brain-derived neurotrophic factor (BDNF) in patients with cerebral infarction (CI).MethodsA total of 90 patients with CI were admitted to our hospital from March 2019 to March 2021. According to the random number table method, 90 patients were divided into a control group (was treated with transient electrical acupuncture stimulation intervention treatment) and a therapy group (was treated with rehabilitation training on the basis of the control group), with 45 cases in each group. NIHSS score to detect neurological deficit; FMA score to detect motor function recovery; the clinical efficacy of the two groups of patients were compared; blood rheology analyzer to detect whole blood high shear viscosity, whole blood low shear viscosity, platelet aggregation rate and fibrinogen indicators; ELISA detects the content of BDNF in serum.ResultsThere was no significant difference in NIHSS score, FMA score, clinical efficacy, hemorheology index, and BDNF content between the two groups of patients before treatment (P > 0.05). After treatment, the NIHSS score, whole blood high shear visible, whole blood low shear visible, platelet aggregation rate and fibrinogen index of the two groups were lower than those before treatment, and the FMA score and BDNF content of the two groups were higher than those before treatment, and all the above indicators in the therapy group changed significantly compared with the control group (P < 0.05). After treatment, the clinical efficacy of the therapy group was better than that of the control group (P < 0.05).ConclusionThe combination of transient electrical acupuncture stimulation and rehabilitation training can inhibit the blood flow index of patients with CI, improve the nerve function, increase the content of BDNF in the patient's serum, and restore the patient's nerve function.

Tropomyosin receptor kinase B-mediated signaling in integration of neuropathic pain and obesity in diabetic polyneuropathy.

ABSTRACTObjective:To assess the quantitative serum levels of tropomyosin receptor kinase receptor B, and to estimate its association with serum concentration of brain-derived neurotrophic factor and obesity in patients with painful and painless forms of diabetic polyneuropathy.Methods:We examined 70 patients with diabetic polyneuropathy with confirming peripheral nerve dysfunction by electroneuromyography and measuring of serum levels tropomyosin receptor kinase receptor B and brain-derived neurotrophic factor by enzyme immunoassay. Diabetic polyneuropathy was diagnosed using the modified Toronto Consensus (2011) criteria, while neuropathic pain was assessed using an 11-point Numerical Pain Rating Scale. The patients were divided into two groups according to presence or absence of neuropathic pain. Control Group consisted of 14 healthy persons.Results:The serum levels of tropomyosin receptor kinase receptor B and brain-derived neurotrophic factor in patients with diabetic polyneuropathy are significantly higher than healthy controls (p=0.000). Hyperexpression of brain-derived neurotrophic factor in serum was associated with painful form of diabetic polyneuropathy (R=0.392, p=0.012) and obesity (R=0.412, p=0.001). On the contrary high concentration of tropomyosin receptor kinase receptor B in serum associated with painless diabetic polyneuropathy by Pain DETECT (R=-0.354, p=0.015), low body weight (R=-0.354, p=0.015) and severe demyelization of nerve fibers (R=-0.574, p=0.001), indicated “non-working” receptor detected in serum.Conclusion:Tropomyosin receptor kinase receptor B signaling is involved in the modulation of neuropathic pain and obesity in diabetic polyneuropathy.

Serum and aqueous humor levels of brain-derived neurotrophic factor in patients with primary open-angle glaucoma and normal-tension glaucoma.

This study was designed to compare the levels of brain-derived neurotrophic factor (BDNF) in the serum and aqueous humor (AH) of patients with primary open-angle glaucoma (POAG) and normal-tension glaucoma (NTG). This prospective, observational study consists of 30 patients with POAG, 30 patients with NTG, and 30 healthy controls. The serum and AH BDNF levels were assessed using an enzyme-linked immunosorbent assay. BDNF levels in serum and AH were markedly lower in the glaucoma groups (POAG and NTG) than in the control group (p <0.05). When comparing the NTG and POAG groups, the average serum BDNF level was significantly lower in the NTG group than in the POAG group (p <0.05). The difference in the mean BDNF levels in AH between the POAG and NTG groups was not statistically significant. (p = 0.538). We confirmed that serum BDNF levels were lower in patients with NTG than in those with POAG. BDNF could be a causative systemic biomarker in NTG.