Brain-derived Neurotrophic Factor Levels In Patients 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.

Brain-derived Neurotrophic Factor Level and Gene Polymorphism as Risk Factors for Depression in Patients with type 2 Diabetes Mellitus- A Case-Controlled Study.

Diabetes mellitus and depression are comorbidities that can be caused by each other. Brain-derived neurotrophic factor (BDNF) functions as a neuronal growth factor. It maintains the functional integrity of the nervous system. To study the possible association between BDNF levels and gene polymorphism with depression in patients diagnosed with type 2 diabetes mellitus. The Elisa technique measured BDNF, and rs6265 gene polymorphism was detected using real-time PCR. Depression was assessed utilizing a clinical interview tool designed to establish the diagnosis of depression and differentiate it from other psychiatric diseases. BDNF levels were significantly lower in patients with type 2 diabetes mellitus and symptoms of depression than in patients with type 2 diabetes mellitus and no symptoms of depression (82.6±16.1. Vs 122± 17.47, p˂ 0.001). There was a statistically significant difference in BDNF levels in patients with diabetes among the three genotypes of the BDNF gene (p-value < 0.001). Val/ Val carriers had the highest serum BDNF levels, and Met/ Met carriers had the lowest serum BDNF levels. Subgroup analysis showed statistically significant genotype-related differences in serum BDNF levels among the three subgroups in the Depression group. Val/ Val carriers had the highest serum BDNF levels, and Met/ Met carriers had the lowest serum BDNF levels. BDNF Val66Met polymorphism had no significant association with the presence of depression, yet there was a trend towards significance (p = 0.05) Conclusion: In this pilot, Low levels of BDNF were associated with depression in patients with type 2 diabetes. Carriers of the Met/ Met allele have the lowest serum BDNF levels. Multicenter studies with more participants are required.

The Influence of Electroconvulsive Therapy (ECT) on Brain-Derived Neurotrophic Factor (BDNF) Plasma Level in Patients with Schizophrenia-A Systematic Review and Meta-Analysis.

The main aim of this systematic review and meta-analysis is to establish whether there is a correlation between the brain-derived neurotrophic factor (BDNF) level and electroconvulsive therapy (ECT) treatment and the reduction in psychotic symptoms in patients diagnosed with schizophrenia. A systematic search of PubMed/Medline, Cochrane Library, Web of Science, Scopus and Embase was conducted up to March 2023. Inclusion criteria: studies in which adult patients with schizophrenia treated with antipsychotic medication received ECT therapy and had the BDNF level measured before and after ECT treatment. Exclusion criteria: animal and in vitro studies or studies not involving complete information about the treatment and concentration of BDNF in plasma. The risk of bias was assessed using Egger's regression-based test for meta-analysis with continuous outcomes. Six studies comprising 248 individuals with schizophrenia were included. A statistically significant increase in BDNF levels after ECT treatment was observed only in two studies (p < 0.001 and p < 0.027, respectively), whereas in four other studies, an upward trend without statistical significance was noticed. The estimated overall size effect revealed that ECT therapy caused a slight change in the BDNF level but without statistical significance (ES = -0.328). Different numbers of ECT procedures (4-10), final measurement of the BDNF level made at a different time point, using bilateral or unilateral electrode positioning during ECT and treatment with different combinations of typical or atypical antipsychotic medications may be potential reasons for the lack of statistical significance in the changes in BDNF levels after treatment. Data regarding the measurement of BDNF levels pre and post ECT therapy in patients with schizophrenia are very limited without an extended follow-up period and evaluation of mental health change. Our meta-analysis showed that treatment with ECT therapy and antipsychotic medication increases serum BDNF levels in patients with drug-resistant schizophrenia compared to patients treated with medication only; however, this effect is not statistically significant.

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.

BDNF as potential biomarker of epilepsy severity and psychiatric comorbidity: pitfalls in the clinical population

BackgroundSeveral studies implicate brain-derived neurotrophic factor (BDNF) in the pathophysiology of epilepsy. In particular, preclinical data suggest that lower serum BDNF is a biomarker of epilepsy severity and psychiatric comorbidities. We tested this prediction in clinical epilepsy cohorts. MethodsPatients with epilepsy were recruited from 4 epilepsy centers in France and serum BDNF was quantified. Clinical characteristics including epilepsy duration, classification, localization, etiology, seizure frequency and drug resistance were documented. Presence of individual anti-seizure medications (ASM) was noted. Screening for depression and anxiety symptoms was carried out in all patients using the NDDI-E and the GAD-7 scales. In patients with positive screening for anxiety and/or depression, detailed psychiatric testing was performed including the Mini International Neuropsychiatric Interview (MINI), STAI-Y, Holmes Rahe Stressful Events Scale and Beck Depression Interview. Descriptive analysis was applied. Spearman’s test and Pearson’s co-efficient were used to assess the association between BDNF level and continuous variables. For discrete variables, comparison of means (Student’s t-test, Mann-Whitney u-test) was used to compare mean BDNF serum level between groups. Multivariate analysis was performed using a regression model. ResultsNo significant correlation was found between serum BDNF level and clinical features of epilepsy or measures of depression. The main group-level finding was that presence of any ASM at was associated with increased BDNF; this effect was particularly significant for valproate and perampanel. ConclusionPresence of ASM affects serum BDNF levels in patients with epilepsy. Future studies exploring BDNF as a possible biomarker of epilepsy severity and/or psychiatric comorbidity must control for ASM effects.

Blood levels of brain-derived neurotrophic factor (BDNF) in systemic lupus erythematous (SLE): a systematic review and meta-analysis

ObjectivesBDNF has been implicated in the pathophysiology of systemic lupus erythematosus (SLE), especially its neuropsychiatric symptoms. The purpose of this study was to investigate the profile of blood BDNF levels in patients with SLE.MethodsWe searched PubMed, EMBASE, and the Cochrane Library for papers that compared BDNF levels in SLE patients and healthy controls (HCs). The Newcastle–Ottawa scale was used to assess the quality of the included publications, and statistical analyses were carried out using R 4.0.4.ResultsThe final analysis included eight studies totaling 323 healthy controls and 658 SLE patients. Meta-analysis did not show statistically significant differences in blood BDNF concentrations in SLE patients compared to HCs (SMD 0.08, 95% CI [ − 1.15; 1.32], P value = 0.89). After removing outliers, there was no significant change in the results: SMD -0.3868 (95% CI [ − 1.17; 0.39], P value = 0.33. Univariate meta-regression analysis revealed that sample size, number of males, NOS score, and mean age of the SLE participants accounted for the heterogeneity of the studies (R2 were 26.89%, 16.53%, 18.8%, and 49.96%, respectively).ConclusionIn conclusion, our meta-analysis found no significant association between blood BDNF levels and SLE. The potential role and relevance of BDNF in SLE need to be further examined in higher quality studies.

The role of the brain-derived neurotrophic factor (BDNF) in anorexia nervosa

The brain-derived neurotrophic factor (BDNF) is a growth factor belonging to the neurotrophin family which plays a pivotal role in the differentiation, survival, and plasticity of neurons in the central nervous system. Evidence suggests that BDNF is an important signal molecule in the regulation of energy balance and thus implicated in body weight control. The discovery of BDNF-expressing neurons in the paraventricular hypothalamus which is important in the regulation of energy intake, physical activity, and thermogenesis gives more evidence to the suggested participation of BDNF in eating behavior. Until now it remains questionable whether BDNF can be used as a reliable biomarker for eating disorders such as anorexia nervosa (AN) as available findings on BDNF levels in patients with AN are ambiguous. AN is an eating disorder characterized by a pathological low body weight in combination with a body image disturbance typically developing during adolescence. A severe drive for thinness leads to restrictive eating behavior often accompanied by physical hyperactivity. During therapeutic weight restoration an increase of BDNF expression levels seems desirable as it might improve neuronal plasticity and survival which is essential for learning processes and thereby essential for the success of the psychotherapeutic treatment of patients. On the contrary, the well-known anorexigenic effect of BDNF might favor relapse in patients as soon as the BDNF levels significantly increase during weight rehabilitation. The present review summarizes the association between BDNF and general eating behavior and especially focuses on the eating disorder AN. In this regard findings from preclinical AN studies (activity-based anorexia model) are outlined as well.

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

The Effect of Electrical Stimulation Therapy on Brain Derived Neurotrophic Factor in Patients with Tinnitus.

Introduction: The aim of this study was to determine the effect of electric stimulation therapy on brain-derived neurotrophic factor (BDNF) in patients with tinnitus. Materials and methods: In this before-after clinical trial study, 45 patients aged 30-80 years old with tinnitus were involved. The hearing threshold, loudness, and frequency of tinnitus were assessed. Tinnitus Handicap Inventory (THI) questionnaire was completed by the patients. Before holding electrical stimulation sessions, the patients were evaluated for serum brain-derived neurotrophic factor (BDNF) level. Patients underwent five electrical stimulation sessions of 20min for 5 consecutive days. After completion of electrical stimulation session, THI questionnaire was re-completed by the patients and they were evaluated for serum BDNF level. Results: Mean BDNF level before and after the intervention was (1238 ± 494.2) and (1148.2 ± 496.7), respectively (P = 0.04). Mean loudness score before and after the intervention was (6.36 ± 1.47) and (5.27 ± 1.68), respectively (P = 0.01). Mean THI score before and after the intervention was (58.21 ± 11.8) and (53.17 ± 15.19), respectively (p = 0.01). In patients with severe THI1, there was a significant difference between serum BDNF level (p = 0.019) and loudness (p = 0.003) before and after the intervention. However, in patients with mild, moderate, and very severe THI1, no such effect was observed (p > 0.05). Conclusion: According to the results of the present study, electrical stimulation therapy significantly decreased the mean plasma BDNF level in patients with tinnitus, especially in patients with severe tinnitus so it can be used as a marker to define the response to treatment and determine the severity of tinnitus in primary evaluations.

Moderators of ayahuasca's biological antidepressant action.

The understanding of biological responses to psychedelics with antidepressant potential is imperative. Here we report how a set of acute parameters, namely emotional (depressive symptoms), cognitive (psychedelic experience), and physiological (salivary cortisol), recorded during an ayahuasca dosing session, modulated serum brain-derived neurotrophic factor (BDNF), serum cortisol (SC), serum interleukin 6 (IL-6), plasma C-reactive protein (CRP), and salivary cortisol awakening response (CAR). Results were analyzed 2 days after the psychedelic intervention (ayahuasca) versus placebo in both patients with treatment-resistant depression and healthy volunteers. These measures were assessed as part of a randomized double-blinded, placebo-controlled trial (n = 72). Results revealed that larger reductions of depressive symptoms during the dosing session significantly moderated higher levels of SC in patients. Whereas lesser changes in salivary cortisol levels during the ayahuasca intervention were related to higher BDNF levels in patients with a larger clinical response in the reduction in depressive symptoms. No moderator was found for patient's CAR, IL-6, and CRP responses to ayahuasca and for all biomarker responses to ayahuasca in healthy controls and in the placebo group. In summary, some specific emotional and physiological parameters during experimental ayahuasca session were revealed as critical moderators of the improvement of major depression biomarkers, mainly BDNF and SC two days after ayahuasca intake. These findings contribute to paving the way for future studies investigating the biological antidepressant response to psychedelic therapy.

Effects of acute aerobic exercise on brain-derived neurotrophic factor level in rheumatoid arthritis patients.

The study aimed to investigate the variation of brain-derived neurotrophic factor (BDNF) levels following acute exercise in patients with rheumatoid arthritis (RA). This cross-sectional study was conducted with 88 participants (25 males, 63 females; mean age: 45.1±8.3 years; range, 18 to 65 years) between July 2020 and May 2021. Of the participants, 44 were RA patients, and 44 were age-and sex-matched healthy controls. Aerobic exercise was utilized in all participants for a single session. Depression and anxiety levels were evaluated with the Beck Depression Inventory and Hospital Anxiety and Depression Scale. Blood samples were collected from all subjects before and immediately after the intervention. Serum BDNF levels (both baseline and after exercise) were similar in the RA and control groups. Although serum BDNF levels significantly decreased in both groups after aerobic exercise (Wilcoxon rank p<0.05), ΔBDNF levels were significantly higher in the RA group than in the control group (p=0.047). Additionally, ΔBDNF levels were significantly correlated with the Hospital Anxiety and Depression Scale scores in the RA group (p<0.05) but not in the control group. A single bout of exercise may effectively decrease serum BDNF levels in patients with RA and healthy subjects. The long-term effect of exercise on BDNF levels should be investigated in prospective studies.

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 vitamin D on serum BDNF level in patients with hypothyroidism caused by autoimmune thyroiditis

Background. Hashimoto’s thyroiditis is a chronic autoimmune disease of the thyroid gland caused by an increase in thyroid antibodies. A growing body of research suggests that patients with Hashimoto’s thyroiditis may suffer from cognitive impairment. Therefore, it is important to identify risk factors that contribute to the development of cognitive impairment in patients with autoimmune thyroiditis to diagnose them early and treat. Given that the influence of thyroid hormones on the brain is undeniable, and their deficiency leads to a variety of neurological complications, early diagnosis and treatment of neurological disorders in thyroid diseases is crucial for preventing further progression of these complications. The purpose of the study is to determine the effect of vitamin D on the level of brain-derived neurotrophic factor (BDNF) in blood serum of patients with hypothyroidism caused by autoimmune thyroiditis. Materials and methods. Twenty-eight patients with hypothyroidism caused by autoimmune thyroiditis were included in the study. The serum level of BDNF was quantified using a solid-phase enzyme-linked immunosorbent assay with a highly sensitive Human BDNF ELISA Kit (Elabscience®, United States, Catalog No E-EL-H0010) on E.I.A. Reader Sirio S (Seac, Italy). Results. In our study, the administration of vitamin D and L-thyroxine led to a 7.4-fold increase in BDNF levels (p&lt;0.001). In the group of patients who took only L-thyroxine, serum content of BDNF increased by 2.1 times. In patients who took cholecalciferol and L-thyroxine, the level of BDNF was 2.48 times higher compared to those who took only L-thyroxine (p&lt;0.001). Conclusions. A positive effect of vitamin D on the serum level of BDNF was found in patients with hypothyroidism caused by autoimmune thyroiditis. Treatment of these individuals using additional administration of cholecalciferol on the background of L-thyroxine proved to be more effective compared to the administration of L-thyroxine alone (p&lt;0.001).

Circulating brain-derived neurotrophic factor as a potential biomarker in stroke: a systematic review and meta-analysis

BackgroundStroke, an acute cerebrovascular event, is a leading cause of disability, placing a significant psycho-socioeconomic burden worldwide. The adaptation and reorganization process following any neuronal damage is regarded as neuroplasticity. Among many factors believed to attribute to this process, Brain-derived Neurotrophic Factor (BDNF) is a neurotrophin coordinating neuroplasticity after various neurological disorders such as stroke.MethodsWe conducted a systematic search in the main electronic medical databases in January 2021. Primarily we want to compare BDNF levels between patients with stroke and healthy controls (HC). Additional aims included investigation of (1) longitudinal changes in the BDNF levels post-stroke, (2) effects of physical training, (3) repeated transcranial magnetic stimulation (rTMS), and presence of depression on BDNF levels in patients with stroke.ResultsAmong 6243 reviewed records from PubMed, Web of Science, and Scopus, 62 studies were eligible for inclusion in our systematic review. Subjects with stroke, n = 1856, showed lower BDNF levels compared to HC, n = 1191 (SMD [95%CI] = − 1.04 [− 1.49 to − 0.58]). No significant difference was detected in the level of BDNF through time points past stroke. BDNF levels were lower in the patients with depression compared to non-depressed subjects (SMD [95%CI] = − 0.60 [− 1.10 to − 0.10]). Physical training had an immediate positive effect on the BDNF levels and not statistically significant effect in the long term; SMD [95%CI] = 0.49 [0.09 to 0.88]) and SMD [95%CI] = 0.02 [− 0.43 to 0.47]). Lastly, rTMS showed no effect on the level of BDNF with 0.00 SMD.ConclusionsOur study confirms that stroke significantly decreases the level of BDNF in various domains such as cognition, affect, and motor function. As BDNF is the major representative of neuroplasticity within nervous system, it is believed that stroke has a significant impact on the CNS regeneration, which is permanent if left untreated. This effect is intensified with coexisting conditions such as depression which further decrease the BDNF level but the net impact yet needs to be discovered. We also conclude that exercise and some interventions such as different medications could effectively reverse the damage but further studies are crucial to reach the exact modality and dosage for their optimal effect.

Brain-Derived neurotrophic factor (BDNF) plasma level increases in patients with resistant schizophrenia treated with electroconvulsive therapy (ECT)

Objectives The study aimed to assess the effect of Electroconvulsive Therapy (ECT) on plasma BDNF levels in patients with resistant schizophrenia. Methods It was a cohort study that included 60 patients with resistant schizophrenia fulfilling the DSM-5 criteria of schizophrenia and APA criteria of resistant schizophrenia. They were divided into two groups, followed over 4 weeks, and compared to their baseline assessment. Group (A) included 45 patients who received 4–10 sessions of ECT while Group (B) included 15 patients who received the usual treatment with antipsychotics without ECT. The assessment included the severity of psychotic symptoms assessed by the Positive and Negative Symptom Scale (PANSS) in addition to plasma BDNF level. Results Patients in Group (A) had an increased level of BDNF after treatment with a statistically significant difference in comparison to their baseline BDNF level (P = 0.027). Meanwhile, patients in group (B) showed a non-significant increase in BDNF. Patients in both groups improved significantly in all PANSS subscales after treatment. Conclusions It was concluded that plasma BDNF levels in patients with resistant schizophrenia increase after electroconvulsive therapy in association with clinical improvement. Key points BDNF increases after ECT treatment of resistant schizophrenia. BDNF is not correlated with the severity of psychotic symptoms Patients treated with ECT showed a better response.

Investigation of the Molecular Role of Brain-Derived Neurotrophic Factor in Alzheimer's Disease.

Brain-derived neurotrophic factor (BDNF), or abrineurin, is a member of the neurotrophin family of growth factors that acts on both the central and peripheral nervous systems. BDNF is also well known for its cardinal role in normal neural maturation. It binds to at least two receptors at the cell surface known as tyrosine kinase B (TrkB) and p75NTR. Additional neurotrophins that are anatomically linked with BDNF include neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and nerve growth factor (NGF). It is evident that BDNF levels in patients with Alzheimer's disease (AD) are altered. AD is a progressive disorder and a form of dementia, where the mental function of an elderly person is disrupted. It is associated with a progressive decline in cognitive function, which mainly targets the thinking, memory, and behavior of the person. The degeneration of neurons occurs in the cerebral cortex region of brain. The two major sources responsible for neuronal degeneration are protein fragment amyloid-beta (Aβ), which builds up in the spaces between the nerve cells, known as plaques, disrupting the neuron signaling pathway and leading to dementia, and neurofibrillary tangles (NFTs), which are the twisted fibers of proteins that build up inside the cells. AD is highly prevalent, with recent data indicating nearly 5.8 million Americans aged 65 and older with AD in 2020, and with 80% of patients 75 and older. AD is recognized as the sixth leading cause of death in the USA, and its prevalence is predicted to increase exponentially in the coming years. As AD worsens over time, it becomes increasingly important to understand the exact pathophysiology, biomarkers, and treatment. In this article, we focus primarily on the controversial aspect of BDNF in AD, including its influence on various other proteins and enzymes and the current treatments associated with BDNF, along with future perspectives.

Frontotemporal Transcranial Direct Current Stimulation Decreases Serum Mature Brain-Derived Neurotrophic Factor in Schizophrenia.

Although transcranial direct current stimulation (tDCS) shows promise as a treatment for auditory verbal hallucinations in patients with schizophrenia, mechanisms through which tDCS may induce beneficial effects remain unclear. Evidence points to the involvement of neuronal plasticity mechanisms that are underpinned, amongst others, by brain-derived neurotrophic factor (BDNF) in its two main forms: pro and mature peptides. Here, we aimed to investigate whether tDCS modulates neural plasticity by measuring the acute effects of tDCS on peripheral mature BDNF levels in patients with schizophrenia. Blood samples were collected in 24 patients with schizophrenia before and after they received a single session of either active (20 min, 2 mA, n = 13) or sham (n = 11) frontotemporal tDCS with the anode over the left prefrontal cortex and the cathode over the left temporoparietal junction. We compared the tDCS-induced changes in serum mature BDNF (mBDNF) levels adjusted for baseline values between the two groups. The results showed that active tDCS was associated with a significantly larger decrease in mBDNF levels (mean −20% ± standard deviation 14) than sham tDCS (−8% ± 21) (F = 5.387; p = 0.030; η2 = 0.205). Thus, mature BDNF may be involved in the beneficial effects of frontotemporal tDCS observed in patients with schizophrenia.

Evaluation of plasma levels of BDNF in patients with disorder depressive

IntroductionAccording to the World Health Organization (WHO, 2017) depressive disorder continues to be the most widespread and growing mental illness in the world, also assumes that in 2020 depression will have a prevalence equal to one in six individuals. Studies of neuroanatomy have highlighted structural alterations in the hippocampus, striatal nuclei and prefrontal cortex in patients with mood disorders. This alteration in depressed patients is closely related to the secretion of neurotrophic factors, in particular there is a reduction in BDNF (Brain Derived Neurotrophic Factor).ObjectivesThe objective of this study is to demonstrate which treatments are effective in reducing depressive symptoms that allow the increase of BDNF and consequently the structural homostaticity of the brain.MethodsWe have selected data from the literature of the last decade, collected on major search engines such as: Google Scholar, Research Gate, PubMed, Ebsco. Articles collected by selecting the following Keyword: depression, BDNF (Brain Derived Neurotrophic Factor), neuroimaging cognitive behavior therapy.ResultsThe results show that in patients treated with a single drug treatment or vagus nerve stimulation, repetitive transcranial magnetic stimulation (Lang et al., 2008) or electroconvulsive therapy had improvements in BDNF levels, although compared to drug treatment there are problems of no responders, no compliance and lack of effectiveness in reducing vulnerability to relapse. In addition, the study has shown that patients treated with cognitive behavioral therapy have reported greater changes in the frontal and temporal cortex reducing both depressive symptoms and the risk of relapse.ConclusionsUnderlines the importance of an integrated approach

Serum Levels of BDNF in Patients with Adenoma and Colorectal Cancer.

The present study is aimed at examining the serum levels of brain-derived neurotrophic factor (BDNF) and investigating its role in differential diagnosis of colorectal cancer (CRC). Materials and Methods. In a Chinese population, we conducted a case-control study to compare the diagnostic performance of serum levels of BDNF and carcinoembryonic antigen (CEA) for CRC. We enrolled 61 healthy controls, 31 patients with adenomas, and 81 patients with CRC. We explored the correlation between serum levels of BDNF and several pathological features, such as tumor differentiation and TNM staging. Results. The serum levels of BDNF were significantly (p < 0.0001) higher in patients with CRC (10.64 ± 3.84, n = 81) than in the healthy controls (4.69 ± 1.69 ng/mL, n = 61). Serum BDNF also correlated with tumor size, tumor differentiation, and TNM staging (p < 0.05). For early diagnosis, the combination of BDNF (AUC 0.719; 95% CI, 0.621–0.816) and CEA (AUC 0.733; 95% CI, 0.632–0.909) slightly improved the diagnostic performance for CRC (AUC 0.823; 95% CI, 0.737-0.909). Conclusions. Combined detection of serum BDNF and CEA may thus have the potential to become a new laboratory method for the early clinical diagnosis of CRC.

Brain-Derived Neurotrophic Factor, a New Predictor of Coronary Artery Calcification.

Brain-derived neurotrophic factor (BDNF) plays a functional role in vascular endothelium homeostasis and the alleviation of atherosclerosis. Matrix gla protein (MGP) and Nε-(1-carboxymethyl)-l-lysine (CML) are both confirmed to be VC predictors. This study investigated the association between BDNF, MGP, CML and coronary artery calcification (CAC). Plasma BDNF, MGP, and CML levels were measured in 274 patients who underwent computed tomography to determine the CAC score (Agatston score). It was found that patients with CAC exhibited lower BDNF and MGP and higher CML levels than those without CAC. Plasma BDNF levels in patients with diabetes or hypertension were lower compared with the control groups. In logistic regression analysis, age, hypertension, BDNF, and MGP were independent predictors of CAC. Plasma BDNF and MGP levels were both correlated with the Agatston score even after adjustment for age, total cholesterol level, triglycerides, low-density lipoprotein level, creatinine clearance rate, and the presence of hypertension and diabetes mellitus. In 167 patients with CAC, circulating BDNF level was inversely associated with CML level and positively related to MGP level. In the receiver operating characteristic analysis for CAC, the areas under the curves for BDNF, MGP, and CML were 0.757, 0.777 and 0.653, respectively. In summary, plasma BDNF levels are associated with the Agatston score, and BDNF further predicts the occurrence of CAC.