Serum BDNF Concentrations Research Articles

Effects of combined exercise on cardiovascular risk factors and serum BDNF level in mid-aged women.

[Purpose]The purposes of this study is first to examine a positive effect of long term combined exercise including aerobic and resistance exercise on increasing level of serum BDNF, and investigate how aerobic exercise is related to improving BDNF circulation and resistance exercise improves fat oxidation in mid-aged women.[Methods]Initially, 30 mid-aged women, according to their exercise preference, was randomly assigned as a non-exercise group (n=7, control group; CG) and exercise group (n=23). Then, 23 exercise participants were divided by aerobic exercise group (n=15, AEG) and combination of aerobic and resistance exercise group (n=8, CEG). Prior to the experiment, all participants’maximal oxygen uptake (VO2max), body composition, and blood factors were measured. Changes (Δ delta value) in body composition, fitness level, and serum BDNF level of the different groups were tested through one way ANOVA.[Results]For AEG and CG after 24 weeks, VO2max and high-density lipoprotein cholesterol (HDL-C) were significantly increased. During this period, CEG had significant increase in muscular strength and decrease in triglyceride (TG) total cholesterol (TC)/HDL-C (p=0.013). Continuously, serum BDNF concentration of both AEG and CEG was significantly increased (F=6.328, p=0.001) compared to CG. There, however, was no significant between-group difference.[Conclusion]Although there was no difference in serum BDNF level between AEG and CEG, we confirmed that CEG may have a possibility of positive changes in increase of serum BDNF level in mid-aged women.

Effect of fat free mass on serum and plasma BDNF concentrations during exercise and recovery in healthy young men

Exercise results in release of brain derived neurotrophic factor into the circulation; however, little is known about the changes in serum and plasma brain derived neurotrophic factor concentrations and factors influencing brain derived neurotrophic factor during exercise and recovery. Serum (n=23) and plasma (n=10) brain derived neurotrophic factor concentrations were measured in healthy young men at rest, during steady-rate and after exercise to determine the maximum aerobic power. A two-way analysis of variance was used to investigate brain derived neurotrophic factor levels in blood during exercise and recovery, with one between-subject factor (a median split on: age, height, body mass, fat free mass, body mass index and aerobic fitness), and one within-subject factor (time). Serum brain derived neurotrophic factor concentrations increased in response to exercise and declined rapidly in recovery. Plasma brain derived neurotrophic factor had a greater proportional increase relative to exhaustive exercise compared with serum brain derived neurotrophic factor and was slower to return to near baseline values. There was a significant group-by-time interaction indicating a greater release and faster recovery for serum brain derived neurotrophic factor in high- compared with low-fat free mass individuals.

Brain-derived neurotrophic factor and its relation to leptin in obese children before and after weight loss

ObjectiveBrain-derived neurotrophic factor (BDNF) is a regulator of energy homeostasis and food intake through hypothalamic signaling. Currently, data regarding BDNF in children with obesity are lacking. We evaluated serum BDNF concentrations in obese children, both before and after lifestyle intervention, in reference to those of lean children. MethodsA total of 90 (24 normal weight; 66 obese) children were studied utilizing a cross-sectional clinical outpatient study design. In addition, longitudinal data analysis was performed in 30 obese children participating in a lifestyle intervention for one year. ResultsFasting serum BDNF concentrations were higher in obese vs. normal weight children (BDNF 20.3±1.0 vs. 12.5±1.7ng/mL, respectively, mean±SEM, p<0.001) and correlated significantly to BMI standard deviation score (r=0.426, p<0.001), and leptin (r=0.414, p<0.01). BDNF concentrations were not regulated in response to food, 60min after ingestion of a liquid test meal. After one year lifestyle intervention, delta BDNF correlated significantly to delta leptin (r=0.475, p<0.01), but not to changes of insulin resistance index HOMA-IR, systolic and diastolic blood pressure, HDL, LDL, and triglycerides. In a multiple stepwise linear regression adjusted for pubertal stage, age, sex, and BMI, delta BDNF correlated significantly (p<0.05) to delta leptin and delta triceps skinfold and in tendency to delta subscapularis skinfold thickness (p=0.050). ConclusionsOur results in children do not indicate a significant relationship between BDNF and insulin resistance or cardiovascular risk factors. However, the correlation between changes of BDNF and changes of leptin suggests a relationship between BDNF and fat mass.

Vulnerability to Depression: From Brain Neuroplasticity to Identification of Biomarkers

A stressful event increases the risk of developing depression later in life, but the possible predisposing factors remain unknown. Our study aims to characterize latent vulnerability traits underlying the development of depressive disorders in adult animals. Four weeks after a priming stressful event, serum corticosterone concentration returned to control values in all animals, whereas the other biological parameters returned to basal level in only 58% of animals (called nonvulnerable). In contrast, 42% of animals displayed persistent decreased serum and hippocampus BDNF concentrations, reduced hippocampal volume and neurogenesis, CA3 dendritic retraction and decrease in spine density, as well as amygdala neuron hypertrophy, constituting latent vulnerability traits to depression. In this group, called vulnerable, a subsequent mild stress evoked a rise of serum corticosterone levels and a "depressive" phenotype, in contrast to nonvulnerable animals. Intracerebroventricular administration of 7,8-dihydroxyflavone, a selective TrkB receptor agonist, dampened the development of the "depressive" phenotype. Our results thus characterize the presence of latent vulnerability traits that underlie the emergence of depression and identify the association of low BDNF with normal corticosterone serum concentrations as a predictive biomarker of vulnerability to depression.

No exercise-induced increase in serum BDNF after cycling near a major traffic road

Commuting by bike has a clear health enhancing effect. Moreover, regular exercise is known to improve brain plasticity, which results in enhanced cognition and memory performance. Animal research has clearly shown that exercise upregulates brain-derived neurotrophic factor (BDNF – a neurotrophine) enhancing brain plasticity. Studies in humans found an increase in serum BDNF concentration in response to an acute exercise bout. Recently, more evidence is emerging suggesting that exposure to air pollution (such as particulate matter (PM)) is higher in commuter cyclists compared to car drivers. Furthermore, exposure to PM is linked to negative neurological effects, such as neuroinflammation and cognitive decline. We carried-out a cross-over experiment to examine the acute effect of exercise on serum BDNF, and the potential effect-modification by exposure to traffic-related air pollution. Thirty eight physically fit, non-asthmatic volunteers (mean age: 43, 26% women) performed two cycling trials, one near a major traffic road (Antwerp Ring, R1, up to 260,000 vehicles per day) and one in an air-filtered room. The air-filtered room was created by reducing fine particles as well as ultrafine particles (UFP). PM10, PM2.5 and UFP were measured. The duration (∼20 min) and intensity of cycling were kept the same for each volunteer for both cycling trials. Serum BDNF concentrations were measured before and 30 min after each cycling trial. Average concentrations of PM10 and PM2.5 were 64.9 μg/m 3 and 24.6 μg/m 3 in cycling near a major ring way, in contrast to 7.7 μg/m 3 and 2.0 μg/m 3 in the air-filtered room. Average concentrations of UFP were 28,180 particles/cm 3 along the road in contrast to 496 particles/cm 3 in the air-filtered room. As expected, exercise significantly increased serum BDNF concentration after cycling in the air-filtered room (+14.4%; p = 0.02). In contrast, serum BDNF concentrations did not increase after cycling near the major traffic route (+0.5%; p = 0.42). Although active commuting is considered to be beneficial for health, this health enhancing effect could be negatively influenced by exercising in an environment with high concentrations of PM. Whether this effect is also present with chronic exercise and chronic exposure must be further elucidated.

The early non-increase of serum BDNF predicts failure of antidepressant treatment in patients with major depression: A pilot study

In the treatment of patients with major depressive disorder (MDD), early non-improvement of symptoms after initiation of antidepressant treatment is a highly sensitive and specific marker for final treatment failure. On the other hand, meta-analyses of clinical studies investigating serum BDNF (sBDNF) concentration before and after antidepressant treatment showed an increase of sBDNF during treatment, which was correlated with amelioration of depressive symptoms. No study has yet investigated the predictive value of early changes of sBDNF for final treatment outcome of the individual patient. The aim of this study was to investigate in patients with MDD, whether i) the non-increase of sBDNF in the early course of treatment is a specific and sensitive marker for final treatment failure, ii) whether the sensitivity and specificity of early non-improvement for treatment failure can be increased by combining it with the marker "early non-increase of sBDNF". For this purpose, we performed a pilot study with 41 inpatients with MDD according to DSM-IV, who were treated in a naturalistic setting. Depression severity and sBDNF were measured in weekly intervals from baseline to week six with the 21-item Hamilton Depression Rating Scale (HAMD-21) and ELISA, respectively. The individual markers sBDNF non-increase and HAMD-21 non-improvement from baseline to day 7 or 14 predicted later non-response and non-remission with moderate to high specificity. The combined marker sBDNF non-increase plus HAMD-21 non-improvement at day 14 increased the specificity for non-response and non-remission to 100%. Our data provide the first evidence that the absence of an early increase of sBDNF in conjunction with early non-improvement might be a highly specific peripheral marker predictive for treatment failure in patients with MDD. If replicated, this combined marker could be considered useful for prospective confirmatory trials in patients with MDD.