Reduced brain derived neurotrophic factor (BDNF) concentration is reported to be associated with a cognitive decline in schizophrenia, depending on the stage of the disease. Aim of the study was to ...examine the possible association between plasma BDNF and cognitive decline in chronic stable schizophrenia and mild cognitive impairment (MCI). The study included 123 inpatients of both sexes with schizophrenia, 123 patients with MCI and 208 healthy control subjects. Cognitive abilities were assessed using mini mental state examination (MMSE), Clock Drawing test (CDT) and cognitive subscale of the Positive and Negative Syndrome Scale (PANSS). Plasma BDNF concentration was determined using ELISA. BDNF concentration was lower in patients with schizophrenia and MCI compared to age-matched healthy controls and was similar in carriers of different BDNF Val/66Met genotypes. The MMSE and CDT scores were lower in patients with schizophrenia compared to healthy controls and subjects with MCI. Reduced plasma BDNF was significantly associated with lower MMSE scores in all subjects. BDNF concentration in patients with schizophrenia was not affected by clinical and demographic factors. BDNF Val66Met polymorphism was not associated with the MMSE scores in all participants. Further studies should include longitudinal follow-up and other cognitive scales to confirm these results and offer cognition-improving strategies to prevent cognitive decline in chronic schizophrenia.
► One-bout aerobic exercise induces increased BDNF levels in serum and plasma and within platelets. ► Basal BDNF levels are inversely correlated with cardiorespiratory fitness levels. ► BDNF ...immediately after exercise is positively correlated with cardiorespiratory fitness. ► Cardiorespiratory fitness levels are not correlated with platelet counts.
The most current human-based studies in which brain-derived neurotrophic factor (BDNF) levels in the peripheral blood system are analyzed use it as an indicator that represents BDNF levels in the CNS. However, whether circulating BDNF (serum and plasma) is positively or inversely associated with cardiorespiratory fitness levels (VO2max) is still controversial, and no study has done to investigate exercise effects on the concentration of BDNF stored in circulating platelets which, in fact, store a large amount of circulating BDNF. Thus, the purpose of this study was to determine the relation between VO2max and all circulating BDNF levels (serum, plasma and platelets) in college male students (N=18; age, 19±1 years; height, 173.22±7.65cm; weight, 78.25±14.25kg; body fat percent, 13.82±5.68%). Dual X-ray energy absorptiometry whole body scan was used to measure their body composition. After the overnight fast, all participants were performed VO2max test, and their blood was collected at rest and immediately after the exercise. Our data resulted in significant increases in platelet counts and serum, plasma and platelet BDNF levels immediately after the exercise (p<0.01). VO2max had a significant negative correlation with serum BDNF, plasma BDNF and platelet BDNF at rest (p<0.05) but a significant positive correlation with serum, plasma BDNF, and platelet BDNF immediately after the exercise (p<0.01). However, our data show no correlation between VO2max and platelet count both at rest and immediately after the exercise. In conclusion, this is the first study showing that basal BDNF levels are inversely correlated with cardiorespiratory fitness levels but that the inverse correlations turn into positive correlations with all circulating BDNF levels immediately after the exercise. Moreover, it is the first time to provide evidence that platelet BDNF levels are also positively affected by the exercise. However, future studies will be needed to investigate what tissues provide BDNF into the circulating system and to elucidate the role of circulating BDNF.
The Brain-Derived Neurotrofic Factor (BDNF) is one of the most important neurotrophins in the brain and it is suggested influences the activity of the serotonergic, noradrenergic and dopaminergic ...pathways. In the last few years, it has been hypothesized that BDNF level is related with depression and sleep. Several studies show that depressive subjects present low levels of BDNF in the brain. Poor sleep quality is also related with alterations in the BDNF concentration. Some authors argue that most of the cases show that impaired sleep quality increases the stress and, consequently, the vulnerability to depressive disorders, suggesting that there is a relationship between sleep, depression and BDNF levels.
OBJECTIVEDepression and cognitive impairment are both common non-motor symptoms of Parkinson's disease (PD). Brain-derived neurotrophic factor (BDNF) may play an important role in both cognitive ...function and depression. In this study, we examined BDNF levels, cognitive function, and the relationship between BDNF and cognitive function in PD patients with and without depressive symptoms, which has not been reported yet. METHODSWe recruited 96 PD patients with (n = 46) and without depression (n = 50) and 102 controls and examined the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and BDNF levels in all groups. The Zung Self-Rating Depression Scale (SDS) was used to assess the severity of depression and the Hoehn-Yahr staging test was used to assess motor abilities in PD patients. RESULTSBDNF levels were lower in patients with depressive symptoms than in patients without depressive symptoms (p<0.01). The RBANS total score and the immediate memory, language and attention scores were lower in patients with depressive than in patients without depressive (all p < 0.05). Multiple regression analysis showed that BDNF was independent contributor to immediate memory, language and RBANS total score in the patients with depressive symptoms. BDNF and SDS were independent contributors to attention, and SDS was an independent contributor to delay memory (all p < 0.001). CONCLUSIONSBDNF may be involved in the pathophysiology of PD patients with depressive symptoms. Moreover, the association between BDNF and cognitive performance only in patients with depressive symptoms suggest a close relationship in BDNF, cognition and depressive symptoms in PD patients.
Background: In the learned helplessness (LH) paradigm, approximately 35% of rats are resilient to inescapable stress. Methods: The roles of brain-derived neurotrophic factor (BDNF) and dendritic ...spine density in the brain regions of LH (susceptible) and non-LH rats (resilient) were examined. Western blot analysis and Golgi staining were performed. Results: BDNF levels in the medial prefrontal cortex, CA3, and dentate gyrus (DG) were significantly lower in the LH group than in the control and non-LH groups, whereas BDNF levels in the nucleus accumbens (NAc) in the LH group but not the non-LH group were significantly higher than those in the control group. Furthermore, spine density in the prelimbic cortex, CA3, and DG was significantly lower in the LH group than in the control and non-LH groups, although spine density in the NAc was significantly higher in the LH group than in the control and non-LH groups. Conclusions: The results suggest that regional differences in BDNF levels and spine density in rat brain may contribute to resilience to inescapable stress.
It is unclear how binding of antidepressant drugs to their targets gives rise to the clinical antidepressant effect. We discovered that the transmembrane domain of tyrosine kinase receptor 2 (TRKB), ...the brain-derived neurotrophic factor (BDNF) receptor that promotes neuronal plasticity and antidepressant responses, has a cholesterol-sensing function that mediates synaptic effects of cholesterol. We then found that both typical and fast-acting antidepressants directly bind to TRKB, thereby facilitating synaptic localization of TRKB and its activation by BDNF. Extensive computational approaches including atomistic molecular dynamics simulations revealed a binding site at the transmembrane region of TRKB dimers. Mutation of the TRKB antidepressant-binding motif impaired cellular, behavioral, and plasticity-promoting responses to antidepressants in vitro and in vivo. We suggest that binding to TRKB and allosteric facilitation of BDNF signaling is the common mechanism for antidepressant action, which may explain why typical antidepressants act slowly and how molecular effects of antidepressants are translated into clinical mood recovery.
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•Several antidepressants, including SSRIs and ketamine, directly bind to TRKB•TRKB dimerization at transmembrane region forms a binding pocket for fluoxetine•Antidepressant binding to TRKB facilitates BDNF action and plasticity•Point mutation in TRKB transmembrane region blocks the effects of antidepressants
Direct binding of both typical and fast-acting antidepressants to the BDNF receptor TRKB accounts for cell biological and behavioral actions of antidepressants. This mechanism directly connects antidepressant action to neuronal plasticity and may explain the slow action of typical antidepressants.
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