The growth factor brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase receptor type B (TRKB) are actively produced and trafficked in multiple regions in the adult brain, where they influence neuronal activity, function and survival throughout life. The diverse presence and activity of BDNF suggests a potential role for this molecule in the pathogenesis and treatment of both neurological and psychiatric disorders. This article reviews the current understanding and future directions in BDNF-related research in the central nervous system, with an emphasis on the possible therapeutic application of BDNF in modifying fundamental processes underlying neural disease.
"BDNF in the blood may reflect the level of BDNF in the brain. Together, these findings confirm that BDNF is involved in schizophrenia (Nagahara and Tuszynski, 2011). A further finding of our present study is the increased IL-2, IL-6, and IL-8 levels but decreased TNF-a levels in chronic schizophrenia patients. "
[Show abstract][Hide abstract] ABSTRACT: Brain-derived neurotrophic factor (BDNF) interacts with cytokines. Although both BDNF and cytokines occur at abnormal levels in schizophrenia patients, their interactions have not yet been examined. We therefore compared serum BDNF, TNF-α, interleukin (IL)-2, IL-6, and IL-8 levels in 92 chronically medicated schizophrenia patients and 60 healthy controls. We correlated these serum levels within these subject groups with each other and with clinical symptoms assessed according to the Positive and Negative Syndrome Scale (PANSS). Compared to the control group, the schizophrenia patients had significantly lower BDNF and TNF-α levels, and higher IL-2, IL-6, and IL-8 levels. The patients also showed a significant positive correlation between BDNF and both IL-2 and IL-8 levels, and low BDNF and TNF-α levels together were associated with poor performance on the PANSS cognitive factor. Thus, an interaction between cytokines and neurotrophic factors may be implicated in the pathophysiology of chronic schizophrenia. In particular, the cytokine TNF-α may interact with BNDF causing cognitive impairment.
Brain Behavior and Immunity 09/2015; DOI:10.1016/j.bbi.2015.09.014 · 5.89 Impact Factor
"Our data showed that these two treatment groups exhibited no significant difference on stimulating TrkB phosphorylation 6 h following SAH, while the HIOC group showed improved neurobehavioral outcomes and exerted a tendency of activating TrkB more potently than the BDNF group 24 h post-SAH (Figs. 5, 6). It has been reported that BDNF has poor blood brain barrier penetrability and short serum half-life, and induces TrkB polyubiquitination and degradation, and these features made BDNF's clinical application problematic (Nagahara and Tuszynski, 2011; Shen et al., 2012). From this observation , it seems that HIOC, as a small compound, is more efficient and has prolonged effects on activating TrkB and its downstream effector than BDNF, thus a good candidate for future consideration. "
"Thus, lower levels of BDNF are consistent with the hypothesis that a deficit in this neurotrophic factor may contribute to the structural and functional alterations of brain X.Y. Zhang et al. underlying the psychopathology of schizophrenia (Nagahara and Tuszynski, 2011), supporting the hypothesis of a neurodegenerative process in schizophrenia. A further finding of our present study is decreased activities of SOD and GSH-Px and unchanged CAT in chronic patients with schizophrenia, which is in agreement with some recent studies finding a decrease of erythrocyte SOD and GSH-Px levels (Ranjekar et al., 2003; Zhang et al., 2006; Ben Othmen et al., 2008). "
[Show abstract][Hide abstract] ABSTRACT: Neurodegenerative processes may be involved in the pathogenesis of schizophrenia. Brain-derived neurotrophic factor (BDNF), the most widely distributed neurotrophin and oxidative stress (OS) may be critical for several pathological manifestations of neurodegenerative disorders. Accumulating evidence suggests that both BDNF and OS may be involved in the pathophysiology of schizophrenia. However, the possible interaction between BDNF and OS has been under-investigated. Serum BDNF, plasma malondialdehyde (MDA) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were analyzed using established procedures in 164 chronic medicated schizophrenia and 50 healthy controls. Schizophrenic symptoms were assessed by the Positive and Negative Syndrome Scale (PANSS) with cognitive and depressive factors derived from the five factor model of the PANSS. Compared to the control group, the patients exhibited a significant decrease in BDNF levels, in the activities of SOD and GSH-Px but a significant increase in MDA levels. In patients, but not in controls, we observed a significant negative correlation between BDNF and SOD. Furthermore, the interaction between BDNF and CAT was associated with the PANSS cognitive factor, and the interaction between BDNF and GSH-Px with the PANSS depressive factor. Both decreased BDNF levels and OS may be implicated in the pathophysiology of chronic schizophrenia. Their inverse association only in the schizophrenia group may reflect a pathological mechanism involving an interaction of oxidative damage and neurotrophin dysfunction. Moreover, OS may interact with the BDNF system to influence the clinical symptoms and cognitive impairment in schizophrenia, which is line with the neurodevelopmental hypothesis of schizophrenia.
Nazi Chen, Jishen Ma, Yang Zhao, Meiyu Wu, Huanhuan Yang, Weiyue Gong, Jiang Chao, Xiaokun Li
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