Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family (consisting of nerve growth factor, BDNF, neurotrophin-3, and neurotrophin-4), has been intenselystudied concerning its positive effect on survival promotion and synaptic regulation in the central nervous system. TrkB, a high affinity receptor for BDNF, and its downstream signals including phosphoinositide 3-kinase (PI3K)/Akt, extracellular signal-regulated kinase (ERK) and phospholipase C pathways, are activated to maintain neuronal survival and regulate synaptic plasticity. Evidence suggests that decreased BDNF and TrkB-related signaling are involved in the pathogenesis ofneurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and Huntington’s disease (HD), establishing this neurotrophin as a therapeutic target in treating neurodegeneration. Dr. Tadahiro Numakawa comes from National Center of Neurology and Psychiatry, Japan considered that natural and small compounds activating the BDNF/TrkB system are promising therapeutic targets for the treatment of neurodegenerative diseases. On the other hand, much more in vitro and vivo studies to characterize the functioning of natural compounds as TrkB agonists are needed. Recently, glial production and secretion of growth factors including BDNF, stimulated by a variety of flavonoids, has been reported. In treating HD, the transplantation of stem cells overexpressing growth factors is considered to be a novel approach to improve disease symptoms. In addition, involvement of altered BDNF forms (proBDNF precursor or mature BDNF) in the pathophysiology of mental disorders and AD has been suggested. Precursor proneurotrophins, before proteolysis into mature neurotrophins, bind to the low affinity common receptor p75 with high affinity, ultimately causing cell death. To accelerate development of novel therapeutic agents for neurodegenerative diseases, not only are investigations of underlying mechanisms of BDNF upregulation in neurons necessary, but also studies investigating natural compounds using another cell population (glia and neural stem cells) and biosynthesis of BDNF. The relevant study has been published in the Neural Regeneration Research (Vol. 9, No. 16, 2014).
Article: "Possible protective action of neurotrophic factors and natural compounds against common neurodegenerative diseases" by Tadahiro Numakawa (Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1, Ogawa-Higashi, Kodaira, Tokyo, Japan)
Numakawa T. Possible protective action of neurotrophic factors and natural compounds against common neurodegenerative diseases. Neural Regen Res. 2014;9(16): 1506-1508.
Contact: Meng Zhao
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脑源性神经营养因子，是神经营养蛋白家族中的一员，包括神经生长因子、脑源性神经营养因子、神经营养因子-3和神经营养蛋白-4等，已经有大量研究证实了它们在中枢神经系统中对促进存活和调节突触的积极影响。TrkB，一种脑源性神经营养因子的高亲和力受体，其下游信号有磷酸肌醇3 - 激酶/ Akt蛋白和细胞外信号调节激酶及磷脂酶C途径，它们的被激活有助于维持神经元存活和调节突触可塑性。有证据表明，营养因子及其受体相关信号传导的减少与神经退行性疾病如阿尔茨海默氏病和帕金森氏病的发病机制有关，因此这种神经营养因子可作为治疗神经退行性变的治疗靶。来自日本国立神经科学与精神障碍研究所的Tadahiro Numakawa教授认为，天然和小化合物活化脑源性神经营养因子TrkB系统是可用于治疗神经退行性疾病的极有希望的治疗靶标。但同时，也需要有能够表现天然化合物作为TrkB活化剂功能特性的体外和体内研究。最近，已有研究报道了生长因子，包括脑源性神经营养因子的神经胶质产物与分泌物可经由多种黄酮类化合物刺激。想要加快能够用于神经退行性疾病新治疗剂的发展，不仅需要对神经元中BDNF表达上调机制进行研究，还需要研究天然化合物用于另一种细胞群（神经胶质细胞和神经干细胞）以及脑源性神经营养因子的生物合成。相关研究内容发表在2014年8月第16期《中国神经再生研究（英文版）》杂志上。
Article: "Possible protective action of neurotrophic factors and natural compounds against common neurodegenerative diseases" by Tadahiro Numakawa (Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1, Ogawa-Higashi, Kodaira, Tokyo, Japan)
Numakawa T. Possible protective action of neurotrophic factors and natural compounds against common neurodegenerative diseases. Neural Regen Res. 2014;9(16):1506-1508.
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