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Psychiatric Disorders in Women
Published in Michelle Tollefson, Nancy Eriksen, Neha Pathak, Improving Women's Health Across the Lifespan, 2021
Gia Merlo, Hanjun Ryu, Ariyaneh Nikbin
The precise mechanism by which these physiological changes occur in the brain is not fully known. However, evidence suggests that increases in neurotrophic factors such as insulin-like growth factor and brain-derived neurotrophic factor (BDNF) play a vital role.50 BDNF is upregulated in exercise and may explain the increase in neurogenesis. BDNF exerts its effects by binding to tropomyosin receptor kinase B (TrkB), which is highly expressed in hippocampal neurons. After binding, the BDNF-TrkB complex is internalized into the neuron and serves as a docking site for numerous cell signaling cascades.51,52 Through these effects, BDNF appears to promote neurogenesis and reduce neuroinflammation, increase volume of white matter, promote learning and memory, and potentially reduce symptoms of psychiatric disease.53 BDNF has in fact been hypothesized to play a major role in bipolar disorder, and all primary antidepressant modalities, as well as the mood stabilizers lithium and valproate, have been shown to increase BDNF while stressors decrease BDNF.54 Additionally, in mice, increases in BDNF from exercise were shown to decrease depressive-like behavior in chronically stressed rats.55 Therefore, it appears that exercise may be a potential modality for preventing and treating psychiatric disease through the effects of BDNF.
Cognition Enhancers
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Ramneek Kaur, Rashi Rajput, Sachin Kumar, Harleen Kaur, R. Rachana, Manisha Singh
Neurotrophins (NTs) are the family of proteins that help in functioning, survival, and development of neurons. Levi-Montalcini and Cohen discovered the nerve growth factor (NGF) (the first NT) in 1950s. After 30 years, brain-derived neurotrophic factor (BDNF) was discovered which was followed by NT-3, NT-4, then central neurotrophic factor (CNF), and members of glial cell line neurotrophic factor family. The widely studied NT pertaining to restoration of synapse is BDNF. The BDNF messenger ribonucleic acid (mRNA) are reduced during AD (Murray et al., 1994; Phillips et al., 1991; Connor et al., 1997) and process of aging (Calabrese et al., 2013). Similarly, another receptor of BDNF was tropomyosin receptor kinase B (TrkB). Phosphorylated TrkB is down-regulated in aged rats (Calabrese et al., 2013). PKC phosphorylates co-activator associated arginine methyltransferase 1 (CARM1), which is a protein that methylates HuD (RNA binding protein) that enhances the expression and stability of NT-3, NGF, and BDNF. The expression of these proteins has displayed an increase in development of hippocampal neurons in the culture (Lim and Alkon, 2012). Therefore, BDNF can be increased by modulating the receptor of NT and NT mRNA pharmacologically.
The Role of Nutraceuticals in Depression during Pregnancy and Postpartum Well-Being
Published in Priyanka Bhatt, Maryam Sadat Miraghajani, Sarvadaman Pathak, Yashwant Pathak, Nutraceuticals for Prenatal, Maternal and Offspring’s Nutritional Health, 2019
Fourthly, the neurotrophin family, particularly the brain-derived neurotrophic factor (BDNF), which binds with the tropomyosin receptor kinase B (TrkB) receptor, and the nerve growth factor (NGF), which binds with the tropomyosin receptor kinase A receptor, are important in the protection, survival, and proper function of the synaptic cell in the central and peripheral nervous systems (13,14). Low concentrations of some nutraceuticals increase down-regulation of neurotrophic factors and may, therefore, increase depressive symptoms (2).
Neuroprotective effect of Morin via TrkB/Akt pathway against diabetes mediated oxidative stress and apoptosis in neuronal cells
Published in Toxicology Mechanisms and Methods, 2022
Brain-derived neurotrophic factor (BDNF) is a neurotrophin that released from the central nervous system plays an important role in cell proliferation, synaptic function, morphogenesis, neurotransmission and protect neuronal cells from oxidative stress-mediated via TrkB (Tyrosine kinase receptor B) pathway (Murillo Ortíz et al. 2016). TrkB is a member of the tropomyosin-related kinase family. BDNF has high affinity to the TrkB receptor. It promotes cell survival, synaptic plasticity, development and differentiation of neurons. Binding BDNF to TrkB receptor elicits various intracellular signaling pathways, including phosphatidylinositol 3-kinase (PI3K)-Akt pathway (Meng et al. 2017; Baek and Kim 2020). Akt, a serine/threonine-protein kinase B (PKB), is the primary protein effector downstream of the PI3K signaling pathway. Akt has a vital role in glucose metabolism by regulating the biological function of insulin (Meng et al. 2017). Akt persuade the translocation of glucose transporter type 4 (GLUT4) to the plasma membrane, thereby mediating glucose uptake. Besides, Akt phosphorylates and inhibits the activity of glycogen synthase kinase 3 (GSK3), which enhance the activity of glycogen synthase and stimulates glycogen synthesis. As well, Akt being the major apoptosis-inhibiting protein, previous experimental studies have shown that the Akt signaling pathway is concerned with the pathophysiological processes of diabetes mellitus and its complications (He et al. 2017; Meng et al. 2017; Lu et al. 2017; Sifuentes-Franco et al. 2018).
Identification of vascular dementia and Alzheimer's disease hub genes expressed in the frontal lobe and temporal cortex by weighted co-expression network analysis and construction of a protein–protein interaction
Published in International Journal of Neuroscience, 2022
Xiaodou Tian, Yao Qin, Yuling Tian, Xiaoyan Ge, Jing Cui, Hongjuan Han, Long Liu, Hongmei Yu
SH3GL2 In synergy with SH3GL2, BDNF-NTRK2 mediate early endocytosis and early signal transduction. Brain derived neurotrophic factor (BDNF) is the dominant neurotrophic factor in the brain, which plays an important role in brain differentiation, regeneration and plasticity [48]. In nerve cells, BDNF binds with high affinity to the tropomyosin related kinase B (TrkB) receptor, leading to phosphorylation of TrkB and activation of three important downstream intracellular signaling cascades. These include phosphatidylinositol kinase/protein kinase B (PI3K/Akt) [49,50], phospholipase C-γ (PLC γ) and mitogen activated protein kinase/extracellular signal related kinase (MAPK/ERK) pathways. Such activated nerve cells can inhibit the endoplasmic reticulum stress response leading to neuron cell death [51,52]. This is a highly toxic mechanism caused by the accumulation of Aβ in AD [53].
Sex-biased transgenerational transmission of betaine-induced epigenetic modifications in glucocorticoid receptor gene and its down-stream BDNF/ERK pathway in rat hippocampus
Published in Nutritional Neuroscience, 2022
Yang Yang, Shu Yang, Yimin Jia, Chao Yin, Ruqian Zhao
Brain-derived neurotrophic factor (BDNF) is critical for hippocampal neurogenesis and synaptic plasticity [12,13]. BDNF binds to its receptor tropomyosin receptor kinase B (TrκB) and triggers the activation of two major signaling pathways involving phosphatidylinositol-3-kinase (PI3 K)/AKT and extracellular signal-regulated kinase 1/2 (ERK1/2) [14]. It was reported that maternal low-protein diet reduces BDNF expression in the brains of the neonatal rat offspring [15]. Maternal bisphenol A exposure induces impairment of object recognition memory, which is related to an inhibition of hippocampal BDNF and AKT/ERK pathway [16]. In contrast, maternal folate supplementation ameliorates maternal high-fat diet-induced behavior disorders through modulating DNA methylation of BDNF gene in offspring hippocampus [17]. Moreover, our previous study showed that maternal folate supplementation induces GR promoter hypomethylation, leading to GR activation and thereby BDNF/AKT/ERK1/2 up-regulation and hippocampal neurogenesis in mouse offspring [18].