Echeverria Valentina, Barreto George E, Avila-Rodriguezc Marco, Tarasov Vadim V, Aliev Gjumrakch
Facultad de Cs de la Salud, Universidad San Sebastian, Lientur 1457, Concepcion, 4030000, Chile.
Research and Development, Bay Pines VA Healthcare System, Bay Pines, FL, USA.
Curr Alzheimer Res. 2017;14(11):1155-1163. doi: 10.2174/1567205014666170329113007.
The vascular endothelial growth factor (VEGF) is a neuroprotective cytokine that promotes neurogenesis and angiogenesis in the brain. In animal models, it has been shown that environmental enrichment and exercise, two non-pharmacological interventions that are beneficial decreasing the progression of Alzheimer disease (AD) and depressive-like behavior, enhance hippocampal VEGF expression and neurogenesis. Furthermore, the stimulation of VEGF expression promotes neurotransmission and synaptic plasticity processes such as neurogenesis. It is thought that these VEGF actions in the brain, may underly its beneficial therapeutic effects against psychiatric and other neurological conditions.
In this review, evidence linking VEGF deficit with the development of AD as well as the potential role of VEGF signaling as a therapeutic target for cotinine and other interventions in neurodegenerative conditions are discussed.
血管内皮生长因子(VEGF)是一种神经保护细胞因子,可促进大脑中的神经发生和血管生成。在动物模型中,研究表明环境富集和运动这两种有益减少阿尔茨海默病(AD)进展和抑郁样行为的非药物干预措施,可增强海马体中VEGF的表达和神经发生。此外,VEGF表达的刺激可促进神经传递和突触可塑性过程,如神经发生。人们认为VEGF在大脑中的这些作用,可能是其对精神疾病和其他神经疾病产生有益治疗效果的基础。
在本综述中,讨论了将VEGF缺乏与AD的发展联系起来的证据,以及VEGF信号作为可替宁和其他神经退行性疾病干预措施的治疗靶点的潜在作用。