Joshi Rajeev, Salton Stephen R J
Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Front Mol Neurosci. 2022 Jul 15;15:932497. doi: 10.3389/fnmol.2022.932497. eCollection 2022.
This article reviews the current progress in our understanding of the mechanisms by which growth factors, including brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF), and select neurotrophin-regulated gene products, such as VGF (non-acronymic) and VGF-derived neuropeptides, function in the central nervous system (CNS) to modulate neuropsychiatric and neurodegenerative disorders, with a discussion of the possible therapeutic applications of these growth factors to major depressive disorder (MDD) and Alzheimer's disease (AD). BDNF and VEGF levels are generally decreased regionally in the brains of MDD subjects and in preclinical animal models of depression, changes that are associated with neuronal atrophy and reduced neurogenesis, and are reversed by conventional monoaminergic and novel ketamine-like antidepressants. Downstream of neurotrophins and their receptors, VGF was identified as a nerve growth factor (NGF)- and BDNF-inducible secreted protein and neuropeptide precursor that is produced and trafficked throughout the CNS, where its expression is greatly influenced by neuronal activity and exercise, and where several VGF-derived peptides modulate neuronal activity, function, proliferation, differentiation, and survival. Moreover, levels of VGF are reduced in the CSF of AD subjects, where it has been repetitively identified as a disease biomarker, and in the hippocampi of subjects with MDD, suggesting possible shared mechanisms by which reduced levels of VGF and other proteins that are similarly regulated by neurotrophin signaling pathways contribute to and potentially drive the pathogenesis and progression of co-morbid neuropsychiatric and neurodegenerative disorders, particularly MDD and AD, opening possible therapeutic windows.
本文综述了我们目前对生长因子(包括脑源性神经营养因子(BDNF)和血管内皮生长因子(VEGF))以及特定神经营养因子调节的基因产物(如VGF(非首字母缩略词)和VGF衍生的神经肽)在中枢神经系统(CNS)中发挥作用以调节神经精神疾病和神经退行性疾病机制的理解进展,并讨论了这些生长因子在重度抑郁症(MDD)和阿尔茨海默病(AD)中的可能治疗应用。在MDD患者的大脑以及抑郁症临床前动物模型中,BDNF和VEGF水平通常在局部区域降低,这些变化与神经元萎缩和神经发生减少有关,并可被传统的单胺能和新型氯胺酮类抗抑郁药逆转。在神经营养因子及其受体的下游,VGF被鉴定为一种神经生长因子(NGF)和BDNF诱导的分泌蛋白及神经肽前体,它在整个CNS中产生和运输,其表达受神经元活动和运动的极大影响,并且几种VGF衍生的肽可调节神经元活动、功能、增殖、分化和存活。此外,AD患者脑脊液中VGF水平降低,在那里它已被反复鉴定为疾病生物标志物,在MDD患者的海马中也是如此,这表明VGF和其他受神经营养因子信号通路类似调节的蛋白质水平降低可能存在共同机制,导致并可能驱动共病的神经精神疾病和神经退行性疾病(特别是MDD和AD)的发病机制和进展,从而开启了可能的治疗窗口。