School of Life Sciences, BS Abdur Rahman Crescent Institute of Science and Technology, Chennai, Tamil Nadu, India.
Cell Biochem Funct. 2021 Jul;39(5):613-622. doi: 10.1002/cbf.3630. Epub 2021 Mar 1.
In recent years, neurodegeneration has been recognized as a clinical condition that is characterized by neuronal death, dementia, and gradual diminish of cognitive function, poor body coordination and motor disorders. Several studies deciphering cellular and molecular mechanisms show a promising insight for several kinds of damages including neurodegeneration in central nervous system. In addition, there has been an inflammatory key mechanism involved in neurodegenerative disorders. There is a paucity of literature in both cellular- and molecular-mediated targets in damaged neurons at both in vitro and in vivo research models. It has been notified that CNS has a very restricted magnitude of regeneration. Numerous key factors have also been studied and considered as possible culprit of neurodegeneration. Autophagy is a well-known degradation process wherein vesicular machinery as autophagosome transports cytoplasmic contents to the lysosomes. In earlier reports, a bridging connection between autophagy and its associated mechanism has been established. Natural compounds as a neuro-therapeutics have been recognized in neurodegeneration. In our review, we discuss the mechanisms for the onset and progression in neurodegeneration, via inflammation and autophagic machine available in cellular compartments in CNS. This review also discusses about the neuroprotective efficacy of natural compounds against neurodegeneration episodes displays in neuronal platform.
近年来,神经退行性疾病已被认为是一种临床病症,其特征是神经元死亡、痴呆以及认知功能逐渐下降、身体协调能力差和运动障碍。一些研究揭示了细胞和分子机制,为包括中枢神经系统神经退行性病变在内的多种损伤提供了有希望的见解。此外,神经退行性疾病还涉及炎症的关键机制。在体外和体内研究模型中,受损神经元的细胞和分子介导靶点的文献都很少。据报道,中枢神经系统的再生能力非常有限。许多关键因素也被研究并认为是神经退行性变的可能罪魁祸首。自噬是一种众所周知的降解过程,其中囊泡机制(自噬体)将细胞质内容物运输到溶酶体。在早期的报告中,已经建立了自噬与其相关机制之间的桥梁连接。天然化合物作为神经治疗药物已在神经退行性疾病中得到认可。在我们的综述中,我们讨论了通过中枢神经系统细胞区室中的炎症和自噬机制,神经退行性疾病的发病和进展的机制。本综述还讨论了天然化合物对神经元平台上显示的神经退行性病变发作的神经保护作用。