Autophagy as an Anti-senescent in Aging Neurocytes

Abstract

Abstract: Neuron homeostasis is crucial for the organism, and its maintenance is multifactorial, including autophagy. The turnover of aberrant intracellular components is a fundamental pathogenetic mechanism for cell aging. Autophagy is involved in the acceleration of the neurocyte aging process and the modification of cell longevity. Neurocyte aging is a process of loss of cell identity through cellular and subcellular changes that include molecular loss of epigenetics, transcriptomic, proteomic, and autophagy dysfunction. Autophagy dysfunction is the hallmark of neurocyte aging. Cell aging is the credential feature of neurodegenerative diseases. Pathophysiologically, aged neurocytes are characterized by dysregulated autophagy and subsequently neurocyte metabolic stress, resulting in accelerated neurocyte aging. In particular, chaperone- mediated autophagy perturbation results in upregulated expression of aging and apoptosis genes. Aged neurocytes are also characterized by the down-regulation of autophagy-related genes, such as ATG5-ATG12, LC3-II / LC3-I ratio, Beclin-1, and p62. Slowing aging through autophagy targeting is sufficient to improve prognosis in neurodegenerative diseases. Three primary anti-senescent molecules are involved in the aging process: mTOR, AMPK, and Sirtuins. Autophagy therapeutic effects can be applied to reverse and slow aging. This article discusses current advances in the role of autophagy in neurocyte homeostasis, aging, and potential therapeutic strategies to reduce aging and increase cell longevity.