Abstract
With aging, the nervous system gradually undergoes degeneration. Increased oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, and cell death are considered to be common pathophysiological mechanisms of various neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), organophosphate-induced delayed neuropathy (OPIDN), and amyotrophic lateral sclerosis (ALS). Autophagy is a cellular basic metabolic process that degrades the aggregated or misfolded proteins and abnormal organelles in cells. The abnormal regulation of neuronal autophagy is accompanied by the accumulation and deposition of irregular proteins, leading to changes in neuron homeostasis and neurodegeneration. Autophagy exhibits both a protective mechanism and a damage pathway related to programmed cell death. Because of its “double-edged sword”, autophagy plays an important role in neurological damage and NDDs including AD, PD, HD, OPIDN, and ALS. Melatonin is a neuroendocrine hormone mainly synthesized in the pineal gland and exhibits a wide range of biological functions, such as sleep control, regulating circadian rhythm, immune enhancement, metabolism regulation, antioxidant, anti-aging, and anti-tumor effects. It can prevent cell death, reduce inflammation, block calcium channels, etc. In this review, we briefly discuss the neuroprotective role of melatonin against various NDDs via regulating autophagy, which could be a new field for future translational research and clinical studies to discover preventive or therapeutic agents for many NDDs.
Highlights
Neurodegenerative diseases (NDDs) represent a variety of aging-related non-curable diseases that selectively target different neuron populations in the central nervous system (CNS)
This review briefly discussed the role of autophagy in neuronal cell death, focusing on the dual role of autophagy in neurons
As an important neuroprotective agent, melatonin can exhibit beneficial effects on various NDDs, suggesting that melatonin regulates the autophagy process through different mechanisms (Figure 2)
Summary
Neurodegenerative diseases (NDDs) represent a variety of aging-related non-curable diseases that selectively target different neuron populations in the central nervous system (CNS). Autophagy is a catabolic process to degrade the cytoplasmic components and remove dysfunctional components, such as damaged organelles and proteins [7,8]. It is closely linked with cell growth, development, and various diseases, depending on the cellular contexts, environments, and exposures to certain agents. Impaired autophagy in humans leads to the aggregation and accumulation of beta-amyloid (Aβ), cytoskeleton-related protein tau, and β-synuclein in neuronal cells and tissues, even though the contributing role of these aggregated proteins is not well understood in the specific etiology of each NDD. To explore the roles of autophagy and identify protective factors in various NDDs is of great significance for early diagnosis, prevention, and development of effective therapeutic methods
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