Keywords
Neuronal Homeostasis; Amyotrophic Lateral Sclerosis; Huntington’s disease
Abstract
As the expansion of global aging population with improved lifespan and loaded social burden, the incidence of neurological disorders including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD) and Amyotrophic Lateral Sclerosis (ALS) presents a continuous climbing trend [1]. All of these neurological disorders afflicting health status and quality of life for elderly and increasing medical burden to their family and society are highly associated with protein quality control, because damaged, mis-folded or aggregated proteins can cause the proteotoxic stress for cell functional impairment and the intracytoplasmic deposition of aggregate-prone proteins or dysfunctional mitochondria in neurons with limited treatment strategies [2].
Autophagy is a cellular self-consumption process characterized by sequestration of bulk cytoplasm, long-lived proteins and damaged cellular organelles in double membrane vesicles called autophagosomes, which are delivered to lysosomes for the degradation [3,4]. Protein quality control via autophagy is particularly important for the timely removal of aggregated forms of pathogenic proteins in neurodegenerative diseases, including tau in AD, α-synuclein in PD and polyQ-Htt in HD [5,6]. It is also a powerful and selective degradation process for dysfunctional mitochondria in neurons for maintaining mitochondrial homeostasis. A decline in autophagic function is a common trait of the aging process
Citation
Kou X and Chen N. Autophagy as the Modulator of Neuronal Homeostasis and Neurodegenerative Disorders. SM J Neurol Disord Stroke. 2016; 2(1): 1005.