Autophagic defects are a hallmark of neurodegenerative disorders, such as Parkinson's disorder (PD). Enhancing autophagy to remove impaired mitochondria and toxic protein aggregation is an essential component of PD treatment. In particular, activation of autophagy confers neuroprotection in cellular and preclinical models of neurodegenerative diseases. In this study, we investigated the therapeutic mechanisms of electroacupuncture (EA) treatment in mice with established PD and evaluated the relationship between EA, autophagy, and different neurons in the mouse brain. We report that EA improves PD motor symptoms in mice and enhances (1) autophagy initiation (increased Beclin 1), (2) autophagosome biogenesis (increased Atg5, Atg7, Atg9A, Atg12, Atg16L, Atg3, and LC3-II), (3) autophagy flux/substrate degradation (decreased p62), and (4) mitophagy (increased PINK1 and DJ-1) in neurons of the substantia nigra, striatum, hippocampus, and cortex (affected brain areas of PD, Huntington disease, and Alzheimer's disease). EA enhances autophagy initiation, autophagosome biogenesis, mitophagy, and autophagy flux/substrate degradation in certain brain areas. Our findings are the first to show that EA regulates neuronal autophagy and suggest that this convenient, inexpensive treatment has exciting therapeutic potential in neurodegenerative disorders.
Keywords: Autophagy; Electroacupuncture; Mitophagy; Neurodegenerative Disease; Neuroprotection; Parkinson’s Disease.