Sleep is an evolutionarily conserved phenomenon which has survived tremendous evolutionary pressures. Its disruption has deleterious implications for human health. The importance of sleep is illustrated by the fact that sleep deprivation in many animals leads to death. While sleep is tightly regulated by a combination of intrinsic and extrinsic factors it becomes progressively disrupted in old age and in neurodegenerative diseases including Alzheimer’s disease (AD), frontotemporal dementia (FTD), Parkinson’s disease (PD) and Huntington’s disease (HD). One of the key effects of sleep disruption is increased levels of reactive oxygen/nitrogen species (ROS/RNS) and accumulation of protein aggregates, such as Amyloid β and alpha-Synuclein. A possible mechanism of protein plaque clearance is its autophagic degradation through endo-lysosomal pathways. In this review, we will discuss how sleep disruption is intimately linked with neurodegenerative diseases. We will also discuss the evidence that cellular autophagy and antioxidant defense are regulated by sleep, making it a target for future intervention strategies to tackle neurodegenerative diseases.
ROS, RNS, REM, NREM, Autophagy, Glia