Table 1.

Neurodegenerative diseases that display alterations in protein homeostatic regulation and sleep disruptions.

Disease	Evidence of ER stress in disease phenotypes	Sleep disruptions observed
Alzheimer’s Disease (AD)	Increased BiP expression in neurons of AD patients (Hoozemans et al., 2005) Increased CHOP leads to proapotosis in AD (Lee et al., 2010) Reduction of PERK rescues memory and cholinergic neurodegeneration (Devi and Ohno, 2014) Excessive eIF2α phosphorylation associated with memory loss in models of AD (Costa-Mattioli et al., 2009; Ma et al., 2013; Trinh and Klann, 2013)	Fragmented sleep, increased daytime sleepiness, REM disruptions (Prinz et al., 1982; Vitiello and Prinz, 1989; Bliwise, 2004)
Parkinson’s Disease (PD)	Neuron loss in an α-Synuclein model of PD occurs concomitantly with ER chaperone induction (Colla et al., 2012) ATF4 induction in rat dopamine neurons of the substantia nigra results in degeneration (Gully et al., 2016) ER stress in pink1/parkin models of PD leads to neurodegeneration (Celardo et al., 2016)	REM disruptions, excessive daytime sleepiness (Gagnon et al., 2002; Iranzo, 2011)
Frontotemporal Dementia (FTD)	The rTg4510 mouse model of FTD displays an increase in levels of ATF4, p-PERK, p-eIF2α, and BiP (Abisambra et al., 2013; Radford et al., 2015)	Insomnia, sleep disordered breathing, excessive daytime sleepiness (McCarter et al., 2016)
Huntington’s Disease (HD)	BiP and CHOP are upregulated in HD patient brains (Carnemolla et al., 2009) Soluble oligomers of htt activate ER stress (Leitman et al., 2013)	Increased latency to sleep, frequent nocturnal awakening, reduced sleep efficiency (Wiegand et al., 1991; Morton et al., 2005)
Amyotrophic Lateral Sclerosis (ALS)	Elevated levels of ER stress markers, CHOP, XBP1s, and BiP/GRP78 in motor neurons in an animal model of ALS (Ito et al., 2009; Wang et al., 2011; Das et al., 2015)	Daytime sleepiness, sleep disordered breathing (Ferguson et al., 1996; Lo Coco et al., 2011)