The spectrum of sleep disorders in parkinson disease: a review Annie C Lajoie, Anne-Louise Lafontaine, Marta Kaminska Chest 159 (2), 818-827, 2021 There is increasing interest in the effects of sleep and sleep disturbances on the brain, particularly in relation to aging and neurodegenerative processes. Parkinson disease (PD) is the second most common neurodegenerative disorder, with growing prevalence worldwide. Sleep disorders, including sleep-disordered breathing (SDB), are among the most frequent non-motor manifestations of PD. They can substantially impair quality of life and possibly affect the course of the disease. This article reviews the etiology, implications, and management of … View at sciencedirect.com Cited by 12 Related articles All 5 versions embopress.org SGK1 inhibition in glia ameliorates pathologies and symptoms in Parkinson disease animal models Oh‐Chan Kwon, Jae‐Jin Song, Yunseon Yang, Seong‐Hoon Kim, Ji Young Kim, Min‐Jong Seok, Inhwa Hwang, Je‐Wook Yu, Jenisha Karmacharya, Han‐Joo Maeng, Jiyoung Kim, Eek‐hoon Jho, Seung Yeon Ko, Hyeon Son, Mi‐Yoon Chang, Sang‐Hun Lee EMBO molecular medicine 13 (4), e13076, 2021 Astrocytes and microglia are brain‐resident glia that can establish harmful inflammatory environments in disease contexts and thereby contribute to the progression of neuronal loss in neurodegenerative disorders. Correcting the diseased properties of glia is therefore an appealing strategy for treating brain diseases. Previous studies have shown that serum/ glucocorticoid related kinase 1 (SGK1) is upregulated in the brains of patients with various neurodegenerative disorders, suggesting its involvement in the pathogenesis of those diseases. In this study, we show that inhibiting glial SGK1 corrects the pro‐inflammatory properties of glia by suppressing the intracellular NFκB‐, NLRP3‐inflammasome‐, and CGAS‐STING‐mediated inflammatory pathways. Furthermore, SGK1 inhibition potentiated glial activity to scavenge glutamate toxicity and prevented glial cell senescence and mitochondrial damage, which have recently been reported as critical pathologic features of and therapeutic targets in Parkinson disease (PD) and Alzheimer disease (AD). Along with those anti‐inflammatory/neurotrophic functions, silencing and pharmacological inhibition of SGK1 protected midbrain dopamine neurons from degeneration and cured pathologic synuclein alpha (SNCA) aggregation and PD‐associated behavioral deficits in multiple in vitro and in vivo PD models. Collectively, these findings suggest that SGK1 inhibition could be a useful strategy for treating PD and other neurodegenerative disorders that share the common pathology of glia‐mediated neuroinflammation.