Molecular Mechanisms of REM Sleep

Yamada, Rikuhiro G.; Ueda, Hiroki R.

doi:10.3389/fnins.2019.01402

Cited by 32 publications

(14 citation statements)

References 133 publications

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“…The dopamine receptor-signaling pathway regulating sleep, learning, and its plasticity are well known [84,85]. Sleep disorders and sleep deprivation have been correlated with dopaminergic, cholinergic, and GABAergic regulation of synaptic transmission, each of which were terms that were significantly enriched for genes that were downregulated in our study [86–90]. These observations support our hypothesis that REM sleep loss negatively affect the gens and processes related to synaptic homeostasis in brain.…”

Section: Discussionsupporting

confidence: 87%

Differential gene expression in brain and liver tissue of Wistar rats after rapid eye movement sleep deprivation

Pandey

Oliver

Kar

2019

Preprint

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Short title:REM sleep deprivation differentially affects the genes of liver and brain in rats. Highlights of the study: Microarray analysis compared the expression pattern of genes related to many biological, molecular and physiological processes in brain and liver. Analysis revealed about the basic genetic tool-kit involved with REM sleep deprivation and its loss in brain and liver. Many of the genes involved in critical physiological processes like apoptosis and circadian rhythms are found differentially expresses in brain and liver. AbstractFundamental questions about sleep and its universal existence remain elusive. The common presence of sleep across phyla suggests that it must serve some indispensable cellular and/or molecular function needed for survival. Microarray studies, performed in several model systems, have identified classes of genes that are believed to regulate "sleep-state" or viceversa. This has led to the following concepts: first, a function of sleep is to maintain synaptic homeostasis; second, sleep is a stage of macromolecule biosynthesis which is needed during the waking period; third, extending wakefulness leads to the downregulation of several important metabolic pathways which needs to be balanced for extended survival; and, fourth, extending wakefulness leads to endoplasmic reticulum stress. In human sleep studies, microarrays are being pragmatic to the identification of biomarkers for sleepiness and for the common sleep disorders. This study tries to find out the correlative processes which happen across different tissue system in the maintenance of sleep. We compared the gene expression profile in brain and liver due to REM sleep deprivation. Our result suggests that sleep deprivation affects a different set of genes in the brain and liver.

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Section: Discussionsupporting

confidence: 87%

Differential gene expression in brain and liver tissue of Wistar rats after rapid eye movement sleep deprivation

Pandey

Oliver

Kar

2019

Preprint

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“…Although this may be a valuable aspect to take into consideration, further studies including functional analysis of the gene effect on the toxicity of beta-amyloid and other AD proteins remains to be performed. The recent discovery of muscarinic receptor genes as crucial for REM sleep [17] and that on the importance of night sleep for removing brain debris [18]. This and earlier studies may miss the genes involved in the mechanism of sleep and others, while non-coding RNAs [19] are also identified, including miR142 [1,8,13].…”

Section: Discussionmentioning

confidence: 99%

Evidence-Based Genetics and Identification of Key Human Alzheimer’s Disease Alleles with Co-morbidities

Le¹,

Crouch²,

Villanueva³

et al. 2020

J Neurol Exp Neurosci

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Advancements in biomedical research have contributed to increasing the life expectancy of humans, but we now observe an increase in age-related diseases such as Alzheimer's disease. Genome-Wide Association Studies (GWAS) and linkage studies have identified human genes associated with Alzheimer's disease (referred to as AD genes). A previous study by Vahdati in 2017 has revealed the human AD genes and counterparts in model species [1]. Thus, we further investigate the co-morbidity genes and alleles. Using ontology analysis combined with cluster analysis, the study identified functional pathways enriched among the human AD genes, including 179 genes out of 695 human AD genes (26%) that were associated with one or more of the four neurological diseases including Amyotrophic lateral sclerosis, Multiple sclerosis, Parkinson's disease, and Schizophrenia [1]. More importantly, the results indicate co-morbidities with Late-Onset Alzheimer's Disease (LOAD) and other neurological conditions, implying the complexity of the phenotypes in the human AD. The co-morbidity genes may account for mixed symptoms for human AD as well as age-related risks of infections. Of them, the three genes are well conserved (Angiotensin I Converting Enzyme gene, ACE; Methylenetetrahydrofolate Reductase gene, MTHFR; and tumor necrosis factor gene, TNF). In this study, we confirmed the comorbidity of the three genes associated with AD. We further identified the comorbidity of two alleles in the MTHFR gene, C677T and A222V, significantly associated with Alzheimer's disease. This study provides an example of evidencebased analysis that is cost-effective and may be an effective approach to develop cure-alls for multiple diseases.

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“…One of the reasons would be that current animal models are reflecting only in part RTT, for example, in animal models one may alter a single gene whereas in RTT likely more genes are affected (Ehrhart et al., 2016). Alternatively, the brain structures responsible for REM sleep generation and maintenance such as the mesopontine tegmentum (Yamada & Ueda, 2019) may show minimal misexpression by the gene(s). No publications on Foxg1 mutation models investigating sleep were found.…”

Section: Discussionmentioning

confidence: 99%

Sleep problems in Rett syndrome animal models: A systematic review

Zhang

Lin

Spruyt

2020

J of Neuroscience Research

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Rett Syndrome (RTT, MIM 312750), a progressive neurodevelopmental disease, has an approximately incidence rate of 1 in 10,000 (Neul et al., 2010) in live female births. RTT becomes visible through a neurodevelopmental regression following 6 to 18 months apparent normal developmental period. Loss of acquired language skills, stereotypic hand movements, and comprehensive cognitive, social, motor skill

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Molecular Mechanisms of REM Sleep

Cited by 32 publications

References 133 publications

Differential gene expression in brain and liver tissue of Wistar rats after rapid eye movement sleep deprivation

Differential gene expression in brain and liver tissue of Wistar rats after rapid eye movement sleep deprivation

Evidence-Based Genetics and Identification of Key Human Alzheimer’s Disease Alleles with Co-morbidities

Sleep problems in Rett syndrome animal models: A systematic review

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