Similar Datasets
Project description:Hyperexcitable arousal circuits cause sleep instability during aging
| PRJNA673632 | ENA
Project description:Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors
| PRJNA580049 | ENA
Project description:Alterations in metabolism, sleep patterns, body composition, and hormone status are all key features of aging. The hypothalamus is a well-conserved brain region that controls these homeostatic and survival-related behaviors. Despite the importance of this brain region in healthy aging, little is known about the intrinsic features of hypothalamic aging. Here, we utilize single nuclei RNA-sequencing to assess the transcriptomes of 40,064 hypothalamic nuclei from young and aged female mice. We identify cell type-specific signatures of aging in neurons, astrocytes, and microglia, as well as among the diverse collection of neuronal subtypes in this region. We uncover key changes in cell types critical for metabolic regulation and body composition, as well as in an area of the hypothalamus linked to cognition. In addition, our analysis reveals female-specific changes in sex chromosome regulation in the aging brain. This study identifies critical cell-specific features of the aging hypothalamus in mammals.
2022-05-20 | GSE188646 | GEO
Project description:To investigate the prevalence of binge viewing, its association with sleep and examine arousal as an underlying mechanism of this association.Four hundred twenty-three adults (aged 18-25 years old, 61.9% female) completed an online survey assessing regular television viewing, binge viewing, sleep quality (Pittsburgh Sleep Quality Index), fatigue (Fatigue Assessment Scale), insomnia (Bergen Insomnia Scale), and pre-sleep arousal (Pre-Sleep Arousal Scale). Regression analyses were conducted. Mediation analysis was performed using PROCESS Macro.There were 80.6% who identified themselves as a binge viewer. Among those who binge viewed (n = 341), 20.2% had binge viewed at least a few times a week during the past month. Among poor sleepers (Pittsburgh Sleep Quality Index > 5), 32.6% had a poor sleep quality associated with being a binge viewer. Higher binge viewing frequency was associated with a poorer sleep quality, increased fatigue and more symptoms of insomnia, whereas regular television viewing was not. Cognitive pre-sleep arousal fully mediated these relationships.New viewing styles such as binge viewing are increasingly prevalent and may pose a threat to sleep. Increased cognitive arousal functions as the mechanism explaining these effects. Measures of media exposure should take into account the user's level of engagement with media. Interventions aimed at (1) alerting viewers about excessive viewing duration and (2) reducing arousal before sleep may be useful ways to tackle sleep problems in binge viewers.
| S-EPMC5529125 | biostudies-other
Project description:Imprinted genes are highly expressed in the hypothalamus, however whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at the chromosome 15q11-q13, characterised with a hypothalamic insufficiency. Here we investigate the role of paternally expressed Snord116 gene within the context of sleep and metabolic abnormalities of PWS, and we report a novel role of this imprinted gene in the function and organisation of the two main neuromodulatory systems of the lateral hypothalamus (LH), namely the orexin (OX) and the melanin concentrating hormone (MCH). We observe that the dynamic between neuronal discharge in the LH and sleep-wake states of mice carrying the paternal deletion of the Snord116 (PWScrm+/p-) is compromised. This abnormal state-dependent neuronal activity is paralleled by a significant reduction of OX neurons in LH of mutants. Therefore, we propose that unbalance between OX- and MCH- expressing neurons in the LH of mutants reflects in a series of deficits manifested in the PWS, such as dysregulation of rapid eye movement (REM) sleep, food intake and temperature control.
2020-05-25 | GSE139524 | GEO
Project description:The aim of the study was to assess the cellular composition and transcriptional changes at single-cell resolution of the female reproductive tract during ageing in ovary, oviduct and uterus. Tissues of aged mice were collected at the age of 9,12 and 15 months. All tissues were collected and digested using a collagenase and trypsin protocol to obtain single cell suspension. Libraries were prepared using the 10x scRNA-seq protocol.
2024-01-31 | E-MTAB-12889 | biostudies-arrayexpress
Project description:Aging leads to time-dependent functional decline of all major organs. In particular, the aging brain is susceptible to cognitive decline and several neurodegenerative diseases. To characterize the aging process and understand the underlying molecular mechanisms, numerous studies have examined changes in gene expression in the aging mouse brain using high-throughput sequencing. However, microRNA-mediated post-transcriptional regulation of gene expression has not yet been comprehensively elucidated. In this study, we performed global analysis of mRNA and microRNA expression simultaneously in the hypothalamus and hippocampus of young and aged mice. We identified aging-dependent differentially expressed genes, most of which were specific to the hypothalamus or hippocampus.
2023-09-12 | GSE231582 | GEO
Project description:Comparative transcriptomics of the garden dormouse hypothalamus during early torpor, late torpor and interbout arousal of hibernation
2023-11-13 | GSE207494 | GEO
Project description:Sir2 is a highly conserved NAD+-dependent histone deacetylase that functions in heterochromatin formation and promotes replicative lifespan (RLS) in the budding yeast, Saccharomyces cerevisiae. Within the yeast rDNA locus, Sir2 is required for efficient cohesin recruitment and maintaining stability of the tandem array. In addition to the previously reported depletion of Sir2 in replicatively aged cells, we discovered that subunits of the Sir2 containing complexes, SIR and RENT, were depleted. Several other rDNA structural protein complexes also exhibited age-related depletion, most notably the cohesin complex. We hypothesized that mitotic chromosome instability (CIN) due to cohesin depletion could be a driver of replicative aging. ChIP assays of the residual cohesin (Mcd1-13xMyc) in moderately aged cells showed strong depletion from the rDNA and initial redistribution to the point centromeres, which was then lost in older cells. Despite the shift in cohesin distribution, sister chromatid cohesion was partially attenuated in aged cells and the frequency of chromosome loss was increased. This age-induced CIN was exacerbated in strains lacking Sir2 and its paralog, Hst1, but suppressed in strains that stabilize the rDNA array due to deletion of FOB1 or through caloric restriction (CR). Furthermore, ectopic expression of MCD1 from a doxycycline-inducible promoter was sufficient to suppress rDNA instability in aged cells and to extend RLS. Taken together we conclude that age-induced depletion of cohesin and multiple other nucleolar chromatin factors destabilize the rDNA locus, which then results in general CIN and aneuploidy that shortens RLS.
2019-03-12 | GSE117037 | GEO
Project description:Humans and animals lacking orexin neurons exhibit daytime sleepiness, sleep attacks, and state instability. While the circuit basis by which orexin neurons contribute to consolidated wakefulness remains unclear, existing models posit that orexin neurons provide their wake-stabilizing influence by exerting excitatory tone on other brain arousal nodes. Here we show using in vivo optogenetics, in vitro optogenetic-based circuit mapping, and single-cell transcriptomics that orexin neurons also contribute to arousal maintenance through indirect inhibition of sleep-promoting neurons of the ventrolateral preoptic nucleus. Activation of this subcortical circuit rapidly drives wakefulness from sleep by differentially modulating the activity of ventrolateral preoptic neurons. We further identify and characterize a feedforward circuit through which orexin (and co-released glutamate) acts to indirectly target and inhibit sleep-promoting ventrolateral preoptic neurons to produce arousal. This revealed circuitry provides an alternate framework for understanding how orexin neurons contribute to the maintenance of consolidated wakefulness and stabilize behavioral state.
| S-EPMC9293990 | biostudies-literature