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Shift work schedules alter immune cell regulation and accelerate cognitive impairment during aging.

J Neuroinflammation

January 2025

Department of Neuroscience and Experimental Therapeutics, School of Medicine, Texas A&M Health Science Center, Bryan, TX, 77807-3260, USA.

Background: Disturbances of the sleep-wake cycle and other circadian rhythms typically precede the age-related deficits in learning and memory, suggesting that these alterations in circadian timekeeping may contribute to the progressive cognitive decline during aging. The present study examined the role of immune cell activation and inflammation in the link between circadian rhythm dysregulation and cognitive impairment in aging.

Methods: C57Bl/6J mice were exposed to shifted light-dark (LD) cycles (12 h advance/5d) during early adulthood (from ≈ 4-6mo) or continuously to a "fixed" LD12:12 schedule.

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Introduction: While risk factor prevalence of individual risk factors for dementia varies between ethnic groups in New Zealand (NZ), it is not known whether the effect of these risks is the same in each group.

Methods: This retrospective cohort study identified incident cases of dementia. Cox regression models calculated the hazard ratio for dementia for each of the risk factors, after adjustment for age and sex.

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Tumor initiation represents the first step in tumorigenesis during which normal progenitor cells undergo cell fate transition to cancer. Capturing this process as it occurs in vivo, however, remains elusive. Here we employ spatiotemporally controlled oncogene activation and tumor suppressor inhibition together with multiomics to unveil the processes underlying oral epithelial progenitor cell reprogramming into tumor initiating cells at single cell resolution.

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Ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX) is a chromatin modifier responsible for regulating the demethylation of histone H3 lysine 27 trimethylation (H3K27me3), which is crucial for human neurodevelopment. To date, the impact of UTX on neurodevelopment remains elusive. Therefore, this study aimed to investigate the potential molecular mechanisms underlying the effects of UTX on neurodevelopment through untargeted metabolomics based on ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS).

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Background: Anti-N-methyl-D-aspartate receptor encephalitis (anti-NMDARE) is a prevalent type of autoimmune encephalitis caused by antibodies targeting the NMDAR's GluN1 subunit. While significant progress has been made in elucidating the pathophysiology of autoimmune diseases, the immunological mechanisms underlying anti-NMDARE remain elusive. This study aimed to characterize immune cell interactions and dysregulation in anti-NMDARE by leveraging single-cell multi-omics sequencing technologies.

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