Introduction: Alterations in multiple subregions of the human prefrontal cortex (PFC) have been heavily implicated in psychiatric diseases. Moreover, emerging evidence suggests that circadian rhythms in gene expression are present across the brain, including in the PFC, and that these rhythms are altered in disease. However, investigation into the potential circadian mechanisms underlying these diseases in animal models must contend with the fact that the human PFC is highly evolved and specialized relative to that of rodents.
View Article and Find Full Text PDFThe intricate interplay between cellular circadian rhythms, primarily manifested in the chloroplast redox oscillations-characterized by diel hyperoxidation/reduction cycles of 2-Cys Peroxiredoxins-and the nuclear transcription/translation feedback loop (TTFL) machinery within plant cells, demonstrates a remarkable temporal coherence. However, the molecular mechanisms underlying the integration of these circadian rhythms remain elusive. Here, we elucidate that the chloroplast redox protein, NADPH-dependent thioredoxin reductase type-C (NTRC), modulates the integration of the chloroplast redox rhythms and nuclear circadian clocks by regulating intracellular levels of reactive oxygen species and sucrose.
View Article and Find Full Text PDFIntroduction: Circadian rhythm disturbances have long been associated with the development of psychiatric disorders, including mood and substance use disorders. Adolescence is a particularly vulnerable time for the onset of psychiatric disorders and for circadian rhythm and sleep disruptions. Preclinical studies have found that circadian rhythm disruption (CRD) impacts the brain and behavior, but this research is largely focused on adult disruptions.
View Article and Find Full Text PDFNPP Digit Psychiatry Neurosci
August 2024
The nature of data obtainable from the commercial smartphone - bolstered by a translational model emphasizing the impact of social and physical zeitgebers on circadian rhythms and mood - offers the possibility of scalable and objective vital signs for major depression. Our objective was to explore associations between passively sensed behavioral smartphone data and repeatedly measured depressive symptoms to suggest which features could eventually lead towards vital signs for depression. We collected continuous behavioral data and bi-weekly depressive symptoms (PHQ-8) from 131 psychiatric outpatients with a lifetime DSM-5 diagnosis of depression and/or anxiety over a 16-week period.
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