Epigenetic events influencing the biological clock: Panacea for neurodegeneration.

The human biological clock is the 24-h internal molecular network of circadian genes in synchronization with other cells in response to external stimuli. The rhythmicity of the clock genes is maintained by positive and negative transcriptional feedback loops coordinating the 24-h oscillation in different tissues. The superchiasmatic nucleus, the central pacemaker of the biological clock diminishes with aging causing alterations in the clock rhythmicity leading to the onset of neurodegenerative diseases mainly Alzheimer's disease, Parkinson's disease, and Huntington's disease.

Embryonic ethanol exposure induces oxidative stress and inflammation in zebrafish model: A dose-dependent study.

Alcohol, or ethanol, is a major contributor to detrimental diseases and comorbidities worldwide. Alcohol use during pregnancy intervenes the developing embryos leading to morphological changes, neurocognitive defects, and behavioral changes known as fetal alcohol spectrum disorder (FASD). Zebrafish have been used as a model to study FASD; however, the mechanism and the impact of ethanol on oxidative stress and inflammation in the zebrafish FASD model remain unexplored.

Intertwined relationship of dynamin-related protein 1, mitochondrial metabolism and circadian rhythm.

In recent years, mitochondria have gained significant interest in the field of biomedical research due to their impact on human health and ageing. As mitochondrial dynamics are strongly controlled by clock genes, misalignment of the circadian rhythm leads to adverse metabolic health effects. In this review, by exploring various aspects of research and potential links, we hope to update the current understanding of the intricate relationship between DRP1-mediated mitochondrial dynamics and changes in circadian rhythmicity leading to health issues.