Findings suggest that PER3 gene variants prevent adrenal adaptation to winter daylight, leading to serotonin disruption and depression-like behaviors. Study: Human PERIOD3 variants lead to winter depression-like behaviours via glucocorticoid signalling . Image Credit: Yanya/Shutterstock.
com A recent study in Nature Metabolism used humanized mice with modified PERIOD3 gene variants (P415A and H417R) to explore the genetic role in winter seasonal affective disorder (SAD). Male mice exposed to short, winter-like daylight showed SAD-like behaviors, validating them as potential models for SAD research. The study revealed that these gene variants increase corticosterone biosynthesis and disrupt HPA axis regulation, leading to elevated glucocorticoid signaling.
This signaling represses Tryptophan hydroxylase 2 (Tph2), resulting in depression-like behaviors. Study background Several human physiological processes and clinical conditions exhibit seasonal rhythms, often linked to increases in pathogen or vector populations (in the case of transmissible diseases) or changes in environmental cues (such as mood and physiological shifts due to jetlag). A growing body of research describes seasonal trends in psychiatric disorders, with conditions like depression, schizophrenia, and suicidal tendencies peaking during specific times of the year and subsiding during others.
The most well-documented of these trends is "winter seasonal affective disorder" (SAD), a relatively rare condition marked.
