Circadian information is stored in mammalian tissues by an autonomous network of transcriptional feedback loops that have evolved to optimally regulate tissue-specific functions. Currently, stable circadian rhythms of the expression of clock genes (Bmal1/Per2/Cry1, etc.), hormones, and metabolic genes (Glut4/leptin, etc.) have been demonstrated. Desynchronoses are disorders of the body's biorhythms, where the direction and degree of shift of various indicators of the oscillatory process are disturbed. Desynchronosis can be caused by natural conditions or man-made causes. The disruption of circadian rhythms is a risk factor for the appearance of physiological and behavioral disorders and the development of diseases, including epilepsy, and metabolic and oncological diseases. Evidence suggests that seizure activity in the epilepsy phenotype is associated with circadian dysfunction. Interactions between epilepsy and circadian rhythms may be mediated through melatonin, sleep-wake cycles, and clock genes. The correction of circadian dysfunction can lead to a decrease in seizure activity and vice versa. Currently, attempts are being made to pharmacologically correct desynchronosis and related psycho-emotional disorders, as well as combined somatic pathology. On the other hand, the normalization of the light regimen, the regulation of sleep-wake times, and phototherapy as additions to standard treatment can speed up the recovery of patients with various diseases.
Keywords: Bmal1; circadian rhythms; clock; desynchronosis; diseases; epilepsy; gene regulation; melatonin.