Associations Between Sleep Deprivation, Circadian Gene Expression, Depressive Symptoms, and Psychomotor Performance—Preliminary Results

Background: Deprivation of sleep (DS) might affect mood and cognitive abilities, including psychomotor functions (PF). Molecular mechanisms underlying these effects remain unclear, though studies suggest that the circadian rhythm plays a role. Methods: Seventy participants underwent polysomnography (PSG) and DS. PF was evaluated using Bimanual Eye–Hand Coordination Test (BEHCT). Mood, PF, and clock gene expression (Circadian Locomotor Output Cycles Kaput (CLOCK), Brain and Muscle ARNT-Like 1 (BMAL1), Period Circadian Regulator 1 (PER1), Cryptochrome Circadian Regulator 1 (CRY1), Nuclear Receptor Subfamily 1 Group D Member 1 (NR1D1), and Neuronal PAS Domain Protein 2 (NPAS2)) were analyzed post-PSG and post-DS. Mood changes after DS classified participants as responders (RE) or non-responders (NR). Results: In NRs, but not REs, the BEHCT error count positively correlated with the expression of BMAL1, CRY1, PER1, NR1D1 (R = 0.60, p = 0.002; R = 0.49, p = 0.018; R = 0.57, p = 0.023; and R = 0.53, p = 0.011, respectively), with PER1 explaining its variability in 57.8% (b = 0.174, R2 = 0.578, F = 20.144, and p < 0.001). Conclusions: Obtained results suggest that altered clock gene expression may contribute to individual differences in mood and PF following DS.