Knowledge, attitudes, and practices regarding mycoplasma pneumoniae pneumonia among family members of affected children.

Sleep is a fundamental physiological process characterized by reduced mental and physical activity with essential neural mechanisms, involved in modulating memory. Accumulating evidence indicates that REM sleep contributes to memory processing and emotional regulation, and that REM sleep disruption can impair both cognitive and affective domains. In rodents, REM sleep deprivation (REM SD) has been repeatedly associated with deficits in recognition-related tasks, including novel object recognition (NOR), as well as increased anxiety- and depressive-like behaviors. Importantly, NOR performance depends on intact encoding and consolidation of object representations, and the memory domain assessed depends on the retention interval; a 24-h delay is commonly used to evaluate long-term recognition memory. At the molecular level, sleep loss alters synaptic plasticity signaling cascades, including pathways converging on cAMP response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF), which are widely implicated in synaptic consolidation and memory-related plasticity. Sleep deprivation has been shown to downregulate components of CaMKII–CREB–BDNF signaling in the prefrontal cortex, supporting the plausibility that impaired plasticity signaling contributes to behavioral phenotypes after REM SD. In addition to hippocampal contributions, the medial prefrontal cortex (mPFC) participates in recognition memory processes and interacts with hippocampal networks during novelty discrimination, making it a mechanistically relevant region for assessing plasticity-related markers in recognition-memory paradigms. Imperatorin (IMP) is a naturally occurring furanocoumarin reported to exert neuroprotective, anti-inflammatory, and antioxidant effects in preclinical models. Prior studies indicate that IMP can mitigate experimentally induced cognitive impairments and modulate neuroinflammation-associated mechanisms, suggesting that IMP may counteract REM SD–related memory and behavioral disturbances. Based on these converging lines of evidence, we investigated whether IMP attenuates REM SD–induced recognition-memory impairment and behavioral alterations, and whether such effects are associated with changes in CREB and BDNF expression in the prefrontal cortex.