In this narrative review article, we discuss the role of sleep deprivation (SD) in memory processing in rodent models. Numerous studies have examined the effects of SD on memory, with the majority showing that sleep disorders negatively affect memory. Currently, a consensus has not been established on which damage mechanism is the most appropriate. This critical issue in the neuroscience of sleep remains largely unknown. This review article aims to elucidate the mechanisms that underlie the damaging effects of SD on memory. It also proposes a scientific solution that might explain some findings. We have chosen to summarize literature that is both representative and comprehensive, as well as innovative in its approach. We examined the effects of SD on memory, including synaptic plasticity, neuritis, oxidative stress, and neurotransmitters. Results provide valuable insights into the mechanisms by which SD impairs memory function.

Sleep disorders are the most widespread mental disorders after stroke and hurt survivors’ functional prognosis, response to restoration, and quality of life. This review will address an overview of the progress of research on the biological mechanisms associated with stroke-complicating sleep disorders. Extensive research has investigated the negative impact of stroke on sleep. However, a bidirectional association between sleep disorders and stroke exists; while stroke elevates the risk of sleep disorders, these disorders also independently contribute as a risk factor for stroke. This review aims to elucidate the mechanisms of stroke-induced sleep disorders. Possible influences were examined, including functional changes in brain regions, cerebrovascular hemodynamics, neurological deficits, sleep ion regulation, neurotransmitters, and inflammation. The results provide valuable insights into the mechanisms of stroke complicating sleep disorders.

Epimedii Folium (Yinyanghuo), a unique and traditional Chinese medicinal plant used in medicine for more than a thousand years, has been traditionally used to tonify the liver and kidneys, strengthen the muscles and bones, and eliminate rheumatism. Its principal active ingredient, icariin, has long been used clinically for impotence and spermatorrhea, weakness of muscles and bones, rheumatism and arthralgia pain, and has recently attracted growing attention for its therapeutic potential against central nervous system diseases. This review summarizes advances over the past five years in the preparation, neuroprotective effects, and pharmacokinetics of icariin. The literature was retrieved from Pubmed, CNKI (China National Knowledge Infrastructure), Web of Science, and Google Scholar using keywords including “icariin”, “Epimedii Folium”, “neuroprotection”, “biosynthesis” and “pharmacokinetics”, and studies were screened for relevance to preparation methods, pharmacological evaluation, and pharmacokinetic properties. Although extraction from plant sources remains the main preparation method, chemical synthesis and biosynthesis are emerging in response to resource scarcity. Accumulating evidence indicates that icariin exerts neuroprotective effects through multiple mechanisms, including anti-neuroinflammation, mitochondrial protection, antioxidant effects, inhibition of neuronal apoptosis, promotion of neuronal proliferation and differentiation and regulation of synaptic plasticity. Its rapid absorption, ability to cross the blood–brain barrier, and low cumulative toxicity provide a favorable pharmacokinetic basis for central nervous system applications. This review highlights synthetic strategies, pharmacological evaluation and pharmacokinetic characteristics of icariin, aiming to support its broader application in CNSDs.