As a severe and highly contagious infectious disease, coronavirus disease 2019 (COVID-19) has caused a global pandemic. Several case reports have demonstrated that the respiratory system is the main target in patients with COVID-19, but the disease is not limited to the respiratory system. Case analysis indicated that the nervous system can be invaded by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and that 36.4% of COVID-19 patients had neurological symptoms. Importantly, the involvement of the CNS may be associated with poor prognosis and disease worsening. Here, we discussed the symptoms and evidence of nervous system involvement (directly and indirectly) caused by SARS-CoV-2 infection and possible mechanisms. CNS symptoms could be a potential indicator of poor prognosis; therefore, the prevention and treatment of CNS symptoms are also crucial for the recovery of COVID-19 patients.

Background: Although numerous microRNAs (miRNAs) have been discovered to participate in the progression of Alzheimer’s disease (AD), they are still difficult to apply in clinical work. Thus, the identification of novel miRNAs and clarification of their clinical significance are importing for improving the diagnosis and treatment of AD. The purpose of this study was to analyze the expression of miR-128 and its diagnostic value in patients with AD. Patients and Methods: In this study, 117 AD patients and 106 controls were enrolled, and the demographic data, biochemical parameters and serum miR-128 levels were collected. These data were then used to build a logistic regression model, and receiver operating characteristic (ROC) curves were drawn to evaluate the diagnostic value of miR-128. The relationships between miR-128 and inflammatory factors (IL-1β/TNF-α) were also analyzed from clinical serum data. Results: Our study found that miR-128 was significantly upregulated in the serum samples of AD patients compared with controls, and that this upregulation was negatively correlated with Mini-Mental State Examination (MMSE) scores (r = − 0.687, P< 0.01). ROC curve showed that the area under the curve of miR-128 was 0.831. Logistic regression analyses showed that glycosylated hemoglobin (HbA1c) levels, low-density lipoprotein (LDL) levels, MMSE scores and serum miR-128 levels were statistically significant (P< 0.01), and the ROC curve of the combined detection of these variables was 0.906. The serum miR-128 levels in AD patients were positively correlated with the serum IL-1β (r=0.798, P< 0.01) and serum TNF-α levels (r=0.733, P< 0.01). Conclusion: Serum miR-128 is a candidate diagnostic biomarker in AD patients who achieved good diagnostic performance when used alone or in combination with other factors and may have the potential to be a novel therapeutic target for neuroinflammation.

Parkinson's disease (PD) is a serious neurodegenerative disorder wherein changes in metabolites related to lipids, glutathione, and energy metabolism occur. Currently, metabolite changes in PD have been reported, yet their role in the prognosis of disease remains poorly understood. Functional metabolites can be used to diagnose diseases, especially PD, and can exert neuroprotective effects. This study used a PD animal model and a lipopolysaccharide (LPS)—mediated inflammatory response model (using the BV-2 mouse microglial cell line) to identify functional metabolites that can identify important metabolic disorders during PD, and comprehensively evaluated their profiles using a metabolomics-based approach. Our results showed that co-treatment with myristic acid and heptadecanoic acid downregulated the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in BV-2 cells. Additionally, myristic acid and 10 μM heptadecanoic acid significantly inhibited the LPS-induced inflammatory response through the nuclear factor-κB pathway in BV-2 microglial cells, which provides a potential approach for PD treatment. Myristic acid and heptadecanoic acid were the active metabolites found by active metabolomics technology, but at present, there is no research report about their function for PD treatment, and our findings offer a novel research strategy for PD diagnosis and treatment.

Synaptotagmin III (Syt3) is a Ca²⁺-dependent membrane-traffic protein that is highly concentrated in synaptic plasma membranes and affects synaptic plasticity by regulating post-synaptic receptor endocytosis. Here, we show that Syt3 is upregulated in the penumbra after ischemia/reperfusion (I/R) injury. Knockdown of Syt3 protects against I/R injury, promotes recovery of motor function, and inhibits cognitive decline. Overexpression of Syt3 exerts the opposite effects. Mechanistically, I/R injury augments Syt3-GluA2 interactions, decreases GluA2 surface expression, and promotes the formation of Ca²⁺-permeable AMPA receptors (CP-AMPARs). Using a CP-AMPAR antagonist or dissociating the Syt3-GluA2 complex via TAT-GluA2-3Y peptide promotes recovery from neurological impairments and improves cognitive function. Furthermore, Syt3 knockout mice are resistant to cerebral ischemia because they show high-level expression of surface GluA2 and low-level expression of CP-AMPARs after I/R. Our results indicate that Syt3-GluA2 interactions, which regulate the formation of CP-AMPARs, may be a therapeutic target for ischemic insults.

Cerebral ischemia/reperfusion injury is an important factor leading to poor prognosis in ischemic stroke patients. Therefore, it is particularly important to find effective remedial measures to promote the health of patients to return to society. Isoflurane is a safe and reliable anesthetic gas with a long history of clinical application. In recent years, its protection function to human body has been widely recognized, and nowadays isoflurane for cerebral protection has been widely studied, and the stable effect of isoflurane has satisfied many researchers. Basic studies have shown that isoflurane’s protection of brain tissue after ischemia/reperfusion involves a variety of signaling pathways and effector molecules. Even though many signaling pathways have been described, more and more studies focus on exploring their mechanisms of action, in order to provide strong evidence for clinical application. This could prompt the introduction of isoflurane therapy to clinical patients as soon as possible. In this paper, several confirmed signaling pathways will be reviewed to find possible strategies for clinical treatment.