IImmunodeficiency and hyperinflammation characterize COVID-19 associated states; thus, repurposing of multiple cytokine and/or anti-cytokine drugs currently being used in other therapeutic areas has been suggested as a potential therapeutic strategy in COVID-19 patients. Clinical trials involving these drugs target the most frequent and life-threatening peripheral consequences of the disease, mainly focusing on lung, heart, and coagulation functions; however, a growing number of reports describe a wide range of COVID-associated neurological manifestations (altogether defined as neuro-COVID) including anosmia, seizures, confusion, stroke, encephalopathy, and paralysis. Notably, the underlying pathophysiological mechanisms for neuro-COVID may also include dysregulation of cytokines/chemokines, deficiencies in the innate immune response, and autoimmunity. This suggests that therapeutic attempts with drugs targeting cytokine-mediated inflammation in peripheral organs could also positively affect neuro-COVID manifestations. As a matter of fact, some of these drugs have also been scrutinized for their potential efficacy in treating neuroinflammatory diseases such as optic neuromyelitis, epilepsy, stroke, and traumatic brain injury, among others. On the other hand, anti-cytokine drugs, by impairing relevant physiological activities exerted by these mediators in the CNS, may also be endowed with significant neurological risk. Therefore, the primary aim of the present manuscript is to review the available preclinical and clinical data regarding the neurological effects of the drugs targeting cytokine-mediated inflammation, in order to raise awareness about their potentially beneficial or detrimental neurological consequences when used to treat COVID-19 patients.

Objective: Current tests available to diagnose fetal hypoxia in-utero lack sensitivity thus un-diagnosing many fetuses at risk. microRNAs derived from the placenta circulate in the maternal blood during pregnancy and may be used as biomarkers for pregnancy complications. To identify putative markers of fetal growth restriction (FGR) and new therapeutic druggable targets, we examined, in maternal blood samples, the expression of a cluster of microRNAs, known to be regulated by hypoxia. Population: Pregnant Caucasian women between 18 and 46 years old hospitalized. Design and Setting: To discriminate between early- and late-onset FGR, the study population was divided into two subgroups according to the gestational age at delivery, group (1) : <32th weeks of gestation; and group (2) from 32th to 37th weeks of gestation. Methods: Ultrasound biometry, Doppler velocimetry, RT-PC-R, Software miRNA-targets predictors Results: Among the microRNA cluster examined, three microRNAs: miR-16-5p, miR-103-3p, and miR-27b-3p were upregulated in FGR blood samples before the 32th week of gestation. Notably, the expression of all miRNAs was increased through gestation in healthy control group, whereas, in the FGR groups, where there was a progressive reduction in the expression of miR-103-3p and miR-107-3p and a slight reduction for miR-16-5p. Main Outcome Measures: miRNA expression Conclusions: Our results showed that measurement of miRNAs in maternal blood may form the basis for a future diagnostic test to determine the degree of fetal hypoxia in FGR, thus allowing the start of appropriate therapeutic.