The effect of SARS-CoV-2 on the nervous system: a review of neurological impacts caused by human coronaviruses

The COVID-19 pandemic has affected millions of people worldwide. While coronaviruses typically have low rates of neurotropic effects, the massive transmission of SARS-CoV-2 suggests that a substantial population will suffer from potential SARS-CoV-2-related neurological disorders. The rapid and recent emergence of SARS-CoV-2 means little research exists on its potential neurological effects. Here we analyze the effects of similar viruses to provide insight into the potential effects of SARS-CoV-2 on the nervous system and beyond. Seven coronavirus strains (HCoV-OC43, HCoV-HKU1, HCoV-229E, HCoV-NL63, SARS-CoV, MERS-CoV, SARS-CoV-2) can infect humans. Many of these strains cause neurological effects, such as headaches, dizziness, strokes, seizures, and critical illness polyneuropathy/myopathy. Certain studies have also linked coronaviruses with multiple sclerosis and extensive central nervous system injuries. Reviewing these studies provides insight into the anticipated effects for patients with SARS-CoV-2. This review will first describe the effects of other coronaviruses that have caused severe disease (SARS-CoV, MERS-CoV) on the nervous system, as well as their proposed origins, non-neurological effects, and neurological infection mechanisms. It will then discuss what is known about SARS-CoV-2 in these areas with reference to the aforementioned viruses, with the goal of providing a holistic picture of SARS-CoV-2.

Exploring CNS effects of American traditional medicines using zebrafish models

: Although American traditional medicine (ATM) has been practiced for millennia, its complex multi-target mechanisms of therapeutic action remain poorly understood. Animal models are widely used to elucidate the therapeutic effects of various ATMs, including their modulation of brain and behavior. Complementing rodent models, the zebrafish (Danio rerio) is a promising novel organism in translational neuroscience and neuropharmacology research. Here, we emphasize the growing value of zebrafish for testing neurotropic effects of ATMs and outline future directions of research in this field. We also demonstrate the developing utility of zebrafish as complementary models for probing CNS mechanisms of ATM action and their potential to treat brain disorders.

Infection and Risk of Parkinson’s Disease

Parkinson’s disease (PD) is thought to be caused by a combination of genetic and environmental factors. Bacterial or viral infection has been proposed as a potential risk factor, and there is supporting although not entirely consistent epidemiologic and basic science evidence to support its role. Encephalitis caused by influenza has included parkinsonian features. Epidemiological evidence is most compelling for an association between PD and hepatitis C virus. Infection with Helicobacter pylori may be associated not only with PD risk but also response to levodopa. Rapidly evolving knowledge regarding the role of the microbiome also suggests a role of resident bacteria in PD risk. Biological plausibility for the role for infectious agents is supported by the known neurotropic effects of specific viruses, particular vulnerability of the substantia nigra and even the promotion of aggregation of alpha-synuclein. A common feature of implicated viruses appears to be production of high levels of cytokines and chemokines that can cross the blood-brain barrier leading to microglial activation and inflammation and ultimately neuronal cell death. Based on multiple avenues of evidence it appears likely that specific bacterial and particularly viral infections may increase vulnerability to PD. The implications of this for PD prevention requires attention and may be most relevant once preventive treatments for at-risk populations are developed.

Mechanisms and Effects of Dietary Restriction on CNS and Affective Disorders

Neuropsychiatric disorders, including depression contribute significantly to global disability and possess high social and health burden. Management is dominated by pharmacotherapy and psychotherapy; nevertheless, such treatments prevent or treat less than half of the patients, suggesting that alternative approaches are required. Emerging data suggest that diet may be an adjustable risk factor for psychiatric disorders. Caloric restriction (CR) possesses protective effects in almost all organs including the brain. However, the precise molecular pathways of these effects remain uncertain. In this review, we will discuss the putative neurobiological mechanisms of CR on the brain. The article will address also the molecular basis of the antidepressant effects of CR, primarily including ghrelin signaling, CREB neurotropic effects and ketone bodies production. Then we will highlight the probable effect of CR on the neuroinflammation, which emerges as a key pathogenetic factor for the majority of neuropsychiatric disorders. Finally, we discuss the so called caloric restriction mimetics, compounds that reproduce properties of CR. Further research will be required to verify the safety and efficacy of CR before a general approval can be proposed to introduce it and its mimetics in clinical practice for the treatment of neuropsychiatric disorders.

Similarity Of Effects On EEG And HRV Parameters Of Aramaic, Greek Catholic And Krishnaic Prayers

The object of observation were 4 men: Greek Catholic priest Father Volodymyr, head of the Church Brotherhood Ivan, a supporter of Krishna Victor, and your obedient servant, the first author to memorize the authentic Lord's Prayer in Aramaic. Results. The neurotropic effects of Prayer are manifested in two inhibitory and three activating patterns. The first inhibitory pattern reflects the decrease in elevated and upper limit levels of SPD of θ-and δ-rhythm in frontal loci and the second - decrease in normal SPD levels of β-and θ-rhythm in the frontal, central, temporal and parietal loci. The first activating pattern reflects a small increase in normal levels of β-rhythm index and asymmetry and SPD entropy in locus C3, as well as a further increase in elevated δ-rhythm SPD levels in loci P3 and T3. The second pattern reflects the slight increase in normal SPD levels of θ-rhythm in loci T3, T5, T6, O2 and α-rhythm in locus T5, as well as their indices and entropy SPD in locus O2. The third pattern reflects a slight increase in amplitude and SPD of α-rhythm in central, frontal, temporal and occipital loci.

Neurotropic Effects of Hepatoprotectors During Alcohol Poisoning

Purpose. To compare the efficacy of metabolic hepatoprotectors at an early stage of acute alcohol poisoning complicated by toxic hepatitis.Material and methods. 80 patients with acute alcohol poisoning complicated by toxic hepatitis who received medical treatment in the toxicology unit of the Republican Research Center of Emergency Medicine during 2015–2017 were examined. The patients were split into 3 groups. At the background of backbone therapy, patients of group I (n=30) received a hepatoprotectors on the basis of inosine, meglumine, methionine, nicotinamide, and succinic acid; patients of group II (n=20) were prescribed to receive drugs based on betaine glucuronate (glucomethamine), diethanol amine (glucodiamine), and nicotinamide ascorbate. Patients of group III (n=30) received the backbone therapy. In all patients, the concentrations of liver enzymes, bilirubin, free ammonia, blood lactate, the condition of vegetative nervous status were analyzed. Psychoastenics was examined using the MMSE score, FAB score and Reitan test.Results. After 48 hours, in group I patients, the concentration of blood lactate became almost normal, in group II patients it decreased to 2.6Ѓ}0.9 mmol/l, and in group III patients it was equal to 2.7Ѓ}0.9 mmol/l. On day 5, in patients of groups I and II the cognitive deficit was almost absent, in patients of group III the MMSE scores were 1.3-fold and 1.4-fold lower than in patients of groups I and II, respectively.Conclusion. The drug used in group I possessed increased antihypoxant properties but smaller hepatoprotective properties than the drug used in group II. When signs of toxic hepatitis are predominant it would be more preferable to use the drug applied in group II and when the signs of tissue hypoxia are predominant the drug applied in group I should be used.

Musashi binding elements in Zika and related Flavivirus 3’UTRs: A comparative studyin silico

ABSTRACTZika virus (ZIKV) belongs to a class of neurotropic viruses that have the ability to cause congenital infection, which can result in microcephaly or fetal demise. Recently, the RNA-binding protein Musashi-1 (Msi1), which mediates the maintenance and self-renewal of stem cells and acts as a translational regulator, has been associated with promoting ZIKV replication, neurotropism, and pathology. Msi1 predominantly binds to single-stranded motifs in the 3’ untranslated region (UTR) of RNA that contain aUAGtrinucleotide in their core. We systematically analyzed the properties of Musashi binding elements (MBEs) in the 3’UTR of flaviviruses with a thermodynamic model for RNA folding. Our results indicate that MBEs in ZIKV 3’UTRs occur predominantly in unpaired, single-stranded structural context, thus corroborating experimental observations by a biophysical model of RNA structure formation. Statistical analysis and comparison with related viruses show that ZIKV MBEs are maximally accessible among mosquito-borne flaviviruses. Our study addresses the broader question of whether other emerging arboviruses can cause similar neurotropic effects through the same mechanism in the developing fetus by establishing a link between the biophysical properties of viral RNA and teratogenicity. Moreover, our thermodynamic model can explain recent experimental findings and predict the Msi1-related neurotropic potential of other viruses.