Mini-review on SARS-CoV-2 infection and neurological manifestations: A Perspective

Author(s):  
Vishal Chavda ◽  
Arif Tasleem Jan ◽  
Dhananjay Yadav

: The Coronavirus, also known as SARS-CoV-2 (Severe Acute Respiratory Syndrome Corona Virus-19), due to its depth impact on acute respiratory dysfunction and mortality, has thrown the world into chaos with its splendid rate of transmission. Recent research findings suggest that the loss of involuntary breathing control in the brainstem, which leads to death, is a clear indicator of neurological involvement.The nose to brain entry is the promising gateway of SARS-CoV-2 to reach the brain via systemic circulatory distribution subsequent infection of the lung. The loss of involuntary control of breathing is a result of an active gateway of systemic blood circulation through the lungs into the brain. Early neurological symptoms like loss of smell, convulsions, and ataxia are the clues of neurological involvement and central nervous system entry of SARS-CoV-2 that further become fatal, life-threatening and require artificial respiration and emergency admissions. As per studies investigated on Wuhan hospitalized patients of SARS-CoV-2, the involvement of SARS-CoV-2 in the central nervous system (CNS) has three major gateways: Direct involvement into CNS includes headache, ataxia, dizziness, altered or impaired consciousness, acute stroke or seizures; peripheral involvement includes impaired taste, smell, vision and altered nociception; and skeletal muscle impairment like skeletal muscle disorders, acute paralysis in a particular area of the body. In the previous era, most studied and researched viruses were beta coronavirus and mouse hepatitis virus, which were studied for acute and chronic encephalitis and multiple sclerosis (MS). Although the early symptoms of SARS-CoV are respiratory pathogenesis, the differential diagnosis should always be considered for neurological perspective to stop mortalities.

2017 ◽  
Vol 91 (22) ◽  
Author(s):  
D. Lori Wheeler ◽  
Jeremiah Athmer ◽  
David K. Meyerholz ◽  
Stanley Perlman

ABSTRACT Viral infection of the central nervous system (CNS) is complicated by the mostly irreplaceable nature of neurons, as the loss of neurons has the potential to result in permanent damage to brain function. However, whether neurons or other cells in the CNS sometimes survive infection and the effects of infection on neuronal function is largely unknown. To address this question, we used the rJHM strain (rJ) of mouse hepatitis virus (MHV), a neurotropic coronavirus that causes acute encephalitis in susceptible strains of mice. To determine whether neurons or other CNS cells survive acute infection with this virulent virus, we developed a recombinant JHMV that expresses Cre recombinase (rJ-Cre) and infected mice that universally expressed a silent (floxed) version of tdTomato. Infection of these mice with rJ-Cre resulted in expression of tdTomato in host cells. The results showed that some cells were able to survive the infection, as demonstrated by continued tdTomato expression after virus antigen could no longer be detected. Most notably, interneurons in the olfactory bulb, which are known to be inhibitory, represented a large fraction of the surviving cells. In conclusion, our results indicated that some neurons are resistant to virus-mediated cell death and provide a framework for studying the effects of prior coronavirus infection on neuron function. IMPORTANCE We developed a novel recombinant virus that allows the study of cells that survive an infection by a central nervous system-specific strain of murine coronavirus. Using this virus, we identified neurons and, to a lesser extent, nonneuronal cells in the brain that were infected during the acute phase of the infection and survived for approximately 2 weeks until the mice succumbed to the infection. We focused on neurons and glial cells within the olfactory bulb because the virus enters the brain at this site. Our results show that interneurons of the olfactory bulb were the primary cell type able to survive infection. Further, these results indicate that this system will be useful for functional and gene expression studies of cells in the brain that survive acute infection.


1990 ◽  
Vol 258 (5) ◽  
pp. E894-E897 ◽  
Author(s):  
G. C. Tombaugh ◽  
R. M. Sapolsky

Glucocorticoids enhance the neurotoxic potential of several insults to the rat hippocampus that involve overactivation of glutamatergic synapses. These hormones also stimulate the synthesis of glutamine synthetase (GS) in peripheral tissue. Because this enzyme helps regulate glutamate metabolism in the central nervous system, glucocorticoid induction of GS in the brain may underlie the observed synergy. We have measured GS activity in the hippocampus and skeletal muscle (plantaris) of adult rats after bilateral adrenalectomy (ADX), corticosterone (Cort) replacement, or stress. No significant changes in GS were observed in hippocampal tissue, whereas muscle GS was significantly elevated after Cort treatment or stress and was reduced after ADX. These results suggest that Cort-induced shifts in GS activity probably do not explain Cort neurotoxicity, although the stress-induced rise in muscle GS may be relevant to certain types of myopathy.


Bioprinting ◽  
2021 ◽  
pp. 98-118
Author(s):  
Kenneth Douglas

Abstract: This chapter recounts bioprinting studies of skin, bone, skeletal muscle, and neuromuscular junctions. The chapter begins with a study of bioprinted skin designed to enable the creation of skin with a uniform pigmentation. The chapter relates two very different approaches to bioprinted bone: a synthetic bone called hyperelastic bone and a strategy that prints cartilage precursors to bone and then induces the conversion of the cartilage to bone by judicious choice of bioinks. Muscles move bone, and the chapter discusses an investigation of bioprinted skeletal muscle. Finally, the chapter considers an attempt to bioprint a neuromuscular junction, a synapse—a minute gap—of about 20 billionths of a meter between a motor neuron and the cell membrane of a skeletal muscle cell. A motor neuron is a nerve in the central nervous system that sends signals to the muscles of the body.


2016 ◽  
Vol 7 (4) ◽  
pp. 253-258 ◽  
Author(s):  
Jing Zhang ◽  
Weizhen Zhang

AbstractIrisin was initially discovered as a novel hormone-like myokine released from skeletal muscle during exercise to improve obesity and glucose dysfunction by stimulating the browning of white adipose tissue. Emerging evidence have indicated that irisin also affects brain function. FNDC5 mRNA and FNDC5/irisin immunoreactivity are present in various regions of the brain. Central irisin is involved in the regulation of neural differentiation and proliferation, neurobehavior, energy expenditure and cardiac function. Elevation of peripheral irisin level stimulates hippocampal genes related to neuroprotection, learning and memory. In this brief review, we summarize the current understanding on neuronal functions of irisin. In addition, we discuss the pros and cons for this molecule as a potential messenger mediating the crosstalk between skeletal muscle and central nervous system during exercise.


1951 ◽  
Vol 97 (409) ◽  
pp. 792-800 ◽  
Author(s):  
L. Crome

The problems of the interdependence and unity of the brain and body have been put on a scientific basis by Pavlov and his successors. Bykov (1947) has, for example, been able to demonstrate that the cortex plays a leading part in the regulation of somatic processes, such as secretion of urine, blood pressure, peristalsis and metabolism. It is therefore reasonable to argue that lesions of the central nervous system will be reflected in the pathogenesis and course of morbid processes in the body. It does not follow, however, that this influence will necessarily be in the direction of greater lability, more rapid pathogenesis or more extensive destruction. The outstanding feature of the central nervous system is its plasticity and power of compensation. It is therefore possible and probable that those parts of the nervous system which remain intact will take over and compensate for the function of the lost ones. Emotion may, for example, lead to polyuria, but it does not follow that urinary secretion will be impaired in a leucotomized patient. The brain may well play an important part in the infective processes of a normal person, but the defence against infection in a microcephalic idiot may remain perfectly adequate, and may even be more effective than in a normal person, provided that the mechanism of the immunity and phagocytosis had been more fully mobilized in the course of his previous life.


2021 ◽  
Vol 17 (2) ◽  
pp. 6-15
Author(s):  
L.A. Dziak ◽  
O.S. Tsurkalenko ◽  
K.V. Chekha ◽  
V.M. Suk

Coronavirus infection is a systemic pathology resulting in impairment of the nervous system. The involvement of the central nervous system in COVID-19 is diverse by clinical manifestations and main mechanisms. The mechanisms of interrelations between SARS-CoV-2 and the nervous system include a direct virus-induced lesion of the central nervous system, inflammatory-mediated impairment, thrombus burden, and impairment caused by hypoxia and homeostasis. Due to the multi-factor mechanisms (viral, immune, hypoxic, hypercoagulation), the SARS-CoV-2 infection can cause a wide range of neurological disorders involving both the central and peripheral nervous system and end organs. Dizziness, headache, altered level of consciousness, acute cerebrovascular diseases, hypogeusia, hyposmia, peripheral neuropathies, sleep disorders, delirium, neuralgia, myalgia are the most common signs. The structural and functional changes in various organs and systems and many neurological symptoms are determined to persist after COVID-19. Regardless of the numerous clinical reports about the neurological and psychiatric symptoms of COVID-19 as before it is difficult to determine if they are associated with the direct or indirect impact of viral infection or they are secondary to hypoxia, sepsis, cytokine reaction, and multiple organ failure. Penetrated the brain, COVID-19 can impact the other organs and systems and the body in general. Given the mechanisms of impairment, the survivors after COVID-19 with the infection penetrated the brain are more susceptible to more serious diseases such as Parkinson’s disease, cognitive decline, multiple sclerosis, and other autoimmune diseases. Given the multi-factor pathogenesis of COVID-19 resulting in long-term persistence of the clinical symptoms due to impaired neuroplasticity and neurogenesis followed by cholinergic deficiency, the usage of Neuroxon® 1000 mg a day with twice-day dosing for 30 days. Also, a long-term follow-up and control over the COVID-19 patients are recommended for the prophylaxis, timely determination, and correction of long-term complications.


1995 ◽  
Vol 198 (12) ◽  
pp. 2527-2536
Author(s):  
D R Nässel ◽  
M Y Kim ◽  
C T Lundquist

We have examined the distribution of two tachykinin-related neuropeptides, callitachykinin I and II (CavTK-I and CavTK-II), isolated from whole-animal extracts of the blowfly Calliphora vomitoria. Extracts of dissected brains, thoracic-abdominal ganglia and midguts of adult blowflies and the entire central nervous system of larval flies were analysed by high performance liquid chromatography (HPLC) combined with enzyme-linked immunosorbent assay (ELISA) for the presence of CavTKs. To identify the two neuropeptides by HPLC, we used the retention times of synthetic CavTK-I and II as reference and detection with an antiserum raised to locustatachykinin II (shown here to recognise both CavTK-I and II). The brain contains only two immunoreactive components, and these have exactly the same retention times as CavTK-I and II. The thoracic-abdominal ganglia and midgut contain immunoreactive material eluting like CavTK-I and II as well as additional material eluting later. The larval central nervous system (CNS) contains material eluting like CavTK-I and II as well as a component that elutes earlier. We conclude that CavTK-I and II are present in all assayed tissues and that additional, hitherto uncharacterised, forms of tachykinin-immunoreactive material may be present in the body ganglia and midgut as well as in the larval CNS. An antiserum was raised to CavTK-II for immunocytochemistry. This antiserum, which was found to be specific for CavTK-II in ELISA, labelled all the neurones and midgut endocrine cells previously shown to react with the less selective locustatachykinin antisera. It is not clear, however, whether CavTK-I and II are colocalised in all LomTK-immunoreactive cells since there is no unambiguous probe for CavTK-I.


2021 ◽  
Author(s):  
G.S. Dzhunusova ◽  
N.U. Sataeva ◽  
S.B. Ibraimov

The studies were carried out on adolescents-mountaineers living in high-mountainous areas (2800 m above sea level, in Naryn, Osh, Issyk-Kul regions, 260 people). The markers of the functional activity of the brain were revealed, which characterize maladjustment functional changes on the EEG. Information databases of EEG parameters of adolescents living at an altitude of 2800 m have been created with the identification of the peculiarities of regional EEG standards, "electronic passports of the functional state of health" of adolescents were developed. The systemic and intersystemic restructuring of the body was identified, allowing to distinguish groups of persons with an unstable functional state, exposed to stressful environmental influences. Key words: hypoxia, adolescents, central nervous system, EEG.


2020 ◽  
Vol 74 ◽  
pp. 517-531
Author(s):  
Wioletta Kazana ◽  
Agnieszka Zabłocka

Brain-derived neurotrophic factor (BDNF) plays an important role in the proper functioning of the nervous system. It regulates the growth and survival of nerve cells, and is crucial in processes related to the memory, learning and synaptic plasticity. Abnormalities related to the distribution and secretion of BDNF protein accompany many diseases of the nervous system, in the course of which a significant decrease in BDNF level in the brain is observed. Impairments of BDNF transport may occur, for example, in the event of a single nucleotide polymorphism in the Bdnf (Val66Met) coding gene or due to the dysfunctions of the proteins involved in intracellular transport, such as huntingtin (HTT), huntingtin-associated protein 1 (HAP1), carboxypeptidase E (CPE) or sortilin 1 (SORT1). One of the therapeutic goals in the treatment of diseases of the central nervous system may be the regulation of expression and secretion of BDNF protein by nerve cells. Potential therapeutic strategies are based on direct injection of the protein into the specific region of the brain, the use of viral vectors expressing the Bdnf gene, transplantation of BDNF-producing cells, the use of substances of natural origin that stimulate the cells of the central nervous system for BDNF production, or the use of molecules activating the main receptor for BDNF – tyrosine receptor kinase B (TrkB). In addition, an appropriate lifestyle that promotes physical activity helps to increase BDNF level in the body. This paper summarizes the current knowledge about the biological role of BDNF protein and proteins involved in intracellular transport of this neurotrophin. Moreover, it presents contemporary research trends to develop therapeutic methods, leading to an increase in the level of BDNF protein in the brain.


2020 ◽  
Vol 18 ◽  
Author(s):  
Vimal Patel ◽  
Vishal Chavda ◽  
Jigar Shah

: Neurology and associated nanotherapeutics is a complex field in terms of therapeutics and neurological disorder complexity. Brain is an intricate appendage and requires more precise embattled treatment for the particular diseases and hence it’s a broad scale for developing more targeted drug deliveries. The brain is one of the most inaccessible tissues of the body due to the existence of the blood-brain barrier (BBB), thus delivery of drugs inside the brain is a striking dare and it is also tricky to treat central nervous system (CNS) complications pharmacologically. The therapeutic aspiration is to accomplish a lowest drug meditation in the brain tissues so as to gain favoured therapeutic results. To devastate this obstacle, nanotechnology is engaged in the field of targeted brain drug delivery and neuropathology targeting. These carriers hold myriad ability as they may augment the drug delivery into the brain by shielding them from degradation and prolonging their transmission in the blood, as well as promoting their transport through the BBB. Nanopharmaceuticals are quickly sprouting as new avenue that is engaged with the drug-loaded nanocarriers to demonstrate unique physicochemical properties and tiny size range for penetrating into the central nervous system. The enchantment behind their therapeutic achievement is the condensed drug dose and inferior toxicity, whereby restricting the therapeutic compound to the specific site. Therefore, in this article we have tried to recapitulate the advances the novel scopes for the brain targeted drug delivery for complex neurological disorders.


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