COVID-19 Beyond the Lungs

2022 ◽  
pp. 109-126
Author(s):  
Omar El Hiba ◽  
Hicham Chatoui ◽  
Nadia Zouhairi ◽  
Lahoucine Bahi ◽  
Lhoussaine Ammouta ◽  
...  

Since December 2019, the world has been shaken by the spread of a highly pathogen virus, causing severe acute respiratory syndrome (SARS-Cov2), which emerged in Wuhan, China. SARS-Cov2 is known to cause acute pneumonia: the cardinal feature of coronavirus disease 2019 (COVID-19). Clinical features of the disease include respiratory distress, loss of spontaneous breathing, and sometimes neurologic signs such as headache and nausea and anosmia, leading to suppose a possible involvement of the nervous system as a potential target of SARS-CoV2. The chapter will shed light on the recent clinical and experimental data sustaining the involvement of the nervous system in the pathophysiology of COVID-19, based on several case reports and experimental data reporting the possible transmission of SARS-CoV2 throughout the peripheral nerves to the brain cardiorespiratory centers. Thus, understanding the role of the nervous system in the course of clinical symptoms of COVID-19 is important in determining the appropriate therapeutic approach to combat the disease.

Author(s):  
Ray Guillery

This chapter introduces two interpretations of how we know about the world. One, the standard, sensory-to-motor view, is that physical actions for sounds, lights, tastes, smells, and so on act on our sense organs to produce messages that are sent through the nervous system to the cerebral cortex, where the relevant structures of the world can be recognized and appropriate motor actions can be initiated. The other is an interactive sensorimotor view where the nervous system records our interactions with the world, abstracting our knowledge about the world from these interactions. These two opposing views have rarely been considered in terms of specific neural pathways or the messages that they carry; that is the plan for this book. Each view leads to different sets of interpretations of experiments and to different sets of research proposals. The final part of the chapter explores a well-studied and widely taught clinical condition that illustrates the confusions that can arise when the dual meaning of the driver messages to the thalamus is not recognized.


2021 ◽  
Vol 22 (14) ◽  
pp. 7287
Author(s):  
Masaki Tanaka ◽  
Shunji Yamada ◽  
Yoshihisa Watanabe

Neuropeptide Y (NPY), an abundant peptide in the central nervous system, is expressed in neurons of various regions throughout the brain. The physiological and behavioral effects of NPY are mainly mediated through Y1, Y2, and Y5 receptor subtypes, which are expressed in regions regulating food intake, fear and anxiety, learning and memory, depression, and posttraumatic stress. In particular, the nucleus accumbens (NAc) has one of the highest NPY concentrations in the brain. In this review, we summarize the role of NPY in the NAc. NPY is expressed principally in medium-sized aspiny neurons, and numerous NPY immunoreactive fibers are observed in the NAc. Alterations in NPY expression under certain conditions through intra-NAc injections of NPY or receptor agonists/antagonists revealed NPY to be involved in the characteristic functions of the NAc, such as alcohol intake and drug addiction. In addition, control of mesolimbic dopaminergic release via NPY receptors may take part in these functions. NPY in the NAc also participates in fat intake and emotional behavior. Accumbal NPY neurons and fibers may exert physiological and pathophysiological actions partly through neuroendocrine mechanisms and the autonomic nervous system.


1996 ◽  
Vol 76 (1) ◽  
pp. 193-244 ◽  
Author(s):  
P. B. Persson

It is generally held that the role of a specific control element can only be understood within its physiological environment. The reviewed studies make it clear that there is a potent interplay between locally produced substances such as adenosine, nitric oxide, prostaglandins, and various others all interacting with the central level of control. This can occur at central sites (e.g., nitric oxide in the brain) or in the periphery (e.g., neural influence on autoregulation). The interactions are more or less pronounced during specific physiological challenges. Furthermore, several of these interactions are altered under pathological circumstances, and in some cases, the interactions seem to maintain or even augment the severity of disease. When more than three parameters participate in an interaction, the resulting regulation may become extremely complex. If these parameters are nonlinearly coupled with each other, the only way to shed light onto the nature of control network is by treating it as a black box. With the use of spectral analysis or nonlinear methods, it is possible to disentangle the fundamental nature of the system in terms of the complexity and stability. Therefore, modern developments in cardiovascular physiology utilizing these techniques, some of which are derived from the "chaos theory," are reviewed.


2018 ◽  
Vol 3 (1) ◽  
pp. 32
Author(s):  
Vita Elysia ◽  
Ake Wihadanto

Local Government of Magelang Regency initiates the Sister Village Program after Mount Merapi Eruption in 2010. The idea of this program is to connect villages at risk from Merapi eruption to partner villages with less risk in the surrounding regions. This program is part of post-disaster recovery initiatives at the local level which includes planned evacuation routes, shelters, provision of food and other daily essentials. This paper aims to shed light on the role of sister village program in promoting community resilience after the volcanic eruption of Merapi. It is found that the system of sister village program can fulfill many aspects of community resilience components. Considering Indonesia is one of the most disaster-prone countries in the world, this program should be regarded as a good example to be replicated in other prone areas in the country.


2020 ◽  
Author(s):  
Yue Shen ◽  
HaiXiang Ma ◽  
XiTing Lian ◽  
LeYuan Gu ◽  
Qian Yu ◽  
...  

AbstractSudden unexpected death in epilepsy (SUDEP) is the fatal cause leading to the death of epilepsy patients with anti-epileptic drug resistance. However, the underlying mechanism of SUDEP remains to be elusive. Our previous study demonstrated that enhancement of serotonin (5-HT) synthesis by intraperitoneal (IP) injection of 5-hydroxytryptophan in brain significantly reduced the incidence of seizure-induced respiratory arrest (S-IRA) in DBA/1 mice SUDEP models. Given that 5-HT2A receptor (5-HT2AR) acts an important role in mediating respiration system in brain, we hypothesized that 5-HT2AR is of great significance to modulate S-IRA and SUDEP. To test this hypothesis, we examined whether the decreased incidence S-IRA evoked by either acoustic stimulation or PTZ by blocking 5-HT2AR by administration with ketanserin (KET), a selective antagonist of 5HT2AR, in DBA/1 mice SUDEP models to test the role of 5-HT2AR modulating S-IRA. Our results suggested that the decreased incidence of S-IRA by 5-Hydroxytryptophan (5-HTP), a precursor for central nervous system (CNS) serotonin (5-HT) synthesis, was significantly reversed by IP and intracerebroventricularly (ICV) injection of ketanserin in our models. Thus, our data suggested that 5-HT2AR in the brain may be a potential and specific target to prevent SUDEP.


Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.


Author(s):  
Patricia S. Churchland ◽  
Terrence J. Sejnowski

This chapter examines the physical mechanisms in nervous systems in order to elucidate the structural bases and functional principles of synaptic plasticity. Neuroscientific research on plasticity can be divided into four main streams: the neural mechanism for relatively simple kinds of plasticity, such as classical conditioning or habituation; anatomical and physiological studies of temporal lobe structures, including the hippocampus and the amygdala; study of the development of the visual system; and the relation between the animal's genes and the development of its nervous system. The chapter first considers the role of the mammalian hippocampus in learning and memory before discussing Donald Hebb's views on synaptic plasticity. It then explores the mechanisms underlying neuronal plasticity and those that decrease synaptic strength, the relevance of time with respect to plasticity, and the occurrence of plasticity during the development of the nervous system. It also describes modules, modularity, and networks in the brain.


Author(s):  
Georg Northoff

Some recent philosophical discussions consider whether the brain is best understood as an open or closed system. This issue has major epistemic consequences akin to the scepticism engendered by the famous Cartesian demon. Specifically, one and the same empirical theory of brain function, predictive coding, entailing a prediction model of brain, have been associated with contradictory views of the brain as either open (Clark, 2012, 2013) or closed (Hohwy, 2013, 2014). Based on recent empirical evidence, the present paper argues that contrary to appearances, these views of the brain are compatible with one another. I suggest that there are two main forms of neural activity in the brain, one of which can be characterized as open, and the other as closed. Stimulus-induced activity, because it relies on predictive coding is indeed closed to the world, which entails that in certain respects, the brain is an inferentially secluded and self-evidencing system. In contrast, the brain’s resting state or spontaneous activity is best taken as open because it is a world-evidencing system that allows for the brain’s neural activity to align with the statistically-based spatiotemporal structure of objects and events in the world. This model requires an important caveat, however. Due to its statistically-based nature, the resting state’s alignment to the world comes in degrees. In extreme cases, the degree of alignment can be extremely low, resulting in a resting state that is barely if at all aligned to the world. This is for instance the case in schizophrenia. Clinical symptoms such as delusions and hallucinations in schizophrenics are indicative of the fundamental delicateness of the alignment between the brain’s resting-state and the world’s phenomena. Nevertheless, I argue that so long as we are dealing with a well-functioning brain, the more dire epistemic implications of predictive coding can be forestalled. That the brain is in part a self-evidencing system does not yield any generalizable reason to worry that human cognition is out of step with the real world. Instead, the brain is aligned to the world accounting for “world-brain relation” that mitigates sceptistic worries.


Author(s):  
Dale Purves

A major challenge in neuroscience today is to decipher the operating principle of the brain and the rest of the nervous system in the same straightforward way that biologists have come to understand the functions of other organs and organ systems (e.g., the cardiovascular system, the digestive system, and so on). The argument here has been that the function of nervous systems is to make, maintain, and modify neural associations that ultimately promote survival and reproduction in a world that sensory systems can’t apprehend. In this way, we and other animals can link the subjective domain of perception to successful behavior without ever recovering the properties of the world. Neural function on a wholly empirical basis may be the key to understanding how brains operate.


2019 ◽  
pp. 7-53
Author(s):  
James W. Jones

Drawing upon clinical psychoanalysis and laboratory research, this chapter develops an “embodied-relational” epistemology. The chapter reviews major research findings on the ways embodiment influences the cognitive processes by which we understand ourselves and the world. It also reviews current neuro-network studies whose findings imply the brain can be understood as a single, interactive system and not simply a collection of relatively autonomous domains. The emphasis here is on the brain’s complexity, integration, and a certain degree of openness. Sensory experience is understood as an active, not passive process, involving an intimate interconnection between self and world. The role of proprioception, as well as the five basic senses, is analyzed. The implications of such research findings for human understanding, and especially religious understanding, are elaborated.


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