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Olfactory dysfunction, also known as anosmia and hyposmia, is one of the most prevalent (80-90%) symptoms reported by patients with COVID-19. Outside the context of COVID-19, chemosensory dysfunction has been associated with decreased quality of life, anxiety, depression, and cognitive impairment. In the setting of COVID-19, decreased sense of smell has been positively associated with mood disorders such as anxiety and depression. The short-term and long-term neuropsychiatric implications of the olfactory dysfunction related to COVID-19 are still largely unexplored. Investigation of the neuropsychiatric sequelae of olfactory dysfunction related to COVID-19 infection is particularly critical to characterize the pathological effects of COVID-19 on brain function and to develop strategies to improve patient’s quality of life and mental wellbeing. In this Research Topic, Frontiers aims to highlight studies that investigate the neuropsychiatric, psychological, and cognitive consequences of COVID-19-related olfactory dysfunction, present current advances in the field, and anticipate health care needs for the development of therapeutic interventions.
The nervous system plays an important role in the regulation of immunity and inflammation. On the other hand unbalanced immune responses in inflammatory and autoimmune conditions may have a deleterious impact on neuronal integrity and brain function. Recent studies have characterized neural pathways communicating peripheral inflammatory signals to the CNS, and brain- and spinal cord-derived circuitries controlling various innate and adaptive immune responses and inflammation. A prototypical neural reflex circuit that regulates immunity and inflammation is the vagus nerve-based “inflammatory reflex”. Ongoing research has revealed cellular and molecular mechanisms underlying these neural circuits and indicated new therapeutic approaches in inflammatory and autoimmune disorders. Pharmacological and bioelectronic modulation of neural circuitry has been successfully explored in preclinical settings of sepsis, arthritis, inflammatory bowel disease, obesity-driven disorders, diabetes and other diseases. These studies paved the way to successful clinical trials with bioelectronic neuronal modulation in rheumatoid arthritis and inflammatory bowel disease. Dysregulated release of cytokines and other inflammatory molecules may have a severe impact on brain function. Brain inflammation (neuroinflammation), imbalances in brain neuronal integrity and neurotransmitter systems, and cognitive impairment are characteristic features of post-operative conditions, sepsis, liver diseases, diabetes and other disorders characterized by immune and metabolic dysregulation. Derangements in cytokine release also play a pivotal role in depression. Characteristic brain reactive antibodies in autoimmune conditions, including systemic lupus erythematosus and neuromyelitis optica, significantly contribute to brain pathology and cognitive impairment. These studies, and the simultaneous characterization of neuro-protective cytokines, identified new therapeutic approaches for treating neurological complications in inflammatory and autoimmune disorders. This Frontiers Research Topic is a forum for publishing research findings and methodological and conceptual advances at the intersection of immunology and neuroscience. We hope that presenting new insight into bi-directional neuro-immune communication in inflammation and autoimmunity will foster further collaborations and facilitate the development of new efficient therapeutic strategies.
The Coronavirus Disease 2019 (COVID-19) global pandemic, caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has led to the identification of a broad range of post-acute Covid neurological symptoms including cognitive impairments, specific executive dysfunctions with sensorimotor deficits (paresthesia, numbness, or weakness of specific body parts), changes in sleep, changes in taste or smell, hallucinations, emotional distress (anxiety, depression), and fatigue/asthenia. Alarmingly, those post-acute sequelae of COVID-19 (PASC) can occur several weeks after infection, arise after severe, mild, or even asymptomatic SARS-CoV2 infection, and are characterized by the persistence, worsening, or new onset of chronic and debilitating neurological symptoms, which have led to the use of NeuroCOVID syndrome terminology. A link between COVID-19-related neurological symptoms and other neurological diseases has not been clearly established, but an increasing number of studies report an increase in mortality post-SARS-CoV-2 infection and an atypical clinical presentation of COVID-19 in patients with dementia. Another intriguing discovery is that survivors that did not suffer from neurodegenerative diseases before the COVID-19 infection seem to be at high risk for subsequent development of neurological disease and in particular Alzheimer’s disease, and to develop early-dementia symptoms. However, the pathophysiology of those associations is not yet delineated, and more research is needed on NeuroCOVID in both the general population and in specific subgroups affected by neurological disorders. As the COVID-19 pandemic could cause a significant rise in the number of dementia patients in the long term, there is an urgent need to understand how PASC is associated with neurodegenerative disorders or with a worsening of neurologic symptoms in neurologically vulnerable populations.
With the invitation to edit this volume, I wanted to take the opportunity to assemble reviews on different aspects of circadian clocks and rhythms. Although most c- tributions in this volume focus on mammalian circadian clocks, the historical int- duction and comparative clocks section illustrate the importance of various other organisms in deciphering the mechanisms and principles of circadian biology. Circadian rhythms have been studied for centuries, but only recently, a mole- lar understanding of this process has emerged. This has taken research on circadian clocks from mystic phenomenology to a mechanistic level; chains of molecular events can describe phenomena with remarkable accuracy. Nevertheless, current models of the functioning of circadian clocks are still rudimentary. This is not due to the faultiness of discovered mechanisms, but due to the lack of undiscovered processes involved in contributing to circadian rhythmicity. We know for example, that the general circadian mechanism is not regulated equally in all tissues of m- mals. Hence, a lot still needs to be discovered to get a full understanding of cir- dian rhythms at the systems level. In this respect, technology has advanced at high speed in the last years and provided us with data illustrating the sheer complexity of regulation of physiological processes in organisms. To handle this information, computer aided integration of the results is of utmost importance in order to d- cover novel concepts that ultimately need to be tested experimentally.
Linking Neuroscience and Behavior in COVID-19 examines the impact of the virus and pandemic on behavior and mental health. Chapters look at those with pre-existing conditions, including dementia and multiple sclerosis, and how the pandemic has burdened them further. There is also discussion on the mental health consequences the pandemic has had and continues to have on the broad populace, including depression and anxiety, as well as neurological effects of the virus itself. Finally, managing care and treatment of conditions - those preceding, caused by, or emerging for the first time during the pandemic are also detailed. - Discusses the impact of the COVID-19 pandemic and the virus itself on behavior and psychology - Examines comorbidities including Parkinson's disease, neuroinflammation, and autism spectrum disorders - Outlines the management and care for coexisting conditions including brain tumors, multiple sclerosis, and ischemic stroke - Features chapters on the severe damage to the nervous system which may be caused by SARS-CoV-2 infection including myelitis - Contains chapters with key facts, dictionary of terms, summary points, applications to other areas pertinent to each chapter, and policies and procedures
This book discusses the organ-specific systemic manifestations of COVID-19. The initial chapters of the book review the origin and evolution of the coronaviruses, followed by pathogenesis and immune response during COVID-19 infection. The book also provides insight into the role of angiotensin-converting enzyme 2 in the onset of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pathogenesis. It summarizes the neurological aspects of SARS-CoV2, including transmission pathways, mechanisms of invasion into the nervous system, and mechanisms of neurological disease. It also delineates the association of severe disease with high blood plasma levels of inflammatory cytokines and inflammatory markers in SARS-CoV-2 infection. Lastly, it discusses the perturbation of gut microbiota by SARS-CoV-2 and uncovers the potential risk of virus infection on reproductive health.
Neurocognitive and neuropsychiatric disorders contribute to a substantial amount of global morbidity and, as such, the identification of their causes is paramount to understanding their underlying pathophysiology as well as treatment and prevention strategies. Infectious Diseases in Neurocognitive and Neuropsychiatric Medicine considers the many infectious diseases that have been associated with cognitive and neuropsychiatric function. In Parts I-III, each chapter focuses on a different disease to cover a range of viral, bacterial, and parasitic diseases in neurocognitive and neuropsychiatric medicine. Part IV considers infectious diseases and clinical conditions and syndromes, while Part V examines the relationship between neurocognitive and neuropsychiatric function and the microbiome and Part VI the relationship with childhood development. In addition to molecular and clinical descriptions of the infectious diseases themselves, many chapters also explore the diseases' basic epidemiological features to consider where they may be exerting the greatest impact on cognitive and neuropsychiatric function. Where they exist, the possible mitigating factors and treatments for the neuropsychiatric and cognitive dysfunction that can be associated with these infectious diseases are also explored. In doing so, this volume examines the neurocognitive and neuropsychiatric disorders associated with infectious disease to better understand the role infections play.