This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.

This book provides comprehensive information, both for clinicians and scientists, on the basic mechanisms, clinical features, and therapeutic approaches to epilepsy as an inflammatory disease. Inflammation has been for many years considered as an etiologic player (and a therapeutic target) for a specific group of epilepsies. However, it turns out that this concept underestimated the impact of inflammation in seizure disorders. Many accepted therapies for non-inflammatory epilepsies act in part as an inflammatory drug. The CNS actively responds to acute immune challenges by altering body temperature, stimulating the HPA axis, as well as up- and down-regulating specific sympathetic pathways.

"Mechanisms of Neuroinflammation" book explains how the neuronal cells become swollen at the moment of the blood-brain barrier disruption and how they lose their immunological isolation. A cascade of cytokines and immune cells from the bloodstream enters the nervous system, inflaming neurons and activating the glia. This produces a neuroinflammatory process that can generate different neurodegenerative diseases. Better understanding of mechanisms that are activated at the time when the damage to the brain occurs could lead to the development of suitable therapies that revert the neuronal inflammation and thus prevent further damage to the nervous system.

This book traces the history of adenosine receptor research from molecular biology to medicinal chemistry to behavior, including their implications in disease and potential strategies as therapeutic targets. It provides the reader with a comprehensive overview of the adenosine receptors that includes information on all subtypes - A1, A2A, A2B and A3. Aspects addressed include the most up to date information on their functional distribution in the nervous and peripheral systems, behavioral roles in inflammation, cancer, pain and neurological diseases such as Huntington’s disease, Epilepsy, Parkinson’s disease and Alzheimer’s disease.

Neuroinflammation, Resolution, and Neuroprotection in the Brain discusses the molecular aspects of neuroinflammation in neurological disorders. The book examines the effect of diet and exercise on neuroinflammatory diseases. Chapters focus on bioactive lipids, cytokines and chemokines, as well as the involvement of neuroinflammation, resolution and neuroprotection in neurotraumatic diseases, neurodegenerative diseases and neuropsychiatric diseases. The comprehensive information in this monograph will help readers understand molecular cross-talk among mediators of phospholipid, sphingolipid and cholesterol metabolism. The book's goal is to jumpstart more studies on molecular mechanisms and the therapeutic aspects of neurological disorders in human subjects. - Discusses the molecular aspects of neuroinflammation, resolution and neuroprotection - Examines the role of diet and exercise on neuroinflammatory diseases - Provides cutting-edge research on signal transduction processes - Explores the treatment of neurological disorders caused by neuroinflammation

Brain Edema: From Molecular Mechanisms to Clinical Practice brings together the most widely recognized experts in experimental and clinical brain edema research to review the current knowledge gathered on the molecular and cellular pathophysiology and clinical management of brain edema. This timely book also discusses future directions of research and treatment. Brain edema is an integral and acutely life-threatening part of the pathophysiology of multiple cerebral and non-cerebral disorders, including traumatic brain injury, cerebral ischemia, brain tumors, cardiac arrest, altitude sickness and liver failure. Affecting millions worldwide, research over the past few years has shown that a plethora of complex molecular and cellular mechanisms contribute to this pathological accumulation of water in the brain parenchyma. In parallel, the development of new neuroimaging tools has provided a new way to examine how edema develops longitudinally and in real time, both in pre-clinical models and in patients. Despite intense research over the past few decades, therapeutic options are still limited and sometimes not effective. - Presents a comprehensive understanding of the molecular mechanisms involved in edema formation and resolution - Discusses the specific role of edema development in several pathologies, including traumatic brain injury, stroke, brain tumors, cardiac arrest, and liver failure - Proposes a new classification of edema based on molecular processes - Discusses clinical management of new clinical trials coming from pre-clinical studies - Addresses the possible link between edema formation, other molecular and cellular processes, including inflammation and neuroinflammation

For long, high dose ionizing radiation was considered as a net immune suppressing agent, as shown, among others, by the exquisite radiosensitivity of the lymphoid system to radiation-induced cell killing. However, recent advances in radiobiology and immunology have made this picture more complex. For example, the recognition that radiation-induced bystander effects, share common mediators with various immunological signalling processes, suggests that they are at least partly immune mediated. Another milestone was the finding, in the field of onco-immunology, that local tumor irradiation can modulate the immunogenicity of tumor cells and the anti-tumor immune responsiveness both locally, in the tumor microenvironment, and at systemic level. These observations paved the way for studies exploring optimal combinations of radiotherapy and immunotherapy in order to achieve a synergistic effect to eradicate tumors. However, not all interactions between radiation and the immune system are beneficial, as it was recognized that many of radiation-induced late side effects are also of immune and inflammatory nature. Currently perhaps the most studied field of research in radiation biology is focused around the biological effects of low doses, where many of the observed pathophysiological endpoints are due to mechanisms other than direct radiation-induced cell killing and are immune-related. Finally, it must not be forgotten that the interactions between the ionizing radiations and the immune system are bi-directional, and activation of the immune system also influences the outcome of radiation exposure. This Research Topic brings together 23 articles and aims to give an overview of the complex and very often contradictory nature of the interactions between ionizing radiation and the immune system. Due to its increasing penetrance in the population both through medical diagnostic or environmental sources or during cosmic travel low dose ionizing radiation exposure is becoming a major epidemiological concern world-wide. Several of the articles within the Research Topic specifically address potential long-term health consequences and the underlying mechanisms of low dose radiation exposure. A major intention of the Editors was also to draw the attention of the non-radiobiological scientific community on the fact that ionizing radiation is by far more than purely an immune suppressing agent.

Traumatic brain injury (TBI) remains a significant source of death and permanent disability, contributing to nearly one-third of all injury related deaths in the United States and exacting a profound personal and economic toll. Despite the increased resources that have recently been brought to bear to improve our understanding of TBI, the developme

Aging is one of the major risk factors for the onset and progression of various neurodegenerative diseases. Neuroinflammation is a common feature of virtually every central nervous system disease, and is acknowledged as a likely mediator of cognitive impairments. Systemic inflammation levels are augmented with advanced age and neurodegeneration. The influence of age on neuroinflammatory responses including glial activation, increased production of proinflammatory cytokines, and aberrant neuronal signaling could magnify the deterioration of the central nervous system microenvironment in disease, and may contribute to enhanced cognitive impairment. This eBook is a collection of highly informative original research articles, providing comprehensive aspect of neuroinflammation and possible therapeutic interventions in rescuing cognitive impairments.