Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Immune responses within the brain are still scarcely explored. Nerve tissue damage is accompanied by the activation of glial cells, primarily microglia and astroglia, and such activation is responsible for the release of cytokines and chemokines that maintain the local inflammatory response and actively recruit lymphocytes and monocytes to the damaged areas. Theoretically, these responses are designed to repair the brain damage. However, alterations, or a chronic perpetuation of these responses may underlie a number of neuro-pathologies. It is thought that each inflammatory scenario within the brain have a specific biochemical footprint characterized by the release of determined cytokines, chemokines and growing factors able to define particular immunological responses. Alongside, glial cells transform their cell body, become larger and develop higher number of branches adopting an active morphological phenotype. These changes are related with the search of interactions with other cells, such as bystander resident cells of the brain parenchyma, but also cells homing from the blood stream. In this process, microglia and astrocytes communicates with other cells by the formation of specific intercellular connections that are still poorly understood. These interactions are complex and entail the arrangement of cytoskeletal compounds, secretory and phagocytic domains. In this particular crosstalk there is a two-way communication in which glial cells and target cells come together establishing interfaces with specific information exchange. This way, glial cells orchestrate the particular response recruiting cellular subsets within the central nervous system and organizing the resolution of the brain damage. In this Frontiers Research Topic, we compile a selection of articles unfolding diverse aspects of glial-derived inflammation, focused on neurodegenerative diseases and other nervous system disorders, with special emphasis on microglia/macrophages as leading actors managing neuro-immunity.

astroglia --- neuroimmunology --- Neuroinflammation --- T cells --- glia --- Microglia

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Immune responses within the brain are still scarcely explored. Nerve tissue damage is accompanied by the activation of glial cells, primarily microglia and astroglia, and such activation is responsible for the release of cytokines and chemokines that maintain the local inflammatory response and actively recruit lymphocytes and monocytes to the damaged areas. Theoretically, these responses are designed to repair the brain damage. However, alterations, or a chronic perpetuation of these responses may underlie a number of neuro-pathologies. It is thought that each inflammatory scenario within the brain have a specific biochemical footprint characterized by the release of determined cytokines, chemokines and growing factors able to define particular immunological responses. Alongside, glial cells transform their cell body, become larger and develop higher number of branches adopting an active morphological phenotype. These changes are related with the search of interactions with other cells, such as bystander resident cells of the brain parenchyma, but also cells homing from the blood stream. In this process, microglia and astrocytes communicates with other cells by the formation of specific intercellular connections that are still poorly understood. These interactions are complex and entail the arrangement of cytoskeletal compounds, secretory and phagocytic domains. In this particular crosstalk there is a two-way communication in which glial cells and target cells come together establishing interfaces with specific information exchange. This way, glial cells orchestrate the particular response recruiting cellular subsets within the central nervous system and organizing the resolution of the brain damage. In this Frontiers Research Topic, we compile a selection of articles unfolding diverse aspects of glial-derived inflammation, focused on neurodegenerative diseases and other nervous system disorders, with special emphasis on microglia/macrophages as leading actors managing neuro-immunity.

astroglia --- neuroimmunology --- Neuroinflammation --- T cells --- glia --- Microglia

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Immune responses within the brain are still scarcely explored. Nerve tissue damage is accompanied by the activation of glial cells, primarily microglia and astroglia, and such activation is responsible for the release of cytokines and chemokines that maintain the local inflammatory response and actively recruit lymphocytes and monocytes to the damaged areas. Theoretically, these responses are designed to repair the brain damage. However, alterations, or a chronic perpetuation of these responses may underlie a number of neuro-pathologies. It is thought that each inflammatory scenario within the brain have a specific biochemical footprint characterized by the release of determined cytokines, chemokines and growing factors able to define particular immunological responses. Alongside, glial cells transform their cell body, become larger and develop higher number of branches adopting an active morphological phenotype. These changes are related with the search of interactions with other cells, such as bystander resident cells of the brain parenchyma, but also cells homing from the blood stream. In this process, microglia and astrocytes communicates with other cells by the formation of specific intercellular connections that are still poorly understood. These interactions are complex and entail the arrangement of cytoskeletal compounds, secretory and phagocytic domains. In this particular crosstalk there is a two-way communication in which glial cells and target cells come together establishing interfaces with specific information exchange. This way, glial cells orchestrate the particular response recruiting cellular subsets within the central nervous system and organizing the resolution of the brain damage. In this Frontiers Research Topic, we compile a selection of articles unfolding diverse aspects of glial-derived inflammation, focused on neurodegenerative diseases and other nervous system disorders, with special emphasis on microglia/macrophages as leading actors managing neuro-immunity.

astroglia --- neuroimmunology --- Neuroinflammation --- T cells --- glia --- Microglia --- astroglia --- neuroimmunology --- Neuroinflammation --- T cells --- glia --- Microglia

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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

Science: general issues --- Neurosciences --- aging --- inflammation --- microglia --- astroglia --- therapies

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This book collects 25 scientific articles from laboratories around the world, all of which use botulinum neurotoxins as the main protagonists of their studies. The use of botulinum neurotoxin in medicine, following its ability to inhibit the effects of various disorders of different etiology on the human organism, constitutes the main topic of each article presented here. This book, which is aimed at both students and medical professionals, attempts to summarize current knowledge about the use of botulinum toxin as a therapeutic agent in many diseases, ranging from spasticity to tremor, form motor dysfunction after stroke to neuropathic pain, from hyperactive muscle to migraine, and so on. Thanks to its simplified writing, accessible to an audience who may not be familiar with the mysteries of science, readers will get new insights into this biological toxin and its multiple applications, not simply relegated to its historical use to correct of face wrinkles. Both review and research articles are presented, not only concerning animal studies, but also clinical reports. This book will provide an up-to-date picture of the state-of-the-art of the possible development of novel applications of botulinum neurotoxins for future therapeutic purposes.

Medicine --- botulinum toxin --- limb tremors --- muscle selection --- biological effect --- various cell types --- neurotransmitter --- dermatology --- novel indication --- botulinum neurotoxin --- masticatory system --- maxillofacial bone --- dental occlusion --- orthognathic surgery --- sialorrhoea --- drooling --- salivary glands --- swallowing --- eccrine glands --- onabotulinumtoxin A --- incobotulinumtoxin A --- botulinum neurotoxins --- botulinum neurotoxin serotype A --- heavy chain --- botulinum neurotoxin serotype a heavy chain (BoNT/A HC) --- spinal cord injury (SCI) --- nerve regeneration --- growth associated protein 43 (GAP-43) --- superior cervical ganglion 10 (SCG10) --- neuronal processes --- neural regeneration --- Schwann cells --- glia --- spinal cord --- immunohistochemistry --- allodynia --- weight bearing --- sciatic static index --- walking track analysis --- itch --- SNARE --- VAMP --- mast cells --- compound 48/80 --- chloroquine --- spasticity --- botulinum toxin type A --- appropriate treatment --- Therapeutic Index --- pruritus --- antipruritic --- clinical --- experimental --- BoNT/A --- astroglia --- interleukins --- microglia --- TLR2 --- TLR4 --- Snap-23 --- pain --- cerebral palsy --- botulinum toxin A --- complex regional pain syndrome --- lumbar sympathetic ganglion block --- chronic pelvic pain --- overactive detrusor --- vaginism --- temporomandibular joint dislocation --- lateral pterygoid muscle --- botulinum toxin therapy --- synaptic transmission --- SNAP-25 --- epilepsy --- Parkinson's disease --- neurotransmission blockade --- electrical activity --- prion disease --- new indications --- formulation --- delivery --- refractory chronic migraine --- tension headache --- medication overuse headache --- prophylactic treatment --- XEOMIN® --- BTX --- central neuropathic pain --- spinal cord injury --- post-stroke shoulder pain --- mouse test --- Clostridium tetani --- botulinum antitoxin --- food safety --- abobotulinumtoxinA --- upper limb spasticity --- post-stroke --- early use --- ONTIME --- clinical trial --- human --- urodynamics --- botulinum neurotoxin-A --- basal ganglia --- interspecies differences in motor behavior --- mouse --- rat --- interneurons --- hand tremor --- treatment --- electromyography --- kinematics --- essential tremor --- dystonic tremor --- tremor --- movement disorders --- Botulinum toxin --- upper limb biomechanics --- joint biomechanics --- diagnostic guidance --- clinical decision support --- spastic paresis --- electrical stimulation --- stroke management --- rehabilitation --- hand --- botulinum toxin --- limb tremors --- muscle selection --- biological effect --- various cell types --- neurotransmitter --- dermatology --- novel indication --- botulinum neurotoxin --- masticatory system --- maxillofacial bone --- dental occlusion --- orthognathic surgery --- sialorrhoea --- drooling --- salivary glands --- swallowing --- eccrine glands --- onabotulinumtoxin A --- incobotulinumtoxin A --- botulinum neurotoxins --- botulinum neurotoxin serotype A --- heavy chain --- botulinum neurotoxin serotype a heavy chain (BoNT/A HC) --- spinal cord injury (SCI) --- nerve regeneration --- growth associated protein 43 (GAP-43) --- superior cervical ganglion 10 (SCG10) --- neuronal processes --- neural regeneration --- Schwann cells --- glia --- spinal cord --- immunohistochemistry --- allodynia --- weight bearing --- sciatic static index --- walking track analysis --- itch --- SNARE --- VAMP --- mast cells --- compound 48/80 --- chloroquine --- spasticity --- botulinum toxin type A --- appropriate treatment --- Therapeutic Index --- pruritus --- antipruritic --- clinical --- experimental --- BoNT/A --- astroglia --- interleukins --- microglia --- TLR2 --- TLR4 --- Snap-23 --- pain --- cerebral palsy --- botulinum toxin A --- complex regional pain syndrome --- lumbar sympathetic ganglion block --- chronic pelvic pain --- overactive detrusor --- vaginism --- temporomandibular joint dislocation --- lateral pterygoid muscle --- botulinum toxin therapy --- synaptic transmission --- SNAP-25 --- epilepsy --- Parkinson's disease --- neurotransmission blockade --- electrical activity --- prion disease --- new indications --- formulation --- delivery --- refractory chronic migraine --- tension headache --- medication overuse headache --- prophylactic treatment --- XEOMIN® --- BTX --- central neuropathic pain --- spinal cord injury --- post-stroke shoulder pain --- mouse test --- Clostridium tetani --- botulinum antitoxin --- food safety --- abobotulinumtoxinA --- upper limb spasticity --- post-stroke --- early use --- ONTIME --- clinical trial --- human --- urodynamics --- botulinum neurotoxin-A --- basal ganglia --- interspecies differences in motor behavior --- mouse --- rat --- interneurons --- hand tremor --- treatment --- electromyography --- kinematics --- essential tremor --- dystonic tremor --- tremor --- movement disorders --- Botulinum toxin --- upper limb biomechanics --- joint biomechanics --- diagnostic guidance --- clinical decision support --- spastic paresis --- electrical stimulation --- stroke management --- rehabilitation --- hand