The Experts below are selected from a list of 9405 Experts worldwide ranked by ideXlab platform

Alexei Verkhratsky - One of the best experts on this subject based on the ideXlab platform.

  • The role of Neuroglia in autism spectrum disorders.
    Progress in molecular biology and translational science, 2020
    Co-Authors: Caterina Scuderi, Alexei Verkhratsky
    Abstract:

    Abstract Neuroglia are a large class of neural cells of ectodermal (astroglia, oligodendroglia, and peripheral glial cells) and mesodermal (microglia) origin. Neuroglial cells provide homeostatic support, protection, and defense to the nervous tissue. Pathological potential of Neuroglia has been acknowledged since their discovery. Research of the recent decade has shown the key role of all classes of glial cells in autism spectrum disorders (ASD), although molecular mechanisms defining glial contribution to ASD are yet to be fully characterized. This narrative conceptualizes recent findings of the broader roles of glial cells, including their active participation in the control of cerebral environment and regulation of synaptic development and scaling, highlighting their putative involvement in the etiopathogenesis of ASD.

  • Neuroglia in Ageing
    Advances in experimental medicine and biology, 2019
    Co-Authors: Alexei Verkhratsky, Robert Zorec, J. J. Rodríguez-arellano, Vladimir Parpura
    Abstract:

    Ageing reduces the functional capacity of all organs, so does that of the nervous system; the latter is evident in the reduction of cognitive abilities, learning and memory. While the exact mechanisms of ageing of the nervous system remain elusive, it is without doubt that morpho-functional changes in a variety of Neuroglial cells contribute to this process. The age-dependent changes in Neuroglia are characterised by a progressive loss of function. This reduces glial ability to homeostatically nurture, protect and regenerate the nervous tissue. Such Neuroglial paralysis also facilitates neurodegenerative processes. Ageing of Neuroglia is variable and can be affected by environmental factors and comorbidities.

  • The Concept of Neuroglia.
    Advances in experimental medicine and biology, 2019
    Co-Authors: Alexei Verkhratsky, Robert Zorec, Vladimir Parpura
    Abstract:

    Neuroglia represent a diverse population of non-neuronal cells in the nervous systems, be that peripheral, central, enteric or autonomic nervous system. Arguably, these cells represent about half of the volume of the human brain. This volumetric ratio, and by extension glia to neurone ratio, not only widely differ depending on the size of the animal species brain and its positioning on the phylogenetic tree, but also vary between the regions of an individual brain. Neuroglia derived from a dual origin (ectoderm and mesodermal) and in an assorted morphology, yet their functional traits can be mainly classified into being keepers of homeostasis (water, ions, neurotransmitters, metabolites, fuels, etc.) and defenders (e.g., against microbial organisms, etc.) of the nervous system. As these capabilities go awry, Neuroglia ultimately define their fundamental role in most, if not, all neuropathologies. This concept presented in this chapter serves as a general introduction into the world of Neuroglia and subsequent topics covered by this book.

  • Neuroglia Molecular Mechanisms in Psychiatric Disorders
    Frontiers Media SA, 2019
    Co-Authors: Mami Noda, Alexei Verkhratsky, Caterina Scuderi
    Abstract:

    Neuropsychiatric disorders have long been considered as specific dysfunctions of neuronal functions. Studies of the recent decade, however, have challenged this simplistic view, highlighting the important role played by Neuroglial cells in the onset and/or progression of neuropsychiatric diseases. In the central nervous system (CNS) non-excitable Neuroglia are represented by cells of ectodermal origin (astrocytes, mainly responsible for CNS homeostasis and oligodendrocytes that provide myelination and support for axons) and mesodermal origin (microglial cells that are scions of foetal macrophages entering the neural tube early in development; these cells provide for CNS defence and contribute to shaping neuronal networks). Pathological changes of Neuroglia are complex; these changes are classified into reactive gliosis (astrogliosis, activation of microglia and hypertrophy of oligodendroglial precursors), gliodegeneration with loss of function and glial pathological remodelling. Combination of these processes defines the evolution of neurological diseases in general and neuropsychiatric disorders in particular.In this research topic we addressed the contribution of Neuroglia to major neuropsychiatric pathologies including major depression, schizophrenia, and addictive disorders

  • Neuroglia in the autistic brain: evidence from a preclinical model
    Molecular autism, 2018
    Co-Authors: Maria Rosanna Bronzuoli, Alexei Verkhratsky, Roberta Facchinetti, Davide Ingrassia, Michela Sarvadio, Sara Schiavi, Luca Steardo, Viviana Trezza, Caterina Scuderi
    Abstract:

    Neuroglial cells that provide homeostatic support and form defence of the nervous system contribute to all neurological disorders. We analyzed three major types of Neuroglia, astrocytes, oligodendrocytes, and microglia in the brains of an animal model of autism spectrum disorder, in which rats were exposed prenatally to antiepileptic and mood stabilizer drug valproic acid; this model being of acknowledged clinical relevance. We tested the autistic-like behaviors of valproic acid-prenatally exposed male rats by performing isolation-induced ultrasonic vocalizations, the three-chamber test, and the hole board test. To account for human infancy, adolescence, and adulthood, such tasks were performed at postnatal day 13, postnatal day 35, and postnatal day 90, respectively. After sacrifice, we examined gene and protein expression of specific markers of Neuroglia in hippocampus, prefrontal cortex, and cerebellum, these brain regions being associated with autism spectrum disorder pathogenesis. Infant offspring of VPA-exposed dams emitted less ultrasonic vocalizations when isolated from their mothers and siblings and, in adolescence and adulthood, they showed altered sociability in the three chamber test and increased stereotypic behavior in the hole board test. Molecular analyses indicate that prenatal valproic acid exposure affects all types of Neuroglia, mainly causing transcriptional modifications. The most prominent changes occur in prefrontal cortex and in the hippocampus of autistic-like animals; these changes are particularly evident during infancy and adolescence, while they appear to be mitigated in adulthood. Neuroglial pathological phenotype in autism spectrum disorder rat model appears to be rather mild with little signs of widespread and chronic neuroinflammation.

Laura Ballerini - One of the best experts on this subject based on the ideXlab platform.

  • 3d organotypic spinal cultures exploring neuron and Neuroglia responses upon prolonged exposure to graphene oxide
    Frontiers in Systems Neuroscience, 2019
    Co-Authors: Mattia Musto, Rossana Rauti, Artur Filipe Rodrigues, Elena Bonechi, Clara Ballerini, Kostas Kostarelos, Laura Ballerini
    Abstract:

    Graphene-based nanomaterials are increasingly engineered as components of biosensors, interfaces or drug delivery platforms in neuro-repair strategies. In these developments, the mostly used derivative of graphene is graphene oxide (GO). To tailor the safe development of GO nanosheets, we need to model in vitro tissue responses, and in particular the reactivity of microglia, a sub-population of Neuroglia that acts as the first active immune response, when challenged by GO. Here, we investigated central nervous system (CNS) tissue reactivity upon long-term exposure to GO nanosheets in 3D culture models. We used the mouse organotypic spinal cord cultures, ideally suited for studying long-term interference with cues delivered at controlled times and concentrations. In cultured spinal segments, the normal presence, distribution and maturation of anatomically distinct classes of neurons and resident Neuroglial cells are preserved. Organotypic explants were developed for 2 weeks embedded in fibrin glue alone or presenting GO nanosheets at 10, 25 and 50 μg/mL. We addressed the impact of such treatments on premotor synaptic activity monitored by patch clamp recordings of ventral interneurons. We investigated by immunofluorescence and confocal microscopy the accompanying glial responses to GO exposure, focusing on resident microglia, tested in organotypic spinal slices and in isolated Neuroglia cultures. Our results suggest that microglia reactivity to accumulation of GO flakes, maybe due to active phagocytosis, may trim down synaptic activity, although in the absence of an effective activation of inflammatory response and in the absence of neuronal cell death.

  • Image_3_3D Organotypic Spinal Cultures: Exploring Neuron and Neuroglia Responses Upon Prolonged Exposure to Graphene Oxide.TIF
    2019
    Co-Authors: Mattia Musto, Rossana Rauti, Artur Filipe Rodrigues, Elena Bonechi, Clara Ballerini, Kostas Kostarelos, Laura Ballerini
    Abstract:

    Graphene-based nanomaterials are increasingly engineered as components of biosensors, interfaces or drug delivery platforms in neuro-repair strategies. In these developments, the mostly used derivative of graphene is graphene oxide (GO). To tailor the safe development of GO nanosheets, we need to model in vitro tissue responses, and in particular the reactivity of microglia, a sub-population of Neuroglia that acts as the first active immune response, when challenged by GO. Here, we investigated central nervous system (CNS) tissue reactivity upon long-term exposure to GO nanosheets in 3D culture models. We used the mouse organotypic spinal cord cultures, ideally suited for studying long-term interference with cues delivered at controlled times and concentrations. In cultured spinal segments, the normal presence, distribution and maturation of anatomically distinct classes of neurons and resident Neuroglial cells are preserved. Organotypic explants were developed for 2 weeks embedded in fibrin glue alone or presenting GO nanosheets at 10, 25 and 50 μg/mL. We addressed the impact of such treatments on premotor synaptic activity monitored by patch clamp recordings of ventral interneurons. We investigated by immunofluorescence and confocal microscopy the accompanying glial responses to GO exposure, focusing on resident microglia, tested in organotypic spinal slices and in isolated Neuroglia cultures. Our results suggest that microglia reactivity to accumulation of GO flakes, maybe due to active phagocytosis, may trim down synaptic activity, although in the absence of an effective activation of inflammatory response and in the absence of neuronal cell death.

Vladimir Parpura - One of the best experts on this subject based on the ideXlab platform.

  • The Concept of Neuroglia.
    Advances in experimental medicine and biology, 2019
    Co-Authors: Alexei Verkhratsky, Robert Zorec, Vladimir Parpura
    Abstract:

    Neuroglia represent a diverse population of non-neuronal cells in the nervous systems, be that peripheral, central, enteric or autonomic nervous system. Arguably, these cells represent about half of the volume of the human brain. This volumetric ratio, and by extension glia to neurone ratio, not only widely differ depending on the size of the animal species brain and its positioning on the phylogenetic tree, but also vary between the regions of an individual brain. Neuroglia derived from a dual origin (ectoderm and mesodermal) and in an assorted morphology, yet their functional traits can be mainly classified into being keepers of homeostasis (water, ions, neurotransmitters, metabolites, fuels, etc.) and defenders (e.g., against microbial organisms, etc.) of the nervous system. As these capabilities go awry, Neuroglia ultimately define their fundamental role in most, if not, all neuropathologies. This concept presented in this chapter serves as a general introduction into the world of Neuroglia and subsequent topics covered by this book.

  • Neuroglia in Ageing
    Advances in experimental medicine and biology, 2019
    Co-Authors: Alexei Verkhratsky, Robert Zorec, J. J. Rodríguez-arellano, Vladimir Parpura
    Abstract:

    Ageing reduces the functional capacity of all organs, so does that of the nervous system; the latter is evident in the reduction of cognitive abilities, learning and memory. While the exact mechanisms of ageing of the nervous system remain elusive, it is without doubt that morpho-functional changes in a variety of Neuroglial cells contribute to this process. The age-dependent changes in Neuroglia are characterised by a progressive loss of function. This reduces glial ability to homeostatically nurture, protect and regenerate the nervous tissue. Such Neuroglial paralysis also facilitates neurodegenerative processes. Ageing of Neuroglia is variable and can be affected by environmental factors and comorbidities.

  • Neuroglia: Functional Paralysis and Reactivity in Alzheimer’s Disease and Other Neurodegenerative Pathologies
    Advances in neurobiology, 2017
    Co-Authors: Alexei Verkhratsky, Robert Zorec, José J. Rodríguez, Vladimir Parpura
    Abstract:

    The most notable finding in neurodegenerative diseases is the progressive death of neurones cells. Yet, Neuroglial changes can precede and facilitate neuronal loss. This is perhaps expected because astroglial cells maintain the brain homoeostasis, and are responsible for defence and regeneration, so that their malfunction manifested as degeneration or asthenia together with reactivity contribute to pathophysiology. Neuroglia may represent a novel target for therapeutic intervention, be that prevention, slowing progression of or possibly curing neurodegenerative diseases.

  • Neuroglia functional paralysis and reactivity in alzheimer s disease and other neurodegenerative pathologies
    Advances in neurobiology, 2017
    Co-Authors: Alexei Verkhratsky, Robert Zorec, José J. Rodríguez, Vladimir Parpura
    Abstract:

    The most notable finding in neurodegenerative diseases is the progressive death of neurones cells. Yet, Neuroglial changes can precede and facilitate neuronal loss. This is perhaps expected because astroglial cells maintain the brain homoeostasis, and are responsible for defence and regeneration, so that their malfunction manifested as degeneration or asthenia together with reactivity contribute to pathophysiology. Neuroglia may represent a novel target for therapeutic intervention, be that prevention, slowing progression of or possibly curing neurodegenerative diseases.

  • editorial Neuroglia as a central element of neurological diseases an underappreciated target for therapeutic intervention
    Current Neuropharmacology, 2014
    Co-Authors: Liang Peng, Vladimir Parpura, Alexei Verkhratsky
    Abstract:

    Neuroglia of the central nervous system (CNS), represented by cells of neural (astrocytes, oligodendrocytes and NG2 glial cells) and myeloid (microglia) origins are fundamental for homeostasis of the nervous tissue. Astrocytes are critical for the development of the CNS, they are indispensable for synaptogenesis, and they define structural organisation of the nervous tissue, as well as the generation and maintenance of CNS-blood and cerebrospinal fluid-blood barriers. Astroglial cells control homeostasis of ions and neurotransmitters and provide neurones with metabolic support. Oligodendrocytes, through the process of myelination, as well as by homoeostatic support of axons provide for interneuronal connectivity. The NG2 cells receive direct synaptic inputs, and might be important elements of adult remyelination. Microglial cells, which originate from foetal macrophages invading the brain early in embryogenesis, shape the synaptic connections through removing of redundant synapses and phagocyting apoptotic neurones. Neuroglia also form the defensive system of the CNS through complex and context-specific programmes of activation, known as reactive gliosis. Many neurological diseases are associated with neurogliopathologies represented by asthenic and atrophic changes in glial cells that, through the loss or diminution of their homeostatic and defensive functions, assist evolution of pathology. Conceptually, neurological and psychiatric disorders can be regarded as failures of Neuroglial homeostatic/ defensive responses, and, hence, glia represent a (much underappreciated) target for therapeutic intervention.

Monique R. Ferguson - One of the best experts on this subject based on the ideXlab platform.

  • Localization of West Nile Virus in monkey brain: double staining antigens immunohistochemically of neurons, Neuroglia cells and West Nile Virus.
    International journal of clinical and experimental pathology, 2009
    Co-Authors: Junping Ren, Monique R. Ferguson
    Abstract:

    West Nile virus (WNV) can cause encephalitis or meningitis that affects brain tissue, which can also lead to permanent neurological damage that can be fatal. To our knowledge, no consistent double immunohistochemical staining of neurons, Neuroglia cells, and WNV has yet been reported. To establish a method for performing double-label immunohistochemical detection of neurons, Neuroglia cells and WNV, examining the pathological characteristics of WNV-infected neurons, Neuroglia cells, and investigating distribution of WNV in monkey brain, paraffin-embedded monkey brain tissue were retrospectively studied by immunohistochemical staining of neurons, Neuroglia cells and WNV. Antibodies against neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP) and WNV were used to develop the method of double-label immunohistochemical staining, which allowed independent assessment of neuron status and WNV distribution. A range of immunohistochemical WNV infection in monkey brain was observed in both neurons and Neuroglia cells in terms of the thickness of lesion staining, and the WNV staining was slightly higher in Neuroglia cells than in neurons. All these findings suggest that WNV invasion in the brain plays a crucial role in neurological damage by inducing central nervous system (CNS) cell dysfunction or cell death directly.

Mattia Musto - One of the best experts on this subject based on the ideXlab platform.

  • 3d organotypic spinal cultures exploring neuron and Neuroglia responses upon prolonged exposure to graphene oxide
    Frontiers in Systems Neuroscience, 2019
    Co-Authors: Mattia Musto, Rossana Rauti, Artur Filipe Rodrigues, Elena Bonechi, Clara Ballerini, Kostas Kostarelos, Laura Ballerini
    Abstract:

    Graphene-based nanomaterials are increasingly engineered as components of biosensors, interfaces or drug delivery platforms in neuro-repair strategies. In these developments, the mostly used derivative of graphene is graphene oxide (GO). To tailor the safe development of GO nanosheets, we need to model in vitro tissue responses, and in particular the reactivity of microglia, a sub-population of Neuroglia that acts as the first active immune response, when challenged by GO. Here, we investigated central nervous system (CNS) tissue reactivity upon long-term exposure to GO nanosheets in 3D culture models. We used the mouse organotypic spinal cord cultures, ideally suited for studying long-term interference with cues delivered at controlled times and concentrations. In cultured spinal segments, the normal presence, distribution and maturation of anatomically distinct classes of neurons and resident Neuroglial cells are preserved. Organotypic explants were developed for 2 weeks embedded in fibrin glue alone or presenting GO nanosheets at 10, 25 and 50 μg/mL. We addressed the impact of such treatments on premotor synaptic activity monitored by patch clamp recordings of ventral interneurons. We investigated by immunofluorescence and confocal microscopy the accompanying glial responses to GO exposure, focusing on resident microglia, tested in organotypic spinal slices and in isolated Neuroglia cultures. Our results suggest that microglia reactivity to accumulation of GO flakes, maybe due to active phagocytosis, may trim down synaptic activity, although in the absence of an effective activation of inflammatory response and in the absence of neuronal cell death.

  • Image_3_3D Organotypic Spinal Cultures: Exploring Neuron and Neuroglia Responses Upon Prolonged Exposure to Graphene Oxide.TIF
    2019
    Co-Authors: Mattia Musto, Rossana Rauti, Artur Filipe Rodrigues, Elena Bonechi, Clara Ballerini, Kostas Kostarelos, Laura Ballerini
    Abstract:

    Graphene-based nanomaterials are increasingly engineered as components of biosensors, interfaces or drug delivery platforms in neuro-repair strategies. In these developments, the mostly used derivative of graphene is graphene oxide (GO). To tailor the safe development of GO nanosheets, we need to model in vitro tissue responses, and in particular the reactivity of microglia, a sub-population of Neuroglia that acts as the first active immune response, when challenged by GO. Here, we investigated central nervous system (CNS) tissue reactivity upon long-term exposure to GO nanosheets in 3D culture models. We used the mouse organotypic spinal cord cultures, ideally suited for studying long-term interference with cues delivered at controlled times and concentrations. In cultured spinal segments, the normal presence, distribution and maturation of anatomically distinct classes of neurons and resident Neuroglial cells are preserved. Organotypic explants were developed for 2 weeks embedded in fibrin glue alone or presenting GO nanosheets at 10, 25 and 50 μg/mL. We addressed the impact of such treatments on premotor synaptic activity monitored by patch clamp recordings of ventral interneurons. We investigated by immunofluorescence and confocal microscopy the accompanying glial responses to GO exposure, focusing on resident microglia, tested in organotypic spinal slices and in isolated Neuroglia cultures. Our results suggest that microglia reactivity to accumulation of GO flakes, maybe due to active phagocytosis, may trim down synaptic activity, although in the absence of an effective activation of inflammatory response and in the absence of neuronal cell death.