Increasing evidence suggests that inflammation in the central nervous system (CNS) is closely associated with the pathogenesis of several neurological disorders. Inflammation affects several important physiological functions such as neurotransmitter metabolism, neuroendocrine function, synaptic plasticity as well as neural circuitry of mood. The hallmark of CNS inflammation, i.e. neuroinflammation, is the activation of glial cells. Glial cells, including non-neuronal cells of the neuroepithelium (oligodendrocytes, astrocytes, oligodendrocyte progenitor cells, ependymal cells), neural crest (peripheral glia), and of myeloid origin (microglia), constitute a large fraction of the CNS. Under physiological conditions, glia cells serve a role of immune surveillance, maintain ionic homeostasis, buffer the action of neurotransmitters, and secrete nerve growth factors. However, these cells respond to neural injuries or immunological challenges by producing a variety of proinflammatory and neurotoxic factors, including cytokines, fatty acid metabolites, free radicals, which target bystander neurons and oligodendrocytes.
Glia-cell mediated neurotoxicity is a complex process. A multiprong research approach evaluating potential molecular mechanisms of glia-mediated neurotoxicity, development of appropriate neuroinflammation-targeted interventions, and clinical trials that can monitor and evaluate the efficacy of these interventions will be vital. This Research Topic will hopefully provide impetus for investigators to take on these.
This Research Topic will welcome research in the following areas:
• In vitro and in vivo model systems to study glia-mediated neurotoxicity
• Recent updates on the molecular mechanisms of glia-mediated neurotoxicity
• Advances in development of in vivo imaging modalities to identify glial activation and resulting pathophysiology
• Targeted anti-inflammatory therapy to inhibit the common neurotoxic mechanisms of glial cell activation
• Glial-restricted progenitor cell-based therapy for diseased brain
Increasing evidence suggests that inflammation in the central nervous system (CNS) is closely associated with the pathogenesis of several neurological disorders. Inflammation affects several important physiological functions such as neurotransmitter metabolism, neuroendocrine function, synaptic plasticity as well as neural circuitry of mood. The hallmark of CNS inflammation, i.e. neuroinflammation, is the activation of glial cells. Glial cells, including non-neuronal cells of the neuroepithelium (oligodendrocytes, astrocytes, oligodendrocyte progenitor cells, ependymal cells), neural crest (peripheral glia), and of myeloid origin (microglia), constitute a large fraction of the CNS. Under physiological conditions, glia cells serve a role of immune surveillance, maintain ionic homeostasis, buffer the action of neurotransmitters, and secrete nerve growth factors. However, these cells respond to neural injuries or immunological challenges by producing a variety of proinflammatory and neurotoxic factors, including cytokines, fatty acid metabolites, free radicals, which target bystander neurons and oligodendrocytes.
Glia-cell mediated neurotoxicity is a complex process. A multiprong research approach evaluating potential molecular mechanisms of glia-mediated neurotoxicity, development of appropriate neuroinflammation-targeted interventions, and clinical trials that can monitor and evaluate the efficacy of these interventions will be vital. This Research Topic will hopefully provide impetus for investigators to take on these.
This Research Topic will welcome research in the following areas:
• In vitro and in vivo model systems to study glia-mediated neurotoxicity
• Recent updates on the molecular mechanisms of glia-mediated neurotoxicity
• Advances in development of in vivo imaging modalities to identify glial activation and resulting pathophysiology
• Targeted anti-inflammatory therapy to inhibit the common neurotoxic mechanisms of glial cell activation
• Glial-restricted progenitor cell-based therapy for diseased brain
