- Prof. Juan C. Sáez
- Departamento de Fisiología, Pontificia Universidad Católica de Chile, Santiago de Chile, Chile.
Interdisciplinary Center for Neuroscience of Valparaíso, Institute of Neuroscience, University of Valparaíso, Valparaíso, Chile.
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Special Issue Introduction
Neuroinflammation is a tissue response to acute or chronic stimuli that can be endogenous or exogenous molecules, microorganisms, or conditions. The tissue response depends on the properties of the stimuli (i.e., intensity and duration) as well as the characteristics of the affected cells. It is relevant to recognize that a non-detrimental acute stimulus (i.e., low intensity) could promote phenotypic changes, which up to a threshold, trigger cell phenotype changes that make the organ more resistant to the same or an even stronger stimulus (i.e., with more intensity than the previous one), a phenomenon known as preconditioning. Under these conditions, the stimulus promotes a protective outcome but increases its duration and/or intensity, so that the response overcomes such threshold and could unfold a deleterious tissue response frequently recognized by massive cell death mediated by necrosis. Besides, a delay wave of cell death could propagate from the edge of necrotic focus to neighboring areas being apoptosis the main mechanism of cell death, providing a time-window in which it is possible to intervene to stop the progression of this phenomenon. A somewhat slower cell death progression that also propagates to initially unaffected tissue domains can be recognized under chronic neuropathological conditions such as those associated with metabolic unbalances (e.g., diabetes), expression of unfolding proteins (e.g., Alzheimer´s and Parkinson´s diseases), or gestational and post-partum stress, which are highly associated to neurobehavioral diseases (e.g., schizophrenia and depression). Although numerous neuro center efforts have been made to reduce or stop the neuroinflammatory response, many unanswered questions remain to be solved. During the last two decades, it has been proposed that glia (Astrocytes and oligodendrocytes) and immune cells (mast cells and microglia) could play a relevant role in the development of neuroinflammation. In addition, the neuroinflammatory response is progressive, meaning that the main protagonists and consequences change over time and they alter the scenario in different ways. Nonetheless, neuroinflammation can be recognized as a common factor of diverse pathological conditions of the nervous system. However, its relative contribution to the resulting brain dysfunction remains to be demonstrated. Possibly, a clear cut demonstration is waiting for the discovery of relevant molecular targets and anti-inflammatory drugs suitable for long-lasting treatment without undesired side effects. Since the CNS present much localized and low regeneration capacity, the best strategy to avoid its putative detrimental effects is to prevent as early as possible to avoid its progression before it overpasses the functional compensatory capacity of the nervous tissue that is very high but not endless. This special issue aims to gather theories and pieces of evidence that could offer new events, which might reveal the role of microglia and astrocytes in the neuroinflammatory response of diverse pathological conditions of the nervous system.
Outline of possible topics of interest:
. Influence of the microbiome on microglia and astrocytes during neuroinflammation
. Role of non-selective channels on reactive microglia and astrocytes in neuroinflammation
. Involvement of microglia and astrocytes in neuroinflammation of channelopathies
. Chronic viral infections on microglia and astrocytes during neuroinflammation
. Effects of stress on microglia and astrocytes
. Epigenetic transfer of neuroinflammation
. Connectome and consequence of neuroinflammation on connectome formation
. Exosome- and TNT-mediated cell-cell communication in neuroinflammation
. New molecular targets and treatments to prevent or stop neuroinflammation
Submission Deadline30 Apr 2021