About this Research Topic
This Research Topic is the first part of the article collection series, Modulating Glial Cells Phenotype: New Findings and Therapies, Volume II.
Aging and neurodegenerative diseases are closely related, and the common point between both scenarios is neuroinflammation. Chronic inflammation causes per se functional consequences, such as cognitive deficits, alterations in mood and behavior, loss of neurotransmitters, and even neuronal death. Reported evidence shows a detrimental role of neuroinflammatory responses in the development of neurodegenerative disorders and aging. Glial cells, specifically microglia and astrocytes, seem to have a key role in this process. While it is becoming clear that activation of microglia and astroglia with the concomitant expression of proinflammatory cytokines and chemokines are often associated with disease, is it not fully understood which mechanism leads to glial cells activation. Moreover, there are controversies about the use of the term activation, as astroglia and microglia can be polarized in a so called “good” or “bad” phenotype or even a dystrophic one. The present literature refers to A1 or M1 polarization for the bad phenotype and A2 or M2 for the good one, in astrocytes and microglia respectively.
The study of glial cells has therefore emerged as a hot topic in the last years. Even though there are many original papers or reviews that discuss the implication of astrocytes and microglial cells on neurodegenerative diseases, there remain important gaps in the understanding of that process. Specifically, the unanswered question is whether there is a common pathway to the different phenotypes that could acquire glia, and if these phenotypes correlate with worsening of neurodegenerative diseases or aging. Precisely, which phenotype is better for a healthy brain?
Therefore, it is currently a great area of interest to identify the mechanisms whereby glial cells reactive phenotype acquisition could be detrimental or neuroprotective in the context of inflammatory processes that are closely related with the development of neurodegenerative diseases and aging. The comprehension of these processes represents an area of intense focus for the development of therapeutics to halt the progression of the inflammation or even slow down the process of aging.
This Research Topic will be focused in reviewing current issues and novel findings in the modulation of glial cells and the pathways able to promote a healthy aging and will aim to provide a better understanding of cellular and molecular mechanism towards a neuroprotective or a deleterious glial phenotype. More specifically, this Research Topic will include articles (both experimental and reviews) that describe the process of microglia and astroglia polarization towards neurotoxic or neuroprotective phenotypes, as well as therapeutic interventions that could modified glial phenotype in neurodegenerative diseases and aging brain.
Aging and neurodegenerative diseases are closely related, and the common point between both scenarios is neuroinflammation. Chronic inflammation causes per se functional consequences, such as cognitive deficits, alterations in mood and behavior, loss of neurotransmitters, and even neuronal death. Reported evidence shows a detrimental role of neuroinflammatory responses in the development of neurodegenerative disorders and aging. Glial cells, specifically microglia and astrocytes, seem to have a key role in this process. While it is becoming clear that activation of microglia and astroglia with the concomitant expression of proinflammatory cytokines and chemokines are often associated with disease, is it not fully understood which mechanism leads to glial cells activation. Moreover, there are controversies about the use of the term activation, as astroglia and microglia can be polarized in a so called “good” or “bad” phenotype or even a dystrophic one. The present literature refers to A1 or M1 polarization for the bad phenotype and A2 or M2 for the good one, in astrocytes and microglia respectively.
The study of glial cells has therefore emerged as a hot topic in the last years. Even though there are many original papers or reviews that discuss the implication of astrocytes and microglial cells on neurodegenerative diseases, there remain important gaps in the understanding of that process. Specifically, the unanswered question is whether there is a common pathway to the different phenotypes that could acquire glia, and if these phenotypes correlate with worsening of neurodegenerative diseases or aging. Precisely, which phenotype is better for a healthy brain?
Therefore, it is currently a great area of interest to identify the mechanisms whereby glial cells reactive phenotype acquisition could be detrimental or neuroprotective in the context of inflammatory processes that are closely related with the development of neurodegenerative diseases and aging. The comprehension of these processes represents an area of intense focus for the development of therapeutics to halt the progression of the inflammation or even slow down the process of aging.
This Research Topic will be focused in reviewing current issues and novel findings in the modulation of glial cells and the pathways able to promote a healthy aging and will aim to provide a better understanding of cellular and molecular mechanism towards a neuroprotective or a deleterious glial phenotype. More specifically, this Research Topic will include articles (both experimental and reviews) that describe the process of microglia and astroglia polarization towards neurotoxic or neuroprotective phenotypes, as well as therapeutic interventions that could modified glial phenotype in neurodegenerative diseases and aging brain.
Keywords: Microglia, Astrocytes, Neuroinflammation, Aging, Neurodegeneration
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
