Microglial cells play a key role in maintaining and regulating the homeostasis of the central nervous system (CNS). These cells respond to pathogens, injury, and disease by changing their morphology, migrating to the site of infection/injury and undergoing transcriptional changes. In pathological conditions, these changes contribute to the neural damage by inducing neuroinflammation and releasing neuroinflammatory molecules, but at the same time, they can repair the damaged tissue by releasing anti-inflammatory cytokines and neurotrophic factors.
Most neurological disorders feature microglial reactivity, aimed at containing CNS damage and promoting repair, but often resulting in an exacerbation of the inflammatory response that propagates the neurodegenerative process. Our understanding of the microglial functions in the context of many diseases including Alzheimer's disease (AD) and other neuroinflammatory/neurodegenerative conditions such as multiple sclerosis (MS) or stroke, has widened steadily in the last decade by way of new tools, biomarkers and techniques that help us to distinguish microglia from other myeloid cells. However, there are still many knowledge gaps that need to be filled to fully elucidate the spectrum of microglial functions in these diseases. This is essential to identify new therapeutic targets that can lead to new drugs to facilitate the development of emerging therapies.
This Research Topic aims to bring together articles (Original Research, Reviews, Perspectives, etc.) that uncover gaps in our current knowledge of microglial function and dysfunction in the context of disease.
Topics of interest include, but are not limited to:
- Microglia (dys)function in neuroinflammation associated with neurological disorders
- Cellular and molecular mechanisms underlying microglial activation in neurodegenerative diseases and after brain injury
- Novel models, tools, and markers to study microglial activity and function in the context of brain disease
Microglial cells play a key role in maintaining and regulating the homeostasis of the central nervous system (CNS). These cells respond to pathogens, injury, and disease by changing their morphology, migrating to the site of infection/injury and undergoing transcriptional changes. In pathological conditions, these changes contribute to the neural damage by inducing neuroinflammation and releasing neuroinflammatory molecules, but at the same time, they can repair the damaged tissue by releasing anti-inflammatory cytokines and neurotrophic factors.
Most neurological disorders feature microglial reactivity, aimed at containing CNS damage and promoting repair, but often resulting in an exacerbation of the inflammatory response that propagates the neurodegenerative process. Our understanding of the microglial functions in the context of many diseases including Alzheimer's disease (AD) and other neuroinflammatory/neurodegenerative conditions such as multiple sclerosis (MS) or stroke, has widened steadily in the last decade by way of new tools, biomarkers and techniques that help us to distinguish microglia from other myeloid cells. However, there are still many knowledge gaps that need to be filled to fully elucidate the spectrum of microglial functions in these diseases. This is essential to identify new therapeutic targets that can lead to new drugs to facilitate the development of emerging therapies.
This Research Topic aims to bring together articles (Original Research, Reviews, Perspectives, etc.) that uncover gaps in our current knowledge of microglial function and dysfunction in the context of disease.
Topics of interest include, but are not limited to:
- Microglia (dys)function in neuroinflammation associated with neurological disorders
- Cellular and molecular mechanisms underlying microglial activation in neurodegenerative diseases and after brain injury
- Novel models, tools, and markers to study microglial activity and function in the context of brain disease
