Microglia in Neuroinflammation

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Background

Microglia, the resident innate immune cell population of the central nervous system (CNS), are considered a protective barrier from CNS damage, but also a primary mediator of neuroinflammation. Microglia are derived from yolk sac erythro-myeloid progenitors that migrate to the developing brain prior to formation of the blood brain barrier. Under normal physiological conditions, microglia perform homeostatic functions, such as parenchymal surveillance, neurotrophic support, pathogen or debris removal, and maintenance of synaptic homeostasis and neuronal plasticity. However, in pathological conditions—e.g. exposure to pathogen-associated molecular patterns (PAMPs) or damage associated molecular patterns (DAMPs), microglia can modify their activity and perform either protective or harmful functions, depending on the context. They can increase phagocytosis and breakdown debris. However, in neuroinflammation, microglia activity may become rampant and drive neurodegenerative disease and other chronic CNS pathologies as homeostasis is disrupted and neuronal dysfunction and damage ensue.

However, the notion that microglia, and the neuroinflammation induced by their aberrant activity, are strictly pathogenic players in neurodegenerative disease is rapidly evolving. Further, the oversimplified M1-M2 paradigm of microglial activation, with M1 representing a pro-inflammatory phenotype and M2 representing an anti-inflammatory phenotype, has seriously been called into question. Single cell multi-omic profiling reveals not only regional heterogeneity of microglia and a spectrum of activation states, but the existence of a specialized microglia subset, termed disease-associated microglia (DAM) that arises with age and disease onset in response to what have been called neurodegeneration-associated molecular patterns (NAMPs). Emerging data suggest a protective role for DAM in the early stages of neurodegenerative disease, yet DAM can alter their functional state as disease progresses and play a potentially pathogenic role. Thus, the functional diversity of microglia is more complex than previously appreciated. We are only now scratching the surface regarding the contribution of microglia to neurodegenerative disease and particularly in other CNS pathologies resulting from chronic neuroinflammation.

Here, we call for manuscripts addressing the role of microglia in homeostasis, CNS protection and neuroinflammation. Microglia are at the forefront of research into neuroinflammation associated with neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis, and their role in neuroinflammation associated with other chronic CNS pathologies is under investigation. Thus, we encourage submission of papers interrogating (Original Research articles) or synthesizing the available evidence on (Review articles) microglia-specific roles in neurodegenerative disease as well as other contexts, including, but not limited to:

Cancer, aging, pain, viral infection [SARSCoV2, West Nile, HIV], neuropsychiatric lupus, schizophrenia, autism, prion diseases, epilepsy, sepsis, traumatic brain injury, stroke, diabetes, glaucoma and other eye diseases, chemotherapy-induced cognitive impairment and drug/alcohol abuse.

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.

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