BMC Neurology and BMC Neuroscience welcomed submissions to our Collection on Neuroinflammation and Brain Disease. Inflammation is a biological process that dynamically alters the surrounding microenvironment, including participating immune cells. As a well-protected organ surrounded by specialized barriers and with immune privilege properties, the central nervous system (CNS) tightly regulates immune responses. In neuroinflammatory conditions, pathogenic immunity can disrupt CNS structure and function. Neuroinflammation has a key role in the onset and/or progression of several neurological disorders, including stroke, Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's condition, Multi-sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS).
Microglia are critical cells involved in the brain inflammation and specifically in inflammatory neurodegenerative diseases. Under the influence of exogenous and endogenous factors (trauma, stroke, chronic infections, disease related proteins like Aβ, Tau/p-Tau or α-syn,), the activation of microglia triggers several signal transduction pathways, including phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR), leading to NF-κB activation. The subsequent production of pro-inflammatory cytokines, chemokines, inducible enzymes (e.g., iNOS) and COX-2 drives to neuroinflammation.
Numerous studies have indeed documented the increased production of different cytokines including interleukin-1β (IL-1β), IL-6, IL-18, IL-12, IL-23, IL-33 and tumor necrosis factor-α (TNF-α) in various neurological and neuropsychiatric disorders. For example, an high expression of IL-1β in microglia cells surrounding Aβ plaques was observed in AD patients. Moreover, the neuroinflammation observed in neurological disorders has a pivotal role in exacerbating Aβ burden and tau hyperphosphorylation, suggesting that stimulating cytokines in response to an undesirable external response could be a checkpoint for treating neurological disorders.
The purpose of this collection was to provide the most updated research on crucial molecular pathways involved in neuroinflammation. Deciphering inflammatory biomarkers and their function in the CNS pathophisiology has important implications for understanding the pathogenesis of most of important CNS disorders.
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