The inflammasome, a multiprotein complex, is indispensable in innate immunity. It can be activated by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), including viruses, fungi, ATP, monosodium urate, silica crystals, fibrillar amyloid-β peptides, and aluminum salt crystals. Activation of the inflammasome regulates maturation and secretion of pro-inflammatory cytokines (such as interleukin (IL)-1β and IL-18) and GSDMD-mediated pyroptosis. Activation of the inflammasome plays an important role in the body's resistance to pathogen infection and recognition of danger signals. Still, its overactivation or uncontrolled regulation is closely related to many inflammatory diseases, such as gout, type 2 diabetes, atherosclerosis, nonalcoholic steatohepatitis, Parkinson's disease (PD), Alzheimer's disease (AD), and a variety of autoimmune diseases. In recent years, hyperactivation of inflammasome complexes has been increasingly demonstrated to contribute to sustained neuroinflammation and neurodegenerative disease progression. We focus on why aberrant activation of inflammasome complexes amplifies pathology in neuroinflammation and neurodegeneration and highlight prospects for neurotherapeutic interventions based on targeting inflammasome pathways.
The goal of this Research Topic is to provide a forum to advance research on the contribution of inflammasome (such as NLRP3, NLRC4, NLRP1, and AIM2) activation to the genesis and development of neuroinflammation and neurodegeneration, as well as to explore innovative gut-oriented pharmacological interventions in the attempt to achieve a beneficial impact on neuroinflammation and neurodegeneration.
The Research Topic had the bullet points below:
1) Inflammasome activation promotes the pathogenesis of neuroinflammation and neurodegeneration
2) The inhibitors of inflammasome activation alleviate the pathogenesis of neuroinflammation and neurodegeneration
3) Neuroinflammation and neurodegeneration regulate inflammasome activation
4) Negative regulation of inflammasome activation in neurological diseases
Keywords:
Neuroinflammation, Neurodegeneration, Inflammasome
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.
The inflammasome, a multiprotein complex, is indispensable in innate immunity. It can be activated by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), including viruses, fungi, ATP, monosodium urate, silica crystals, fibrillar amyloid-β peptides, and aluminum salt crystals. Activation of the inflammasome regulates maturation and secretion of pro-inflammatory cytokines (such as interleukin (IL)-1β and IL-18) and GSDMD-mediated pyroptosis. Activation of the inflammasome plays an important role in the body's resistance to pathogen infection and recognition of danger signals. Still, its overactivation or uncontrolled regulation is closely related to many inflammatory diseases, such as gout, type 2 diabetes, atherosclerosis, nonalcoholic steatohepatitis, Parkinson's disease (PD), Alzheimer's disease (AD), and a variety of autoimmune diseases. In recent years, hyperactivation of inflammasome complexes has been increasingly demonstrated to contribute to sustained neuroinflammation and neurodegenerative disease progression. We focus on why aberrant activation of inflammasome complexes amplifies pathology in neuroinflammation and neurodegeneration and highlight prospects for neurotherapeutic interventions based on targeting inflammasome pathways.
The goal of this Research Topic is to provide a forum to advance research on the contribution of inflammasome (such as NLRP3, NLRC4, NLRP1, and AIM2) activation to the genesis and development of neuroinflammation and neurodegeneration, as well as to explore innovative gut-oriented pharmacological interventions in the attempt to achieve a beneficial impact on neuroinflammation and neurodegeneration.
The Research Topic had the bullet points below:
1) Inflammasome activation promotes the pathogenesis of neuroinflammation and neurodegeneration
2) The inhibitors of inflammasome activation alleviate the pathogenesis of neuroinflammation and neurodegeneration
3) Neuroinflammation and neurodegeneration regulate inflammasome activation
4) Negative regulation of inflammasome activation in neurological diseases
Keywords:
Neuroinflammation, Neurodegeneration, Inflammasome
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.