Inflammasomes are multiprotein complexes that play critical roles in activation of the innate immune system. Many inflammasomes have been identified, NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) are the most fully characterized inflammasome. Recently, NLRP3 inflammasome caught neuroscientists’ attention as NLRP3 is widely expressed in the microglia and has been demonstrated to mediate neuroinflammation in neurodegenerative diseases.
NLRP3 inflammasome is composed of intracellular innate immune receptor NLRP3, junction protein ASC and protease caspase-1 (cysteine aspartate protease 1). Activated NLRP3 inflammasomes can induce the maturation and secretion of pro-inflammatory factors, such as IL-1ß and IL-18 in microglia, thus promoting the neuroinflammation associated with neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). Therefore, NLRP3 inflammasome progressively moved in the spotlight leading to the creation of a new research scope on neurodegenerative diseases’ etiology.
Previous studies have found that mitochondrial impairment is an important driving force leading to excessive activation of NLRP3 inflammasome. Recently, more and more studies have been devoted to better understand the NLRP3 inflammasome-mediated neuroinflammation and the relationship with mitochondrial damage in neurodegenerative diseases. Despite these efforts, the detailed biological mechanisms behind NLRP3 inflammasome on the disease’s progression and how to maintain mitochondrial homeostasis to prevent excessive activation of NLRP3 remain unclear both in vivo and in vitro.
This Research Topic aims to provide an overview of the NLRP3 inflammasome’s roles in the development and progression of neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and stroke. Articles that focus on biomarkers, genetics and / or drugs that regulate NLRP3 inflammasome-related damage in vivo and in vitro are also welcome. Although this Research Topic mainly focuses on the NLRP3 inflammasome changes, we also welcome studies related to other inflammasomes and interactions with mitochondrial dysfunctions, inflammation and innate immunity cells. In addition, we are also interested in the research on psychotic disorders, affective diseases, and new medications on these disorders.
Inflammasomes are multiprotein complexes that play critical roles in activation of the innate immune system. Many inflammasomes have been identified, NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) are the most fully characterized inflammasome. Recently, NLRP3 inflammasome caught neuroscientists’ attention as NLRP3 is widely expressed in the microglia and has been demonstrated to mediate neuroinflammation in neurodegenerative diseases.
NLRP3 inflammasome is composed of intracellular innate immune receptor NLRP3, junction protein ASC and protease caspase-1 (cysteine aspartate protease 1). Activated NLRP3 inflammasomes can induce the maturation and secretion of pro-inflammatory factors, such as IL-1ß and IL-18 in microglia, thus promoting the neuroinflammation associated with neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). Therefore, NLRP3 inflammasome progressively moved in the spotlight leading to the creation of a new research scope on neurodegenerative diseases’ etiology.
Previous studies have found that mitochondrial impairment is an important driving force leading to excessive activation of NLRP3 inflammasome. Recently, more and more studies have been devoted to better understand the NLRP3 inflammasome-mediated neuroinflammation and the relationship with mitochondrial damage in neurodegenerative diseases. Despite these efforts, the detailed biological mechanisms behind NLRP3 inflammasome on the disease’s progression and how to maintain mitochondrial homeostasis to prevent excessive activation of NLRP3 remain unclear both in vivo and in vitro.
This Research Topic aims to provide an overview of the NLRP3 inflammasome’s roles in the development and progression of neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and stroke. Articles that focus on biomarkers, genetics and / or drugs that regulate NLRP3 inflammasome-related damage in vivo and in vitro are also welcome. Although this Research Topic mainly focuses on the NLRP3 inflammasome changes, we also welcome studies related to other inflammasomes and interactions with mitochondrial dysfunctions, inflammation and innate immunity cells. In addition, we are also interested in the research on psychotic disorders, affective diseases, and new medications on these disorders.
