Editorial: Neurological, Metabolic and Inflammatory Disorders: A Common Root in Inflammasome

A Common Root in InflammasomeSeveral lines of evidence highlight the relevance of inflammasomes in the pathophysiology of a plethora of diseases, including autoinflammatory syndromes (i.e., cryopyrin-associated autoinflammatory syndromes [CAPS]), neurological diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS) and major depressive disorder (MDD), metabolic disorders, such as obesity and type 2 diabetes, and chronic inflammatory diseases, including gout, psoriasis and intestinal inflammation (Pellegrini et al., 2019).In particular, inflammasome complexes, consisting of nucleotide-binding oligomerization domain leucine rich repeat and pyrin domain-containing protein 3 (NLRP3), NLRP6, NLRP1, NLRC4 or absent in melanoma 2 (AIM2) subunit, adaptor protein apoptosis-associated speck-like protein (ASC) and pro-caspase-1, through the processing and release of interleukin (IL)-1β and IL-18 and the induction of pyroptosis, acts as a key player both in maintaining the host physiology and in the triggering the immune/inflammatory responses in neurological, metabolic, and inflammatory diseases (Pellegrini et al., 2019).In addition, besides canonical caspase-1 dependent inflammasome signalling, non-canonical activations, which depend on caspase-11 in mice (caspase 4 and caspase 5 in humans) or caspase-8 have been found to be involved in the immune/inflammatory responses associated with such disorders (Pellegrini et al., 2019).In this setting, several studies included in our Research Topic have provided new insights on the role of inflammasome pathways in the pathophysiology of neurological and inflammatory diseases as well as on the effects of phytochemicals acting on inflammasome signalling in the counteracting central neuroinflammation and immune/inflammatory responses in such diseases.An interesting bibliometric analysis of 1,222 documents performed by Chen et al. has reported that inflammasome activation and the induction of pyroptosis in brain cells, including microglia, astrocytes, neurons, are pivotally involved in the coordinating physiological processes as well as in the promoting the pathophysiological events associated with brain disease, such as traumatic brain injuries, stroke, AD, and PD (Chen et al.).In addition, they observed that the activation of inflammasome signalling, including NLRP3, NLRC4 and NLRP3, and pyroptosis in brain disorders is associated with the increase in endoplasmic reticulum (ER) stress, oxidative stress, and mitochondrial dysfunction (Chen et al.).In support of this view, the review article by Holbrook et al. has highlighted the role of NLRP3 inflammasome in neurodegenerative diseases, including PD, AD, Huntington's disease, ALS, and prion diseases.In particular, pooling together human and preclinical investigations, they observed that NLRP3 inflammasome overactivation and dysregulation is a common path of several neurodegenerative diseases and they suggest NLRP3 inhibition as a suitable pharmacological strategy for the management of these brain disorders (Holbrook et al.).However, Piancone et al. showed that the treatment monomeric or aggregated α-synuclein to peripheral blood mononuclear cells (PBMCs) from PD patients increased IL-1β and IL-18 as compared to

Abstract licence: CC BY

2 more references, whose wording the paper’s licence keeps private.

A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.