Genes associated with amyloid-beta-induced inflammasome-mediated neuronal death identified using functional gene trap mutagenesis approach

Yap, Jeremy Kean Yi; Pickard, Ben; Gan, Sook Yee; Chan, Elaine Wan Ling

doi:10.1016/j.biocel.2021.106014

Cited by 1 publication

(1 citation statement)

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“…A gene trap mutagenesis screen approach revealed the contribution of three genes— ROTH1 (atypical mitochondrial Ras homolog family member T1), TGF-βR1 , and SNW1 (SNW domain containing 1)—as relevant contributors to pyroptotic neuronal death mediated by Aβ-induced NLRP1 signaling (Yap and others 2021). Yet, the NLRP1 expression levels did not change in an AD-like model induced via STZ injections in male Wistar rats (Saadi and others 2020).…”

Section: Nlrp1 Inflammasomementioning

confidence: 99%

“Other Than NLRP3” Inflammasomes: Multiple Roles in Brain Disease

et al. 2022

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Human neuroinflammatory and neurodegenerative diseases, whose prevalence keeps rising, are still unsolved pathobiological/therapeutical problems. Among others, recent etiology hypotheses stressed as their main driver a chronic neuroinflammation, which is mediated by innate immunity-related protein oligomers: the inflammasomes. A panoply of exogenous and/or endogenous harmful agents activates inflammasomes’ assembly, signaling, and IL-1β/IL-18 production and neural cells’ pyroptotic death. The underlying concept is that inflammasomes’ chronic activation advances neurodegeneration while their short-lasting operation restores tissue homeostasis. Hence, from a therapeutic standpoint, it is crucial to understand inflammasomes’ regulatory mechanisms. About this, a deluge of recent studies focused on the NLRP3 inflammasome with suggestions that its pharmacologic block would hinder neurodegeneration. Yet hitherto no evidence proves this view. Moreover, known inflammasomes are numerous, and the mechanisms regulating their expression and function may vary with the involved animal species and strains, as well as organs and cells, and the harmful factors triggered as a result. Therefore, while presently leaving out some little-studied inflammasomes, this review focuses on the “other than NLRP3” inflammasomes that participate in neuroinflammation’s complex mechanisms: NLRP1, NLRP2, NLRC4, and AIM2. Although human-specific data about them are relatively scant, we stress that only a holistic view including several human brain inflammasomes and other potential pathogenetic drivers will lead to successful therapies for neuroinflammatory and neurodegenerative diseases.

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Section: Nlrp1 Inflammasomementioning

confidence: 99%