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dc.contributor.authorVenegas, Carmen
dc.contributor.authorHeneka, Michael T
dc.date.accessioned2026-02-24T08:29:03Z
dc.date.available2026-02-24T08:29:03Z
dc.date.issued2019
dc.identifier.urihttps://hdl.handle.net/10481/111432
dc.description.abstractHistorically neurodegenerative diseases, Alzheimer's disease (AD) in particular, have been viewed to be primarily caused and driven by neuronal mechanisms. Very recently, due to experimental, genetic, and epidemiologic evidence, immune mechanisms have entered the central stage and are now believed to contribute significantly to risk, onset, and disease progression of this class of disorders. Although immune activation of microglial cells may over time engage various signal transduction pathways, inflammasome activation, which represents a canonical and initiating pathway, seems to be one of the first responses to extracellular β-amyloid (Aβ) accumulation. Here we review the current understanding of inflammasome activation in ADes_ES
dc.language.isoenges_ES
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs 3.0 Licensees_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es_ES
dc.titleInflammasome-mediated innate immunity in Alzheimer's diseasees_ES
dc.typejournal articlees_ES
dc.rights.accessRightsembargoed accesses_ES
dc.identifier.doi10.1096/fj.201900439


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