Inflammation context in Alzheimer’s disease, a relationship intricate to define

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dc.article.number39
dc.catalogadorpva
dc.contributor.authorNovoa Fernández, Catalina
dc.contributor.authorSalazar Torres, Paulina Isabel
dc.contributor.authorCisternas, Pedro
dc.contributor.authorGherardelli Brooks, Camila
dc.contributor.authorVera Salazar, Roberto
dc.contributor.authorZolezzi, Juan M.
dc.contributor.authorInestrosa Cantín, Nibaldo
dc.date.accessioned2023-03-06T20:13:13Z
dc.date.available2023-03-06T20:13:13Z
dc.date.issued2022
dc.date.updated2022-12-25T01:02:24Z
dc.description.abstractAlzheimer’s disease (AD), the most common form of dementia, is characterized by the accumulation of amyloid β (Aβ) and hyperphosphorylated tau protein aggregates. Importantly, Aβ and tau species are able to activate astrocytes and microglia, which release several proinflammatory cytokines, such as tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), together with reactive oxygen (ROS) and nitrogen species (RNS), triggering neuroinflammation. However, this inflammatory response has a dual function: it can play a protective role by increasing Aβ degradation and clearance, but it can also contribute to Aβ and tau overproduction and induce neurodegeneration and synaptic loss. Due to the significant role of inflammation in the pathogenesis of AD, several inflammatory mediators have been proposed as AD markers, such as TNF-α, IL-1β, Iba-1, GFAP, NF-κB, TLR2, and MHCII. Importantly, the use of anti-inflammatory drugs such as NSAIDs has emerged as a potential treatment against AD. Moreover, diseases related to systemic or local inflammation, including infections, cerebrovascular accidents, and obesity, have been proposed as risk factors for the development of AD. In the following review, we focus on key inflammatory processes associated with AD pathogenesis.
dc.fechaingreso.objetodigital2022-12-25
dc.format.extent18 páginas
dc.fuente.origenAutoarchivo
dc.identifier.citationBiological Research. 2022 Dec 23;55(1):39
dc.identifier.doi10.1186/s40659-022-00404-3
dc.identifier.urihttps://doi.org/10.1186/s40659-022-00404-3
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/66530
dc.identifier.wosidWOS:000903240900001
dc.information.autorucFacultad de ciencias biológicas ; Novoa Fernández, Catalina ; S/I ; 1047136
dc.information.autorucFacultad de ciencias biológicas ; Salazar Torres, Paulina Isabel ; S/I ; 205484
dc.information.autorucFacultad de ciencias biológicas ; Gherardelli Brooks, Camila ; S/I ; 10862
dc.information.autorucFacultad de ciencias biológicas ; Inestrosa Cantín, Nibaldo ; 0000-0003-3118-9726 ; 26312
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final18
dc.pagina.inicio1
dc.revistaBiological Research
dc.rightsacceso abierto
dc.rights.holderThe Author(s)
dc.subject.ddc570
dc.subject.deweyBiologíaes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleInflammation context in Alzheimer’s disease, a relationship intricate to definees_ES
dc.typeartículo
dc.volumen55
sipa.codpersvinculados1047136
sipa.codpersvinculados205484
sipa.codpersvinculados1086258
sipa.codpersvinculados26312
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