Seminario IIBB: "Neuroinflammation and copper in Alzheimer’s disease: the role of mitochondrial oxidative stress".

Event Details

Description

Changes in copper (Cu) homeostasis have been consistently linked to Alzheimer’s disease (AD). Cu can interact with amyloid beta (Ab) exacerbating its neurotoxic effects. In addition, recent evidence suggests that Cu may have both pro- and anti-inflammatory properties, influenced by its proximity to Ab plaques. Key components of the innate immune response are the inflammasomes, large protein complexes that, once assembled, lead to the activation of caspase 1 and the processing of interleukin-1b into its active form. In particular, NLRP3 inflammasome induction has been described in individuals with AD and transgenic mouse models and is suggested to contribute to neuroinflammation and AD progression. In this study, we assessed how Cu overload by increase mitochondrial oxidative stress may regulate Ab-induced inflammasome and sustain the aberrant activation of microglia in AD.

• 18 d'octubre de 2024 
• De 3:00 pm fins 4:00 pm
• Biblioteca IIBB-CSIC
• Link: https://conectaha.csic.es/b/san-ewn-57a-efx.