Titanium dioxide and carbon black nanoparticles disrupt neuronal homeostasis via excessive activation of cellular prion protein signaling.
Fiche publication
Date publication
juillet 2022
Journal
Particle and fibre toxicology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BAILLY Yannick
Tous les auteurs :
Ribeiro LW, Pietri M, Ardila-Osorio H, Baudry A, Boudet-Devaud F, Bizingre C, Arellano-Anaya ZE, Haeberlé AM, Gadot N, Boland S, Devineau S, Bailly Y, Kellermann O, Bencsik A, Schneider B
Lien Pubmed
Résumé
Epidemiological emerging evidence shows that human exposure to some nanosized materials present in the environment would contribute to the onset and/or progression of Alzheimer's disease (AD). The cellular and molecular mechanisms whereby nanoparticles would exert some adverse effects towards neurons and take part in AD pathology are nevertheless unknown.
Mots clés
Alzheimer’s disease, Aβ peptides, Nanoneurotoxicity, Nanoparticles, Neuroinflammation, PrPC receptor, Signaling, TNFα receptors
Référence
Part Fibre Toxicol. 2022 07 15;19(1):48