Autor(es):
Paiva, Isabel ; Cellai, Lucrezia ; Meriaux, Céline ; Poncelet, Lauranne ; Nebie, Ouada ; Saliou, Jean-Michel ; Lacoste, Anne-Sophie ; Papegaey, Anthony ; Drobecq, Hervé ; Le Gras, Stéphanie ; Schneider, Marion ; Malik, Enas M ; Müller, Christa E. ; Faivre, Emilie ; Carvalho, Kevin ; Gomez-Murcia, Victoria ; Vieau, Didier ; Thiroux, Bryan ; Eddarkaoui, Sabiha ; Lebouvier, Thibaud ; Schueller, Estelle ; Tzeplaeff, Laura ; Grgurina, Iris ; Seguin, Jonathan ; Stauber, Jonathan ; Lopes, Luísa V. ; Buee, Luc ; Buée-Scherrer, Valerie ; Cunha, Rodrigo A. ; Ait-Belkacem, Rima ; Sergeant, Nicolas ; Annicotte, Jean-Sébastien ; Boutillier, Anne-Laurence ; Blum, David
Data: 2022
Identificador Persistente: https://hdl.handle.net/10316/100338
Origem: Estudo Geral - Universidade de Coimbra
Projeto/bolsa:
info:eu-repo/grantAgreement/FCT/CEEC IND 2017/CEECIND/PT;
Assunto(s): Epigenetics; Memory; Neuroscience; Pharmacology
Descrição
Caffeine is the most consumed psychoactive substance worldwide. Strikingly, molecular pathways engaged by its regular consumption remain unclear. We herein addressed the mechanisms associated with habitual (chronic) caffeine consumption in the mouse hippocampus using untargeted orthogonal-omics techniques. Our results revealed that chronic caffeine exerts concerted pleiotropic effects in the hippocampus, at the epigenomic, proteomic and metabolomic levels. Caffeine lowers metabolic-related processes in the bulk tissue, while it induces neuronal-specific epigenetic changes at synaptic transmission/plasticity-related genes and increased experience-driven transcriptional activity. Altogether, these findings suggest that regular caffeine intake improves the signal-to-noise ratio during information encoding, in part through a fine-tuning of metabolic genes while boosting the salience of information processing during learning in neuronal circuits.
This work was supported by grants from Hauts-de-France (PARTEN-AIRR, COGNADORA; START-AIRR, INS-SPECT) and Programs d’Investissements d’Avenir LabEx (excellence laboratory) DISTALZ (Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer’s disease) and EGID (European Genomic Institute for Diabetes ANR-10LABX-46). Our laboratories are also supported by ANR (GRAND to LB, ADORATAU, ADORASTrAU, METABOTAU to DB and BETAPLASTICITY to JSA), COEN (5008), Fondation pour la Recherche Médicale, France Alzheimer/Fondation de France, FHU VasCog research network (Lille, France), Fondation Vaincre Alzheimer (ADOMEMOTAU), European Foundation for the Study of Diabetes (EFSD to JSA), Fondation Plan Alzheimer as well as Inserm, CNRS, Université Lille, Lille Métropole Communauté Urbaine, DN2M. KC hold a doctoral grant from Lille University. VG-M was supported by Fondation pour la Recherche Médicale (SPF20160936000). CM was supported by Région Hauts753 30 754 de-France. ALB is supported by CNRS, Unistra (Strasbourg, France), ANR-16-CE92-0031 755 756 757 758 759 760 761 762 (EPIFUS), ANR-18-CE16-0008-02 (ADORASTrAU), Alsace Alzheimer 67, France Alzheimer (AAP SM 2017 #1664). IP is supported by Fondation pour la Recherche Médicale (SPF201909009162). CEM is grateful for the support by the Alzheimer Forschung Initiative e.V. (AFI, Düsseldorf, Germany). LC was funded by SIF Italian Society of Pharmacology. RAC was supported by LaCaixa Foundation (LCF/PR/HP17/52190001) and FCT (POCI-01-0145-FEDER-03127). Santa Casa da Misericórdia (MB-7-2018) and CEECIND/01497/2017 to LVL.
