Astrocyte calcium dysfunction causes early network hyperactivity in Alzheimer’s disease
Disha Shah, Willy Gsell, Jérôme Wahis, Emma S. Luckett, Tarik Jamoulle, Ben Vermaercke, Pranav Preman, Daan Moechars, Véronique Hendrickx, Tom Jaspers, Katleen Craessaerts, Katrien Horré, Leen Wolfs, Mark Fiers, Matthew G. Holt, Dietmar Rudolf Thal, Zsuzsanna Callaerts‐Vegh, Rudi D’Hooge, Rik Vandenberghe, Uwe Himmelreich, Vincent Bonin, Bart De Strooper
Abstract
mice. Crucially, these network disruptions are accompanied by decreased astrocyte calcium signaling. Recovery of astrocytic calcium activity normalizes neuronal hyperactivity and FC, as well as seizure susceptibility and day/night behavioral disruptions. In conclusion, we show that astrocytes mediate initial features of AD and drive clinically relevant phenotypes.
Topics & Concepts
AstrocyteNeurosciencePremovement neuronal activityAlzheimer's diseaseDiseaseAnterior cingulate cortexPhenotypeMedicineBiologyPsychologyInternal medicineCentral nervous systemCognitionBiochemistryGeneAlzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms