Armand Savioz
Function: Privat docent
Nom du groupe: NEURAD
Group type: Main
Affiliations: Faculty of Medicine, Geneva University Hospitals, Department of Psychiatry
Domaines: Development and Plasticity
Mot clés: Alzheimer's disease, degenerative dementia, synapse
Activités de recherche
Our studies deal with molecular mechanisms (e.g. synaptic beta-amyloid hypothesis) involved in vulnerability of neural networks in aging as well as in degenerative dementia (Alzheimer disease and frontotemporal dementia). Starting from observations made in humans, cellular and murine models are used to investigate how synaptic modifications and loss lead to functional alterations according to a synapto-connectionist paradigm, but may be counteracted by cerebral reserve and compensatory mechanisms.
Dernières publications
Inhibition of the mitochondrial pyruvate carrier in astrocytes reduces amyloid and tau accumulation in the 3xTgAD mouse model of Alzheimer's disease.
Preferential Involvement of BRCA1/BARD1, Not Tip60/Fe65, in DNA Double-Strand Break Repair in Presenilin-1 P117L Alzheimer Models.
Neuroprotection against Amyloid--Induced DNA Double-Strand Breaks Is Mediated by Multiple Retinoic Acid-Dependent Pathways.
TSPO and amyloid deposits in sub-regions of the hippocampus in the 3xTgAD mouse model of Alzheimer's disease.
Contact
Département de psychiatrie
HUG
Email: Armand.Savioz@hcuge.ch