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.
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.
Heterozygous Deletion of Chorein Exons 70-73 and GNA14 Exons 3-7 in a Brazilian Patient Presenting With Probable Tau-Negative Early-Onset Alzheimer Disease.
Département de psychiatrie