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.
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.
A Study of Aβ Oligomers in the Temporal Cortex and Cerebellum of Patients with Neuropathologically Confirmed Alzheimer's Disease Compared to Aged Controls.
The Vitamin A Derivative All-Trans Retinoic Acid Repairs Amyloid-β-Induced Double-Strand Breaks in Neural Cells and in the Murine Neocortex.
Département de psychiatrie