Research activities
Alzheimer ’s disease
The laboratory has been involved in preclinical research on Alzheimer’s disease (AD) for many years. This work was performed in collaboration with KULeuven and UCLouvain (Dr. Ilse Dewachter, Dr. Nathalie Pierrot and Dr. Jean-Noël Octave). Because, memory loss is one of the first symptoms observed in AD patients, we were interested in the cellular and molecular mechanisms underlying memory consolidation and memory dysfunction in animal’s models of AS. We developed in the laboratory the in vitro model of memory consolidation: the long-term potentiation of synaptic transmission in the hippocampus (LTP). This methodology allows us to record long-lasting plasticity (8 hours) in the hippocampus at any age and in any model of brain disease. In the field of AD, ABeta toxicity was evaluated in different rodent models of AD. We then focused on Tau aggregation and on the mechanisms of its propagation. We demonstrated the role of prion-like seeding in the propagation of Tau pathology in mice and the interactions between amyloid and tau pathologies. More recently we focused our research on the role of APP, the precursor of amyloid peptide and on its role in the regulation of excitatory/inhibitory balance. This research if funded by the Queen Elisabeth fund for Medical Research. The laboratory if also involved, in collaboration with the Faculty of psychology, in the study of semantic memory in AD patients and in the combination of blood, EEG and neuropsychological biomarkers as tools to better predict conversion from MCI to AD. This research is funded by the ‘ARC’ program and is performed in collaboration with regional hospitals. L.
Multiple Sclerosis
The laboratory is interested in the impact of neuroinflammation on synaptic plasticity and cognition. The experimental autoimmune encephalomyelitis (EAE) is used as a rodent model of multiple sclerosis and neuroinflammation. In this model, immune cells infiltration, cytokine release and cell proliferation in the hippocampus in correlated to the deficit in cognition and in synaptic plasticity of the glutamatergic transmission. This project is funded by the Charcot foundation.
Our unit is also associated with the following UMONS research institutes :
