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 (ref. 2).
Eder-Colli L, Abad-Estarlich N, Pannetier C, Vallet PG, Walzer C, Elder
GA, Robakis NK, Bouras C, Savioz A.
The presenilin-1 familial Alzheimer's disease mutation P117L decreases
neuronal differentiation of embryonic murine neural progenitor cells.
Brain Res Bull. 2009, 80, 296-301.
Savioz A, Leuba G, Vallet PG, Walzer C. Contribution of neural networks to Alzheimer disease's progression.
Brain Res Bull. 2009, 80, 309-314.
Leuba G, Walzer C, Vernay A, Carnal B, Kraftsik R, Piotton F, Marin P,
Bouras C, Savioz A. Postsynaptic density protein PSD-95 expression in Alzheimer's disease and okadaic acid induced neuritic retraction.
Neurobiol Dis. 2008 Jun;30(3):408-19.
Dept. Psychiatrie, Neuropsychiatrie
Email: Armand (dot) Savioz (at) hcuge (dot) ch