Our group is interested in a series of neurodegenerative diseases, such as Alzheimer’s, or brain tumours that are mostly associated with age. From the beginning our studies focused first on neuronal neurodegeneration initiated by amyloid accumulation in Alzheimer’s disease (AD); and second on glia-glioma transformation.
With respect to Alzheimer’s pathology, we have verified that the inhibition of the complex called mTORC1 has a therapeutic effect both in vivo and ex vivo (in primary cultures of neurons and glia) in a transgenic mouse model of AD. This inhibition produces an activation of autophagy that leads to a reduction in the amyloid load both in transgenic mice and in neurons and glia from these mice. At this time our work focuses on the analysis of how different autophagy regulators can modify the generation/secretion of amyloid in this transgenic model.