Protective effects of synaptic stimulation in Alzheimer disease and tauopathies
Loss of synapses and alterations of synaptic plasticity are central events in Alzheimer disease (AD), and they are associated with progressive accumulation of Aβ and tau proteins. Recent studies demonstrated protective effects of neuronal/synaptic activation, via deep brain stimulation (DBS). We have found that synaptic stimulation enhanced auto-lysosomal degradation of oligomeric and hyperphosphorylated tau protecting synapses and we are currently exploring the molecular mechanism(s) responsible for such positive outcomes. Overall, our findings indicate that stimulation of synaptic activity promotes clearance of pathological tau, underlying the protective effect of DBS and supporting the use synaptic stimulation as a therapeutic treatment.
About the speaker
After receiving his Master degree in biology and his PhD in Molecular Medicine from the University of Milan, Davide Tampellini worked as a Post Doc and Assistant Professor at the Weill Cornell Medical School in New York. In 2011, he became Assistant Professor at the Lund University in Sweden and since 2013, he is a Senior Researcher in Neuroscience at the INSERM in Paris. As neuroscientist, Davide Tampellini worked in the field of aging and neurodegenerative diseases for over twenty years. His focus is on the homeostasis of proteins involved in Parkinson’s and Alzheimer’s diseases. Currently, he is investigating the mechanisms of tau and beta-amyloid clearance during deep brain stimulation, a promising therapeutic strategy for several neurological and psychiatric disorders. Exciting results that he recently published demonstrated that synaptic stimulation reduced pathological tau oligomers and protected synapses by enhancing autophagy and lysosomal degrading activity.
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