Dominique Bétemps

This study uses PMCA to show that alpha-synuclein aggregates from mutant mice can seed aggregation in wild-type mice and other substrates, mimicking prion-like behavior.

This study investigates whether β-synuclein overexpression via AAV can inhibit α-synuclein aggregation in a synucleinopathy model, but finds no delay in disease onset and reports specific β-synuclein aggregates in treated mice.