Special LMNN Seminar - Mechanisms of prion-like propagation of protein aggregates

Many neurodegenerative diseases such as Alzheimer’s disease or Parkinson’s disease are associated with the gradual accumulation and characteristic spreading of pathological proteins. Factors involved in the prion-like propagation of protein aggregates remain, however, largely elusive. I will present our ongoing work using the nematode Caenorhabditis elegans as a model system to discover and investigate cellular pathways and molecular components that influence the intercellular spreading of disease-associated proteins (e.g., α-Synuclein). I will further discuss our progress in examining how the disaggregation activity of the human Hsp70 chaperone system is modulating diverse aggregation-prone substrates in vitro and in vivo. A better understanding of the role of the cellular protein quality control system in prion-like propagation of misfolded proteins might identify new druggable targets for the treatment of neurodegenerative diseases.