| Abstract: | ["Numerous neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, are characterized by the accumulation and progressive spreading of protein deposits. The underlying processes are not well understood. My group studies the cell biology of the prion-like propagation of disease-associated proteins like tau and \u03b1-synuclein using Caenorhabditis elegans and cell culture models. \r\nI will present our ongoing research, with a particular focus on a project in which we are investigating molecular chaperones in their attempt to remove protein aggregates. Although molecular chaperones are vital for cellular proteostasis maintenance, our findings suggest a double-edged role: while some chaperones may delay aggregate formation, potentially mitigating disease onset in younger individuals, their disaggregation activity could exacerbate disease progression by generating smaller toxic protein species. \r\nIn addition, I will present unpublished data from a genome-wide RNAi screen using a C. elegans model for Tau spreading, in which we have identified novel genes critical for endo-lysosomal integrity and seeded tau aggregation."] |
