Claudio Soto

The International Dementia Conference Series,  hosted by the McGill Centre for Studies in Aging resumed its biweekly events beginning September 15, 2021, with the Prion Hypothesis and Protein Aggregate Series.
Please join us on October 13, 2021, for a presentation by Claudio Soto, PhD, entitled “The prion principle in neurodegenerative diseases and its use for high-sensitivity biochemical diagnosis.”

Zoom Meeting Link

Meeting ID: 858 9923 2847
Passcode: 505682

The prion principle in neurodegenerative diseases and its use for high-sensitivity biochemical diagnosis

A hallmark event in several neurodegenerative diseases is the cerebral accumulation of misfolded protein aggregates that can spread from cell-to-cell by a prion-like mechanism of templated conversion of the normally folded protein into the abnormal misfolded and aggregated form. Recent evidence indicate that soluble misfolded oligomeric versions of these proteins circulate in biological fluids and may serve as a specific biomarker for sensitive diagnosis. Our group has developed a technology for ultra-sensitive detection of soluble misfolded oligomers implicated in Prion, Alzheimer’s, Parkinson’s diseases and related synucleinopathies and tauopathies. The technique, termed PMCA, is based on the cyclic amplification of protein misfolding, and mimics the prion principle of seeding/nucleation model of aggregation in a highly efficient manner by combining phases of polymer growing with their fragmentation to multiply the number of seeds for the exponential amplification of the reaction. PMCA was first adapted and optimized for amplification of prion protein (PrPSc) implicated in prion diseases and more recently has been extended to detect amyloid-beta, Tau, and α-synuclein misfolded oligomers. In this presentation, I will describe the prion principle and its relevance in neurodegenerative diseases, as well as the PMCA rationale, status, and applications for disease diagnosis.