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This lecture by Helen Saibil delves into the mechanisms of protein aggregation and disaggregation in vivo and in vitro, focusing on the case of huntingtin protein in Huntington's Disease. The presentation covers the formation of different types of aggregates, the role of polyQ repeats in toxicity, and the impact of aggregation on disease progression. Saibil also discusses the importance of cytoplasmic aggregates in disease severity, the heterogeneity of mutant huntingtin aggregates, and the machinery involved in reversing aggregation. Through various microscopy techniques, the lecture reveals the unexpected cellular pathways of huntingtin aggregation and the machinery responsible for disassembling amyloid fibrils.