Renée I. Seinstra

This study shows that alpha-synuclein condensation disrupts lipid metabolism, reduces triacylglycerols, and impairs mitochondrial function in C. elegans, with potential therapeutic implications for Parkinson's disease.

This study identifies that rebalancing excitatory and inhibitory inputs in C. elegans restores movement in a TDP-43 toxicity model by synergizing neurotransmitter system enhancements.

This study shows that defects in DDR pathways in C. elegans lead to protein homeostasis loss, which can be rescued by HSP-16.2, preventing motor impairment.

The paper identifies MOAG-4/SERF as modifiers of amyloid formation through charge complementation, showing that charge interactions drive protein aggregation and toxicity.

This study uses multi-parametric phenotyping to analyze ageing trajectories in C. elegans, revealing divergent ageing patterns in disease models and quantifying health states through phenotypic flexibility.