Ellen A. A. Nollen

This study identifies a PPARγ-like signaling pathway in C. elegans that links lipid metabolism and mitochondrial quality control to maintain neuronal function.

PUMA identifies seven distinct aging dimensions from phenotypic data, showing they predict age-related disease risk better than traditional biomedical factors.

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.

The paper introduces an affordable optogenetic device called OptoArm for manipulating C. elegans worms, showing that cholinergic neurons decline with age while GABAergic neurons and muscle cells remain resilient.

This study shows that SERF2 deletion changes amyloid fibril structure in Alzheimer's mouse models, suggesting SERF's role in modifying amyloid aggregation.

The paper shows that α-synuclein forms liquid droplets that mature into amyloid-rich hydrogels, suggesting Lewy body formation is linked to arrested maturation in the presence of lipids.

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.