Sean P. Curran

This study investigates how actin structure and function affect aging in C. elegans and finds that actin dysfunction accelerates aging hallmarks and correlates with human age-related decline in gait speed.

This study identifies molecular mechanisms by which C. elegans avoid Methylobacterium after ingestion, integrating lipid metabolism and dietary needs to influence food preference.

The paper identifies distinct roles of GABAergic, glutamatergic, and octopaminergic neurons in mediating non-autonomous UPRER through transcriptomic and functional analyses in C. elegans.

This study shows that selecting late progeny in C. elegans over multiple generations reduces stress resistance and lifespan but preserves reproductive output.

The paper shows that constitutive SKN-1 activation in C. elegans leads to serotonin deficiency, causing apathy toward pathogens and reduced survival.

This study shows that SKN-1 activity regulates lipid mobilization in C. elegans, affecting longevity and lipid distribution in response to genetic and environmental factors.

This study shows that loss of WDR23 in mice leads to increased NRF2 stability and antioxidant defense, affecting age-related hippocampal behaviors in sex-dependent ways.

This study shows that Oolonghomobisflavans reduce tau fibrils and improve health in Alzheimer's models.

The paper identifies drh-1 as a mechanism to counteract excessive SKN-1 transcriptional activity in C. elegans, improving healthspan by opposing age-related pathology.

This study shows that loss of Wdr23 in mice increases nuclear-coded mitochondrial proteins and alters gene regulation related to mitochondrial biogenesis and stress responses.

This study identifies ether lipid biosynthesis as a key pathway mediating the longevity benefits of biguanides like metformin in C. elegans.

This study shows that riboflavin depletion in C. elegans extends lifespan and improves metabolic health through multiple pathways.

The paper identifies ALDH4A1 genetic variation as a biomarker for age-related muscle health across species using C. elegans and human data.

This study shows that MAFR-1, an RNA polymerase III regulator, affects sperm quality in C. elegans by influencing spermatid size and fertilization ability, with effects dependent on RNA pol III activity.