Jeremy M. Van Raamsdonk

This study shows that old white adipose tissue can rejuvenate in young hosts through thermogenic remodeling and pathway activation, reversing biological age markers.

This study identifies a mitochondria-to-nucleus kinase signaling pathway that promotes longevity in sod-2 mutants by upregulating innate immunity and cuticle formation genes.

This study identifies 196 upregulated and 62 downregulated aging genes across long-lived C. elegans mutants, revealing distinct gene expression strategies for longevity.

This study identifies FMO-2 as a downstream effector of multiple longevity pathways in C. elegans mitochondrial mutants, showing its requirement for lifespan extension.

This paper identifies Cyrene as a geroprotective compound that extends lifespan and healthspan in C. elegans and Drosophila, improving stress resistance and neuroprotection.

This study shows that mild activation of the mitochondrial unfolded protein response (mitoUPR) through ATFS-1 can increase lifespan without enhancing stress resistance in worms.

This study shows that reducing mitochondrial superoxide in the intestine extends longevity in worms by improving stress resistance.

This study identifies transcriptomic biomarkers of mortality across species and models, revealing common aging mechanisms and rejuvenation signatures.

This study shows that disrupting the mitochondrial fission gene drp-1 during development extends the lifespan of daf-2 mutants by improving mitochondrial function and stress resistance.

This study shows that overexpressing mitochondrial fission or fusion genes increases lifespan and stress resistance in C. elegans, despite causing mitochondrial fragmentation.

This study shows that disrupting TBC-2 reduces lifespan and stress resistance in long-lived mitochondrial mutants in C. elegans, suggesting a role for endosomal trafficking in mitochondrial dysfunction-related longevity.

The paper reanalyzes millions of molecular profiles to identify aging interventions using AI agents, finding over 500 interventions that reduce biological age and revealing patterns in aging modulation.

The paper examines nine long-lived C. elegans mutants to show a strong correlation between stress resistance and longevity, driven by overlapping genetic pathways.

This study shows that altering huntingtin levels affects seizure susceptibility in FVB/N mice, with over-expression preventing seizures and reduction increasing their frequency.

This study identifies novel genetic targets that reduce mitochondrial fragmentation in a C. elegans model of polyglutamine toxicity, improving movement and lifespan.

This study shows that ATFS-1 activates multiple stress response pathways to increase resistance to exogenous stressors but reduces lifespan when chronically active.

The paper investigates how lifespan-extending genetic pathways provide neuroprotection in a nematode model of Parkinson's disease, showing dissociation between lifespan extension and neuroprotection.