Genetics, Aging, and Longevity in Model Organisms

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 develops transcriptome and methylation age clocks using multi-omics data from healthy individuals, achieving better accuracy than existing models.

The paper shows that UNC-1 in C. elegans neurons modulates protein homeostasis by altering fat metabolism through neurohormonal signaling involving NHR-1 and DAF-12.

The paper shows that restricting a single amino acid in Drosophila increases survival during nicotine exposure through mTORC1 and GCN2 signaling pathways.

The paper shows that early life activity of RNA splicing factors and lipid metabolism determine the efficacy of longevity interventions in C. elegans.

A cocktail of rapamycin, acarbose, and phenylbutyrate slowed aging in mice by improving health metrics and reducing age-related lesions.

This study identifies picd-1 as an interacting gene of pry-1 in C. elegans, showing its role in stress response and lifespan regulation through inhibition of CRTC-1 function.

This study shows that minocycline prevents early aging phenotypes in Rp58 hetero-KO mice by mitigating DNA damage and cognitive decline.

The paper shows that mitochondrial fission and PINK-1-mediated mitophagy are necessary for reproductive longevity in daf-2 mutants, but not in wild-type worms.

This study shows that inhibiting mTORC1 specifically in neurons of C. elegans extends lifespan without causing growth or reproductive impairments.

This paper uses machine learning to classify ageing-related genes as CR-related or not based on various predictive features, finding that curated knowledge features are most predictive.

This study identifies CCAR-1's role in regulating germline transcription, reproduction, lifespan, and DNA-damage induced apoptosis in C. elegans using whole transcriptome RNA sequencing.

This paper shows that germline-deficient C. elegans larvae become hypoxia resistant adults through developmental stage-dependent mechanisms involving reduced protein translation.

This study identifies FMO-2's role in promoting longevity in C. elegans by rewiring one carbon metabolism and tryptophan metabolism, linking a single enzyme to metabolic pathways involved in lifespan extension.

This study identifies 3-hydroxyanthranilic acid (3HAA) as a metabolite that extends lifespan and improves health in C. elegans and mice by reducing oxidative stress and activating the Nrf2/SKN-1 pathway.

The paper shows that Rp/+ cells in Drosophila rely on Gr64 gustatory receptors for survival and proteostasis by maintaining autophagy and proteasome function.

This study shows dietary restriction extends lifespan in D. melanogaster by protecting the visual system from age and light-related damage through circadian regulation.

The paper identifies aging mechanisms that predict age-related disease multimorbidities in humans using literature analysis and clinical data integration.

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 measures brood size and male-production rate in 96 C. elegans wild strains across reproductive periods, finding they are not genetically correlated and identifying loci associated with male-production rate.

The paper identifies compounds that block food perception in C. elegans, increasing longevity by modulating serotonin and dopamine signaling, suggesting a mechanism by which dietary restriction mimetics extend lifespan.

This study develops DNA methylation clocks for naked mole-rats and finds that queens age more slowly than non-breeders, suggesting a link between reproductive status and epigenetic aging.

This study compares the effects of Sod loss-of-function mutations and paraquat-induced oxidative stress on neuromuscular physiology in Drosophila, finding distinct impacts on neurotransmission.

This study shows that miR-1 regulates lysosomal v-ATPase and biogenesis in C. elegans muscle to affect contractility during proteotoxic stress and ageing.

This study shows that long-term green tea EGCG consumption improves healthspan and lifespan in mice by reducing cellular senescence, gut dysbiosis, and immunosenescence.

This study shows that fatty acid metabolic reprogramming in C. elegans is essential for development on a specific diet, mediated by acetylcholine signaling and the fatty acid elongase gene elo-6.

This study shows GLP-1R agonism reverses transcriptomic aging in brain cells and reduces AD-associated signatures in microglia.

The paper shows that ninaD, a gene upregulated in gut cells, regulates cholesterol homeostasis and protects against neurodegeneration by a gut-brain axis mechanism.

This study shows DAF-18 is required for age-dependent DAF-16 activation in C. elegans, contributing to immunity and functioning through post-translational modifications.

The paper shows that C. elegans hermaphrodites undergo reproductive death after reproduction, which is suppressed by germline removal and linked to lifespan extension.