Genetics, Aging, and Longevity in Model Organisms

This paper introduces ALaSCA, a platform using Pearlian causal inference to identify molecular drivers of neuronal aging, with an application in Alzheimer's disease.

This study identifies the nuclear RNAi pathway as a regulator of DAF-16/FOXO function, affecting longevity and dauer entry in C. elegans through interactions with the mTORC2-AKT axis.

The paper shows that timing of TORC1 inhibition affects Pol III's role in longevity in C. elegans by influencing progeny production and lifespan.

The paper introduces ImAge, an image-based biomarker of aging and rejuvenation using chromatin and epigenetic patterns, showing correlation with chronological age and response to interventions.

The paper shows that inhibiting hypodermal ribosome synthesis in C. elegans triggers a nutrition-independent growth quiescence response across the organism.

This study identifies male-specific brain aging improvements from reduced neuronal insulin signaling in mice.

This study shows that GPCR signaling in C. elegans promotes stress-induced organismic death through a genetic program involving ZIP-10 and lipid remodeling.

This study shows that having more long-lived ancestors is linked to longer healthspan and better mid-life metabolomic profiles in families.

This study shows a drug cocktail improves cognitive function in aged mice by modulating aging pathways through transcriptomic and molecular analyses.

This study identifies CRTC-1's role in balancing histone trimethylation and acetylation to promote longevity in C. elegans.

The paper identifies hemidesmosome-containing structures that mediate mechanotransduction to regulate ECM homeostasis and promote longevity in C. elegans.

The paper confirms that set-2 mutants in C. elegans extend lifespan when fed HT115 E. coli, but not OP50-1, suggesting diet-dependent regulation of COMPASS complex effects on aging.

The paper shows that aging and lifestyle factors cause genotoxic damage, leading to reduced transcription of long genes across multiple species and tissues.

The paper shows ASI sensory neurons control the CEP-1/p53 DNA damage response in PGCs via TGF-beta signaling, reducing inherited mutations.

This study shows that chromosome XII fragments, not ERCs, drive senescence in yeast, despite rDNA copy number increases with age.

The paper uses supervised machine learning with feature selection to prioritize aging-related genes in C. elegans, identifying known and novel genes associated with cellular dysfunction markers.

The paper identifies CCF-1/CNOT7 as a CCR4-NOT subunit required for C. elegans stress response, interacting with PAL-1 to regulate elt-2 and elt-3 expression.

The paper links growth and aging through a mathematical model showing both processes are tied to the reduction in the fraction of cells dividing, providing insights into aging mechanisms and potential applications in improving vaccine effectiveness in the elderly.

The paper shows that resveratrol and copper reduce multiple ageing and neurodegeneration markers by deactivating cell-free chromatin particles in mice.

The paper investigates the role of XRN-2 endoribonuclease activity in dauer state maintenance and post-dauer life cycle continuity in C. elegans, finding that its disruption leads to metabolic and developmental defects.

This study identifies Spt4 as a factor that accelerates cellular senescence by promoting non-coding RNA transcription in rDNA clusters, leading to genomic instability and reduced lifespan in yeast.

This study shows neuronal HLH-30/TFEB improves thermoresistance in C. elegans by inducing mitochondrial fragmentation in muscles, independent of DAF-16/FOXO.

The paper identifies a heat shock factor, hsalHSF2, that contributes to extended lifespan in reproductive ants and shows its transferable role in enhancing survival in fruit flies.

This study identifies HPK-1 as a neuronal regulator of proteostasis that delays aging through distinct serotonergic and GABAergic pathways.

This study identifies Notch signaling in the distal germline as a root cause of reproductive aging in C. elegans by showing that ectopic expression of the Notch effector gene SYGL-1 delays aging.

This study shows that neuropeptides regulate intestinal integrity and aging in invertebrates, with effects modulated by the germline.

Rapamycin treatment during early life extends lifespan and healthspan in mice and Daphnia magna by slowing development and delaying aging.

This paper shows that glia in C. elegans can induce a heat shock response in peripheral cells, increasing lifespan and stress resistance, independent of neurons and neurotransmitters.

This study identifies JWA as an aging-associated gene whose deficiency disrupts intestinal epithelial homeostasis and accelerates aging in mice through the Notch1/PPARγ/Stat5 axis.

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.