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"claude-sonnet-5-5": false, "gpt-6-astra": true, "gemini-4-argon-high": true, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42808804", "id": "H1", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42808804", "id": "H2", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42808804", "id": "H3", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42808804", "id": "H4", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": true, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42808804", "id": "H5", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42585340", "id": "H1", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42585340", "id": "H2", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42585340", "id": "H3", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": true, "grok-4.5": false, "claude-opus-5-5": true } }, { "task": "R42585340", "id": "H4", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42585340", "id": "H5", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": true, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42669067", "id": "H1", "y": 1, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": true, "gemini-4-argon-high": true, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42669067", "id": "H2", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42669067", "id": "H3", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42669067", "id": "H4", "y": 1, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42669067", "id": "H5", "y": 1, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42811065", "id": "H1", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": true, "gemini-4-argon-high": true, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42811065", "id": "H2", "y": 1, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42811065", "id": "H3", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42811065", "id": "H4", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42811065", "id": "H5", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42841610", "id": "H1", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42841610", "id": "H2", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": true, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": true } }, { "task": "R42841610", "id": "H3", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": false, "gemini-4-argon-high": true, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42841610", "id": "H4", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42841610", "id": "H5", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42806003", "id": "H1", "y": 1, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": true, "gemini-4-argon-high": true, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42806003", "id": "H2", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42806003", "id": "H3", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42806003", "id": "H4", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42806003", "id": "H5", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42806572", "id": "H1", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42806572", "id": "H2", "y": 1, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": true, "gemini-4-argon-high": true, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42806572", "id": "H3", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": false } }, { "task": "R42806572", "id": "H4", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42806572", "id": "H5", "y": 1, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": true, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42748238", "id": "H1", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": true, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42748238", "id": "H2", "y": 1, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": true, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": true, "claude-opus-5-5": true } }, { "task": "R42748238", "id": "H3", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42748238", "id": "H4", "y": 0, "yes": false, "coin": false, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } }, { "task": "R42748238", "id": "H5", "y": 0, "yes": false, "coin": true, "forecasts": { "claude-sonnet-5-5": false, "gpt-6-astra": false, "gemini-4-argon-high": false, "grok-4.5": false, "claude-opus-5-5": false } } ], "selected": [ { "task": "R42605193", "id": "H4", "index": 0, "question": "Which circulating regulator causally promotes cellular senescence and organismal ageing, and through what intracellular signaling mechanism does it act?", "text": "Age-elevated circulating TGF-β1 is a causal driver of multi-tissue cellular senescence and organismal ageing. Chronic exposure of young tissues to aged plasma levels of TGF-β1 is sufficient to induce p16INK4a/p21-positive senescence and accelerate functional decline. Mechanism: Circulating TGF-β1 binds TGFBR1/2, activates Smad2/3–Smad4 complexes that transcriptionally induce CDKN2A/CDKN1A and remodel chromatin toward a stable senescence program, while also reinforcing SASP output that further elevates systemic TGF-β1. Prediction: Neutralizing circulating TGF-β1 (or tissue-specific TGFBR1 deletion) in aged animals will reduce senescence markers across distant organs and improve healthspan metrics more than neutralizing IL-6 or insulin signaling alone; conversely, sustained infusion of TGF-β1 into young animals will recapitulate the aged senescence signature even when inflammatory cytokines remain low.", "articleFinding": "ANGPTL8 directly interacts with AKT2 and activates the AKT–mTOR–S6K pathway, thereby driving cell-autonomous adipocyte senescence. Deleting Angptl8 in mice reduces adipose senescence, delays age-related functional decline, and extends lifespan, while genetic or pharmacological pathway inhibition abolishes ANGPTL8-induced senescence.", "doi": "10.1111/acel.70671", "pmid": "42605193", "articleMatch": 0, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 2 }, { "judge": "claude-opus-5-5", "score": 1 }, { "judge": "gemini-4-argon-medium", "score": 1 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42630044", "id": "H3", "index": 1, "question": "What mechanism limits the anabolic response of aged bone to mechanical loading, and can targeted stimulation restore this response?", "text": "Age-related decline in osteocyte Piezo1 (or associated ion-channel/Ca2+ entry) blunts early mechanotransduction, so downstream anabolic gene programs are not activated by physiological strain. Agonism or overexpression of Piezo1 will restore loading responsiveness in aged bone. Mechanism: Reduced Piezo1-dependent calcium influx and YAP/TAZ or NFAT activation in osteocytes cuts the initiation of load-adaptive transcriptional responses. Prediction: Aged osteocytes will show weaker load-evoked Ca2+ transients and Piezo1-dependent gene induction; Piezo1 activation will rescue formation indices after loading, while Piezo1 loss in young bone will phenocopy the aged loading defect.", "articleFinding": "In aged mouse bone, activation of Piezo1 during mechanical loading promotes its membrane co-localization with connexin 43 and increases connexin 43 hemichannel activity through PI3K-Akt signaling. Hemichannel opening increases PGE2 release, suppresses sclerostin, promotes endosteal bone formation, inhibits resorption, and thereby restores the cortical anabolic response to loading.", "doi": "10.1111/acel.70687", "pmid": "42630044", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42647119", "id": "H1", "index": 0, "question": "How does aging affect injury-induced neuronal reprogramming in the retina, and what mechanisms account for any age-related loss of regenerative capacity?", "text": "Aging reduces injury-induced neuronal reprogramming in the retina because chronic low-grade inflammation progressively impairs Müller glial competence to activate neurogenic programs after injury. Suppressing age-associated inflammatory signaling in old retina should restore reprogramming efficiency toward youthful levels. Mechanism: Persistent innate immune activation (inflammaging) elevates NF-κB/STAT-driven glial reactivity that antagonizes Ascl1 and related neurogenic gene networks required for Müller glia-to-neuron conversion after injury. Prediction: Aged retinas will show higher baseline and post-injury inflammatory cytokine signatures coincident with fewer reprogrammed neurons; neutralizing key inflammatory mediators (e.g., IL-6/TNF or microglial depletion) will increase reprogrammed neuron yield in old but not young animals, whereas adding the same cytokines to young tissue will reduce yield.", "articleFinding": "Aging suppresses Müller glia-to-neuron reprogramming by preventing activation of progenitor programs while promoting reactive and inflammatory glial states and an exaggerated retinal neuroimmune response. Dexamethasone partially restores neurogenesis, confirming that age-associated inflammation is a causal, therapeutically tractable component of the regenerative defect, alongside glial-intrinsic barriers.", "doi": "10.1073/pnas.2612369123", "pmid": "42647119", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 4 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 4 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42647635", "id": "H1", "index": 0, "question": "Does experimentally increasing somatic mitochondrial DNA mutation burden cause premature ageing and shortened lifespan in a large mammal?", "text": "Experimentally elevating the somatic mtDNA mutation rate in a large mammal will accelerate multi-tissue functional decline and shorten median and maximum lifespan relative to isogenic controls with a wild-type mtDNA polymerase proofreading capacity. Mechanism: Proofreading-deficient mtDNA polymerase increases the load of random somatic mtDNA mutations, impairing oxidative phosphorylation, elevating ROS and bioenergetic failure in post-mitotic and stem-cell niches, and thereby driving systemic ageing phenotypes. Prediction: Mutator animals will show dose-dependent earlier onset of sarcopenia, anemia, fertility loss, and cardiac dysfunction together with reduced lifespan, with these traits correlating quantitatively with measured tissue mtDNA mutation burden and respiratory-chain deficiency.", "articleFinding": "Prime-edited pigs expressing proofreading-deficient POLG accumulated elevated somatic mitochondrial DNA mutations and developed systemic premature-ageing phenotypes. These included weight loss, rough hair, anaemia, tissue abnormalities, increased apoptosis, elevated senescence-associated markers, and shortened lifespan.", "doi": "10.1126/sciadv.adu0632", "pmid": "42647635", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 4 }, { "judge": "claude-opus-5-5", "score": 5 }, { "judge": "gemini-4-argon-medium", "score": 4 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42665751", "id": "H3", "index": 0, "question": "How does age-associated mitochondrial dysfunction initiate and propagate inflammatory signaling that causes ovarian functional decline?", "text": "Age-associated mitochondrial DNA damage in oocytes and granulosa cells releases oxidized mtDNA into the cytosol, which activates cGAS–STING and thereby initiates type-I interferon and NF-κB inflammatory programs that impair follicle survival and steroidogenesis. Mechanism: Cytosolic mtDNA sensing by cGAS–STING drives interferon and NF-κB transcription in follicular cells, creating a local inflammatory milieu that reduces oocyte competence and granulosa endocrine function. Prediction: Ovary-specific cGAS or STING deletion (or mtDNA packaging rescue) will reduce follicular inflammatory transcripts and preserve ovulation and estradiol output with age, whereas parallel inflammasome blockade alone will not fully rescue the same endpoints.", "articleFinding": "Ageing-associated mitochondrial DNA leakage from oocytes activates oocyte cGAS, generating cGAMP that triggers STING signaling and passes through gap junctions to activate STING in surrounding granulosa cells. Genetic deletion of oocyte Cgas or pharmacological STING inhibition ameliorates inflammation and ovarian dysfunction, establishing this signaling axis as a causal driver of ovarian ageing.", "doi": "10.1038/s43587-026-01195-y", "pmid": "42665751", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42689491", "id": "H4", "index": 0, "question": "Can in vivo correction of the HGPS-causing mutation rescue molecular, cellular, and structural defects in bone, and how does treatment timing affect efficacy?", "text": "In vivo correction of the HGPS-causing LMNA mutation before a critical developmental window fully restores osteoblast differentiation, bone matrix deposition, and adult bone mechanical integrity because early progerin toxicity primarily impairs formation rather than locking in irreversible structural damage. Mechanism: Progerin-driven nuclear lamina dysfunction and DNA-damage signaling in osteoprogenitors disrupt Runx2/Osterix programs during peak bone accrual; removing progerin early reopens normal lineage progression and mineralization before cortical architecture is permanently compromised. Prediction: Correction in juvenile animals normalizes osteoblast transcriptomes, mineral apposition rate, cortical thickness, and fracture toughness to wild-type levels, whereas identical correction after skeletal maturity leaves residual deficits in geometry and strength despite molecular normalization.", "articleFinding": "Adenine base editing of the pathogenic LMNA variant reduced progerin expression, restored extracellular-matrix deposition and mineralization in progeroid osteoblasts, and partially rescued bone structure and physical properties in mice. In vivo correction was strongly age-dependent, with early postnatal delivery producing substantially greater editing and skeletal benefit than later treatment.", "doi": "10.1111/acel.70700", "pmid": "42689491", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 3 }, { "judge": "gemini-4-argon-medium", "score": 4 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42696595", "id": "H3", "index": 0, "question": "What genetic and molecular mechanism causes natural variation in seed longevity among rice varieties?", "text": "Natural allelic variation in a rice IAA-amido synthetase (OsGH3-family) gene alters free auxin homeostasis in developing seeds, changing seed-coat structure and thereby storage longevity. Accessions carrying a high-activity longevity allele conjugate more IAA, produce a less permeable coat, and retain higher germination after aging. Mechanism: Auxin conjugation reduces free IAA during late seed maturation, remodeling testa cell-wall and cuticle deposition and slowing oxidative aging. Prediction: Near-isogenic lines that differ only at the OsGH3 longevity QTL will show correlated differences in free IAA, seed-coat permeability (tetrazolium uptake), and post-aging germination; CRISPR knockout of the high-longevity allele will shorten longevity without changing primary yield components when auxin is restored chemically.", "articleFinding": "Natural variation at qSL6 causally determines rice seed longevity through SL6, a fatty acyl-ACP thioesterase that changes seed fatty-acid composition and increases resistance to oxidation. Desiccation-induced ABA signaling activates SL6 through VP1, while a virus-derived CT-rich element in the 5′ UTR of the ancestral SL6HHZ allele stabilizes its mRNA bidirectionally and contributes to longevity differences between indica and japonica rice.", "doi": "10.1126/sciadv.aeg8609", "pmid": "42696595", "articleMatch": 0, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 1 }, { "judge": "claude-opus-5-5", "score": 1 }, { "judge": "gemini-4-argon-medium", "score": 1 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42698274", "id": "H4", "index": 0, "question": "What molecular mechanism exacerbates dihydrotestosterone-induced mitochondrial dysfunction, oxidative stress and senescence during androgenetic alopecia?", "text": "Dihydrotestosterone-bound androgen receptor transcriptionally represses PGC-1α in dermal papilla cells, collapsing mitochondrial biogenesis and antioxidant capacity. The resulting electron-transport inefficiency elevates ROS, which accelerates cellular senescence and shortens anagen. Mechanism: AR-dependent transcriptional downregulation of the PGC-1α–NRF1/TFAM biogenesis axis, with secondary loss of SOD2/GPX activity. Prediction: Forced PGC-1α expression or AR DNA-binding blockade will restore mtDNA copy number and oxygen consumption and reduce SA-β-gal/p16 under DHT, whereas NOX or inflammasome inhibitors will not fully rescue biogenesis markers.", "articleFinding": "SFRP2 binds FSTL1 and increases its protein stability, establishing an SFRP2–FSTL1 axis that exacerbates DHT-induced mitochondrial dysfunction, oxidative stress, inflammation and senescence in dermal papilla cells. SFRP2 knockdown alleviated these defects and improved hair regeneration and follicle morphology, while FSTL1 knockdown counteracted the harmful effects of SFRP2 overexpression.", "doi": "10.1111/acel.70666", "pmid": "42698274", "articleMatch": 0, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 2 }, { "judge": "claude-opus-5-5", "score": 0 }, { "judge": "gemini-4-argon-medium", "score": 1 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42717261", "id": "H5", "index": 0, "question": "What mechanism induces pathogenic immune-cell senescence in ulcerative colitis, and does this senescence causally exacerbate the disease?", "text": "In ulcerative colitis, chronic metabolic stress damages mitochondria in lamina propria T cells, releasing mtDNA into the cytosol; cytosolic mtDNA activates cGAS–STING, which drives a senescence program that produces a SASP that amplifies mucosal inflammation and impairs epithelial repair. Mechanism: Mitochondrial damage → cytosolic mtDNA → cGAS–STING → immune-cell senescence → SASP-driven colitis exacerbation Prediction: Selective blockade or genetic deletion of cGAS or STING in T cells will reduce senescence markers (p16, SA-β-gal), lower SASP cytokines in the mucosa, and improve histological colitis scores even when upstream mitochondrial stress persists; exogenous cytosolic mtDNA will recapitulate senescence and worsen disease in a STING-dependent manner.", "articleFinding": "NAD+ metabolic dysregulation causes mitochondrial dysfunction and cytosolic mitochondrial DNA leakage, activating cGAS-STING signaling to drive CD8+ T-cell senescence. These senescent cells exacerbate colitis, while systemic senolytic treatment reduces disease severity; their associated signature also predicts severe disease and non-response to biologic therapy.", "doi": "10.1111/acel.70706", "pmid": "42717261", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 4 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42723546", "id": "H2", "index": 0, "question": "Can a cell-free regenerative treatment alleviate UV-induced skin photoaging, and which causal intracellular mechanism mediates its protective effects?", "text": "A cell-free regenerative preparation alleviates UV-induced photoaging by restoring mitophagy in keratinocytes and fibroblasts, which clears dysfunctional mitochondria and thereby reduces mitochondrial danger-signal release that drives senescence and sterile inflammation. Mechanism: Enhanced PINK1/Parkin-dependent mitophagy lowers mtDNA and ROS leakage, interrupting NLRP3 inflammasome activation and SASP maintenance. Prediction: Pharmacologic or genetic blockade of mitophagy will abolish the therapy’s anti-senescence and anti-inflammatory benefits even when barrier and collagen markers partially recover; mitophagy flux reporters and circulating mtDNA will normalize only in treated, mitophagy-competent skin.", "articleFinding": "Human umbilical cord mesenchymal stem cell secretome protects against UV-induced photoaging by enhancing mitophagy, which clears damaged mitochondria and reduces cytosolic mitochondrial DNA leakage. This suppresses cGAS-STING signaling and downstream inflammatory cytokines; mitophagy inhibition abolishes protection, while STING inhibition restores it.", "doi": "10.1111/acel.70701", "pmid": "42723546", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42805954", "id": "H2", "index": 0, "question": "What causal mechanism contributes to the age-related decline of thermogenic adipocytes in subcutaneous white adipose tissue?", "text": "Age-related loss of sympathetic innervation density and norepinephrine release in subcutaneous white adipose tissue causally impairs β3-adrenergic recruitment of thermogenic (beige) adipocytes. Restoring local catecholaminergic tone would therefore rescue cold- or agonist-induced browning in aged animals. Mechanism: Progressive sympathetic axon rarefaction and reduced vesicular norepinephrine availability lower β3-AR–cAMP–PKA signaling in adipocyte progenitors and mature adipocytes, preventing UCP1 induction and beige differentiation. Prediction: Aged scWAT will show reduced tyrosine hydroxylase+ fiber density and lower tissue norepinephrine; local β3-agonist delivery or chemogenetic reactivation of adipose-projecting sympathetic neurons will restore UCP1+ beige adipocytes and cold-induced energy expenditure without requiring systemic endocrine rescue.", "articleFinding": "Microglial ALKBH5 suppresses Ntf5 expression by demethylating Ntf5 mRNA, thereby limiting activation of PVH TrkB-positive neurons, sympathetic innervation of subcutaneous white adipose tissue, and adipocyte browning. Microglia-specific ALKBH5 knockout preserved brown adipocytes and improved metabolic activity during ageing in male mice.", "doi": "10.1038/s41467-026-77050-w", "pmid": "42805954", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 3 }, { "judge": "gemini-4-argon-medium", "score": 2 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42810392", "id": "H3", "index": 0, "question": "Can direct pharmacological activation of a conserved metabolic target extend lifespan across evolutionarily diverse organisms and induce longevity-associated changes in mammals?", "text": "Selective pharmacological activation of AMPK is sufficient to extend lifespan in evolutionarily distant invertebrates and to induce longevity-associated physiological and molecular signatures in mammals. The longevity benefit is caused by AMPK itself rather than off-target pharmacology of multi-target drugs. Mechanism: Direct AMPK activation increases catabolic programs (fatty-acid oxidation, autophagy, mitochondrial biogenesis) and dampens anabolic growth signaling, shifting cells into a conserved energy-sparing, stress-resistant state that slows aging. Prediction: A highly selective AMPK agonist will extend lifespan in C. elegans and Drosophila and, in mice, raise AMPK activity, improve metabolic healthspan markers, and induce transcriptomic/proteomic aging-delay signatures, whereas chemically related inactive analogs will not.", "articleFinding": "Direct pharmacological activation of AMPK with compound 991 extends lifespan in Drosophila melanogaster, Caenorhabditis elegans, and Schizosaccharomyces pombe. In mice, 991 induces a proteomic profile associated with pro-longevity biology, supporting the translational potential of AMPK activation.", "doi": "10.1111/acel.70721", "pmid": "42810392", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 4 }, { "judge": "claude-opus-5-5", "score": 5 }, { "judge": "gemini-4-argon-medium", "score": 4 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42842666", "id": "H1", "index": 0, "question": "How do the different cellular compartments of the vascular wall causally contribute to distinct features of Hutchinson-Gilford progeria vascular pathology?", "text": "Progerin expression specifically in vascular smooth muscle cells is sufficient to cause medial VSMC depletion and collagen-rich extracellular-matrix accumulation, independently of endothelial or adventitial progerin. Mechanism: Cell-autonomous nuclear lamina disruption in VSMCs triggers DNA damage responses, senescence and apoptosis, while dysregulating matrix gene programs that favor collagen deposition and medial remodeling. Prediction: Mice or vessel organoids with VSMC-restricted LMNA G609G (or equivalent) will reproduce medial VSMC loss and collagen accumulation, whereas endothelium- or adventitia-restricted progerin will not.", "articleFinding": "In trilayer engineered blood vessels, HGPS fibroblasts causally promoted extracellular-matrix dysregulation and fibrotic signaling, while HGPS smooth muscle cells drove collagen accumulation and endothelial cells drove inflammation. Correcting the HGPS-associated mutation by base editing restored many pathological characteristics toward healthy levels.", "doi": "10.1126/sciadv.aeh3785", "pmid": "42842666", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 3 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42844664", "id": "H3", "index": 0, "question": "Through what causal mechanism does time-restricted feeding protect against accelerated cardiovascular ageing?", "text": "Time-restricted feeding protects against accelerated cardiovascular ageing by restoring intestinal epithelial barrier integrity, thereby limiting chronic low-grade endotoxemia that drives endothelial dysfunction and arterial stiffening. The barrier restoration is necessary and sufficient for the vascular benefit under otherwise matched caloric intake. Mechanism: Extended daily fasting upregulates tight-junction proteins (e.g., occludin, claudin-1) and mucus production via circadian and AMPK-dependent pathways in enterocytes; reduced translocation of LPS and other microbial products lowers TLR4/NF-κB signaling in endothelium and vascular smooth muscle, slowing hypertension, stiffening, and maladaptive remodeling. Prediction: In aged or progeroid models, TRF that improves gut barrier markers and lowers plasma LPS will prevent arterial stiffening and endothelial dysfunction, whereas TRF combined with experimental barrier disruption (or chronic low-dose LPS infusion matched to ad libitum levels) will abolish protection despite preserved feeding-window compliance and body weight.", "articleFinding": "Time-restricted feeding enriches acetate-producing Limosilactobacillus, and microbiota-derived acetate is necessary and sufficient for its protection against angiotensin II-induced cardiovascular ageing. Acetate activates GPR43, inhibits HDAC3, increases H4K8 acetylation, and suppresses NLRP3-mediated pyroptosis and cellular senescence.", "doi": "10.1111/acel.70728", "pmid": "42844664", "articleMatch": 0, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 2 }, { "judge": "claude-opus-5-5", "score": 1 }, { "judge": "gemini-4-argon-medium", "score": 2 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42858183", "id": "H1", "index": 0, "question": "Can a defined intervention preserve lysosomal function and protein homeostasis during aging, thereby extending lifespan and maintaining organismal function, and through what mechanism?", "text": "Chronic low-dose Tor inhibition preserves lysosomal acidification and autophagic flux during aging, which sustains protein homeostasis and extends lifespan. The benefit depends on maintained lysosomal protease activity rather than reduced protein synthesis alone. Mechanism: Reduced mTORC1 signaling derepresses TFEB/HLH-30 nuclear translocation, upregulating lysosomal biogenesis and v-ATPase subunits, thereby keeping lumenal pH low and clearance competent with age. Prediction: Genetic or pharmacological blockade of TFEB/HLH-30 or v-ATPase will abolish lifespan extension and lysosomal pH preservation under Tor inhibition, while matching the translation-rate reduction without Tor inhibition will not restore lysosomal competence.", "articleFinding": "20(S)-ginsenoside Rg3 extended lifespan and preserved physiological and neuronal function in Caenorhabditis elegans by restoring lysosomal activity and autophagic flux. Rg3 remodeled neuronal lysosomal phosphoinositide signatures toward increased PI(4)P and reduced PI(3)P, suppressed RSKS-1/S6K–TORC1 signaling, and promoted nuclear HLH-30/TFEB activity, thereby improving proteostasis and resistance to polyglutamine- and α-synuclein-associated toxicity.", "doi": "10.1111/acel.70755", "pmid": "42858183", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42669067", "id": "H1", "index": 0, "question": "How does SIRT1 regulate L1 retrotransposon activity, and does this regulation affect cellular senescence?", "text": "SIRT1 maintains L1 silencing by deacetylating histone H3K9/H4K16 at L1 promoter and 5' UTR chromatin; decline of SIRT1 activity during senescence causes L1 transcriptional derepression that accelerates the senescence program. Mechanism: NAD+-dependent local chromatin deacetylation by SIRT1 preserves repressive chromatin at L1 loci; loss of this mark permits RNA polymerase II access and L1 mRNA production. Prediction: ChIP-seq will show increased H3K9ac/H4K16ac and reduced H3K9me3 specifically at L1 5' UTRs after SIRT1 knockdown or catalytic inhibition, preceding elevated L1 RNA and earlier SA-β-gal/p16 induction; a L1-promoter-targeted deacetylase tether will rescue silencing without restoring global SIRT1 activity.", "articleFinding": "SIRT1 suppresses L1 transcription and retrotransposition by promoting the association and recruitment of Lamin B1 and KAP1 at the L1 5′-UTR, increasing repressive H3K9me3 chromatin. SIRT1 deficiency derepresses L1, activates cGAS–STING signaling, and induces cellular senescence; reverse-transcriptase inhibition with 3TC rescues this phenotype.", "doi": "10.1111/acel.70689", "pmid": "42669067", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 3 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42811065", "id": "H1", "index": 0, "question": "Which local mechanism connects stress-induced sympathetic activity to cellular senescence and impaired osteogenesis, and can it be modulated non-invasively?", "text": "Chronic psychological stress elevates bone-marrow norepinephrine from sympathetic terminals, which acts through β2-adrenergic receptors on mesenchymal stem/progenitor cells to drive p53/p21-dependent cellular senescence and thereby suppress osteogenic differentiation. Non-invasive peripheral neuromodulation that reduces local norepinephrine tone or blocks β2 signaling will reverse marrow senescence and restore bone formation. Mechanism: Sympathetic norepinephrine → β2-AR → cAMP/PKA → ROS/p53/p21 senescence program in osteoprogenitors Prediction: Marrow β2-AR knockout or selective β2 blockade will abolish stress-induced senescence markers (p16, SA-β-gal) and rescue osteogenesis even when circulating catecholamines remain high, whereas β1-selective blockade will not; peripheral nerve stimulation that lowers marrow NE will phenocopy β2 blockade.", "articleFinding": "Sympathetic neuropeptide Y drives stress-induced osteoporosis by activating adipocyte Y1R and inducing senescence in bone marrow adipocytes, which impairs osteogenesis. Pulsed electromagnetic fields activate sensory nerves, causing local semaphorin 3A release that suppresses sympathetic neuropeptide Y secretion through a peripheral circuit independent of central pathways.", "doi": "10.1038/s41467-026-77654-2", "pmid": "42811065", "articleMatch": 0, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 2 }, { "judge": "claude-opus-5-5", "score": 2 }, { "judge": "gemini-4-argon-medium", "score": 2 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42806003", "id": "H1", "index": 2, "question": "What intercellular mechanism causes placental senescence during maternal ageing, and can disrupting this mechanism restore placental and offspring health?", "text": "Maternal ageing elevates CD38 on decidual and circulating immune cells, depleting NAD+ in the shared placental microenvironment and thereby suppressing SIRT1/PARP activity in trophoblasts, which accelerates placental cellular senescence and metabolic failure. Restoring NAD+ or inhibiting maternal CD38 should reverse placental senescence and improve fetal growth. Mechanism: Maternal CD38-driven NAD+ depletion creates a metabolic niche that forces trophoblast senescence. Prediction: Placental NAD+ and SIRT1 activity fall with maternal age in parallel with CD38+ immune infiltration; CD38 inhibition or NAD+ precursors restore trophoblast NAD+/SIRT1, reduce senescence markers, and improve fetal outcomes even when maternal chronological age is unchanged.", "articleFinding": "Early inflammation and senescence-associated secretory phenotype activity induce IRF5-dependent CD38 expression in macrophages, which depletes NAD+ in decidual stromal cells and thereby promotes age-related placental senescence. Genetic or pharmacological disruption of this axis, including CD38 inhibition or NAD+ precursor treatment, reduces placental senescence, rescues intrauterine growth restriction, and improves offspring metabolic outcomes.", "doi": "10.1038/s41467-026-77217-5", "pmid": "42806003", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 4 }, { "judge": "gemini-4-argon-medium", "score": 4 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] }, { "task": "R42806572", "id": "H2", "index": 0, "question": "Can a dose-titratable immune engager safely eliminate senescent cells and alleviate age-related pathology across mice and non-human primates, and what measurement can guide its safe dosing?", "text": "A dose-titratable bispecific immune engager that redirects T cells to a senescence-associated surface antigen will clear a therapeutically relevant fraction of senescent cells in aged mice and non-human primates at exposures below those that trigger systemic cytokine release. Circulating IL-6 and IFN-γ rise steeply only after the efficacious dose window, so their early kinetics can guide safe titration. Mechanism: Target engagement on senescent cells forms an immunological synapse that drives selective cytotoxicity; off-target or excess engagement expands systemic cytokine production once a threshold of T-cell activation is crossed. Prediction: In both species, intermediate engager doses will reduce senescence markers (p16INK4a, SA-β-gal, SASP factors) and improve tissue function without grade ≥2 cytokine release, while cytokine AUC will increase nonlinearly only at higher doses that do not further improve efficacy.", "articleFinding": "A GFD-CD3 bispecific T-cell engager targeting uPAR-positive senescent cells caused dose-dependent senolysis and alleviated age-related pathologies in aged mice and non-human primates at low doses. High doses caused hepatotoxicity through T-cell attack on hepatic endothelial cells, while serum aminotransferase monitoring enabled dosing that retained senolytic efficacy without observed adverse effects.", "doi": "10.1111/acel.70742", "pmid": "42806572", "articleMatch": 1, "judgeScores": [ { "judge": "gpt-5.6-sol", "score": 3 }, { "judge": "claude-opus-5-5", "score": 3 }, { "judge": "gemini-4-argon-medium", "score": 3 } ], "votes": [ { "model": "claude-sonnet-5-5", "yes": true }, { "model": "gpt-6-astra", "yes": true }, { "model": "gemini-4-argon-high", "yes": true }, { "model": "grok-4.5", "yes": true } ] } ] }