task	score	input_score	alternative_score	cue_excerpt	rationale_en	missing_en
R42581103	1	1	2	aged systemic environment causally impair intestinal stem-cell metabolism	The systemic source of the effect and the metabolic impairment in stem cells are specified; the specific inflammatory signal is hidden.	TNF, TNFR1, and suppression of fatty acid oxidation
R42601407	2	2	2	physical activity delay ovarian ageing and extend reproductive lifespan	The intervention and both expected effects from the reference finding are stated directly.	Adiponectin, its receptors, and AdipoRon
R42605193	1	1	1	circulating regulator	The search is restricted to circulating regulators acting through intracellular signalling.	ANGPTL8, AKT2, and the AKT-mTOR-S6K sequence
R42608398	1	1	2	microbiota-derived factor directly cause	The microbial source of the causal factor is given; the substance and the cellular mechanism remain unknown.	Corisin and enhancement of ubiquitin-proteasome degradation
R42627902	0	1	1	shift away from erythroid differentiation and toward platelet-producing lineage programs	The shift in cellular differentiation to be explained is described; the regulator and its mode of action are left unspecified. The background additionally points towards transcriptional regulation.	Pbx1 and suppression of Gata1
R42630044	0	0	1	anabolic response of aged bone to mechanical loading	The physiological response and its age-related decline are named; the request for targeted stimulation leaves the molecule and pathway unspecified.	Piezo1, connexin 43, PI3K-Akt, and PGE2
R42639736	0	1	0	disrupted intracellular homeostasis to DNA damage and senescence	Disrupted homeostasis defines a broad problem; the question leaves calcium and the specific organelle unspecified. The background additionally mentions organelle interactions.	DHCR24, ENKUR, and calcium overload
R42642518	1	1	2	circulating factors that accumulate with age	The accumulation of circulating factors, their causal effect, and the potential for reversibility are given; the composition of the factors is hidden.	Metabolic parameters, tumour markers, and dietary modification
R42642521	2	2	1	age-depleted gut microbe and one of its metabolites causally suppress inflammaging and improve healthspan	The question reproduces the pattern of a microorganism plus its metabolite and the expected effects; only the participants remain to be named.	Bifidobacterium pseudocatenulatum and 5-AVAB
R42647119	0	0	1	aging affect injury-induced neuronal reprogramming in the retina	The tissue and the age-related change under study are given; the inflammatory mechanism and the intervention are hidden.	Inflammatory state of Müller glia and dexamethasone
R42647635	2	2	2	increasing somatic mitochondrial DNA mutation burden cause premature ageing and shortened lifespan	A causal hypothesis linking an increased number of mitochondrial DNA mutations to two outcomes in a large mammal is given directly.	POLG proofreading defect, pigs, and the editing method
R42663085	1	1	0	intrinsic molecular regulator be enhanced to reactivate quiescent hair follicles	Enhancement of an intrinsic regulator and follicle activation from dormancy are given; the type of regulator remains broad.	TPP1, telomere protection, telomerase, and TELODIN
R42664348	1	1	1	excess adiposity promote osteoarthritis progression	The source of the effect in adipose tissue is specified; the mechanism transferring material to chondrocytes is hidden.	Extracellular vesicles, mitochondrial DNA, and cGAS-STING
R42665751	2	2	1	mitochondrial dysfunction initiate and propagate inflammatory signaling	The causal sequence from mitochondrial dysfunction through the spread of an inflammatory signal to ovarian dysfunction is already given.	Mitochondrial DNA release, cGAS-cGAMP-STING, and gap junctions
R42689491	2	2	2	in vivo correction of the HGPS-causing mutation rescue molecular, cellular, and structural defects in bone	Correction of the causal mutation and the expected bone restoration are specified; the importance of treatment timing is cued separately.	Adenine base editing, LMNA, and the advantage of early administration
R42696595	0	0	1	natural variation in seed longevity among rice varieties	Genetic variation defines the phenomenon to be explained; lipids, RNA regulation, and the specific gene are hidden.	SL6, fatty acids, ABA-VP1, and the 5′-UTR element
R42698274	1	1	0	dihydrotestosterone-induced mitochondrial dysfunction, oxidative stress and senescence	The hormonal exposure and cellular impairments that narrow the search are specified; the protein interaction is hidden.	SFRP2, FSTL1, and protein stabilisation
R42717261	1	2	0	immune-cell senescence in ulcerative colitis	The question points towards immune cell senescence as the cause of the disease. The background additionally names mitochondrial damage and the release of components into the cytosol.	NAD+, mitochondrial DNA, cGAS-STING, and CD8+ T cells
R42723546	1	1	2	cell-free regenerative treatment alleviate UV-induced skin photoaging	The class of cell-free interventions and the beneficial effect are named; the sequence of intracellular events is hidden.	Secretome, mitophagy, mitochondrial DNA, and cGAS-STING
R42725837	1	1	1	transmembrane protein	The protein class is specified, while its name and direction of action are omitted.	PTCHD4 and AKT enhancement
R42736449	1	1	2	unannotated protein product	The search is restricted to an unannotated protein product; its locus, cells, and function are hidden.	MKKS microprotein and microglial mitochondrial respiration
R42744804	0	1	0	actively eliminates motor neurons and accelerates mortality in SOD1G93A mice	The outcome and the disease model are described; the mechanism of neuronal engulfment is omitted. The background allows for interaction with surrounding cells.	Microglia, Axl, Mer, phosphatidylserine, and engulfment of live neurons
R42749700	1	1	1	disrupted chromatin regulation	The search is directed towards chromatin regulation; the molecules and the specific mode of regulation are hidden.	HMGA1, USP7, HP1β, ANGPTL2, and the UHP peptide
R42758848	1	1	2	developmentally established epigenetic mechanism preserves metabolic readiness	The epigenetic nature and metabolic function are given; the signalling factor and the histone variant are hidden.	IL-7, GABPα, H2A.Z, and oxidative phosphorylation genes
R42759510	1	1	2	peripheral-to-brain signaling	The direction of signalling from the periphery to the brain and the set of outcomes are given; the source organ and the carrier are hidden.	Spleen, RBMX, miR-10a-5p, and γCaMKII
R42775695	1	1	2	defective mitochondrial quality-control flux	The search is restricted to mitochondrial quality control; the cause of impaired flux and the specific intervention are hidden.	HIF-3α, BNIP3, and mitochondrial transplantation
R42775698	1	1	2	gut microbial community causally reprogram intestinal barrier function, systemic metabolism, and mucosal gene expression	The source of the effect and three groups of outcomes are named; the direction of the changes and the metabolites remain unknown.	Microbiota transplantation, Tyr-Phe, prostaglandin E3, and gene suppression
R42786310	2	2	1	commensal microorganism predicted from integrated human ageing profiles causally extend lifespan and healthspan	The scheme for selecting the microorganism and the list of beneficial effects, including a shift of molecular profiles towards a youthful state, are given.	Neisseria flavescens, live and inactivated bacteria, and the difference between models
R42805954	0	1	0	age-related decline of thermogenic adipocytes	The phenomenon to be explained is named; the neural pathway appears only in the background.	Microglia, ALKBH5, Ntf5, and sympathetic innervation
R42810392	2	2	2	direct pharmacological activation of a conserved metabolic target extend lifespan across evolutionarily diverse organisms	Selective activation, cross-species lifespan extension, and changes in mammals are given; the central causal scheme is already formulated.	AMPK, compound 991, the specific species, and the mouse proteome
R42811497	0	1	0	cellular senescence and fibrosis in localized scleroderma	The question specifies the pathological outcomes and the general possibility of treatment; the molecular process is hidden. The background additionally mentions organelle homeostasis.	Parthenolide, Ero1L, and contacts between the endoplasmic reticulum and mitochondria
R42821663	1	1	2	hypertension accelerate osteoarthritis	The systemic exposure and the sensitivity of injured joints are given; the circulating mediator is hidden.	Vasopressin, AVPR1A, and NR4A3
R42822442	1	1	2	nutrient scarcity	The search is restricted to nutrient deficiency as the cause of senescence in transferred immune cells.	Glucose, Th9, AMPK, ZAK-NIK, and IL-9
R42826184	1	1	2	three-dimensional genome organization	The class of genome structure changes and the direction of the transcriptional effect are specified; the architectural protein and the mode of rearrangement are hidden.	SATB1, TAD boundaries, and CTCF interactions
R42839094	1	1	2	conserved form of lipid remodeling	Lipid remodelling is given as a limit on lifespan; the type of lipid change and the regulator are hidden.	Acyl chain elongation and Plb1
R42841227	1	1	2	gut microbial metabolism causally impair antiviral defense	The microbial metabolic source of impaired antiviral defence is given; the metabolite and the receptors are hidden.	Acetate, FFAR2/FFAR3, and histone H3 acetylation
R42842666	1	1	0	different cellular compartments of the vascular wall	The search is directed towards separating the causal functions of vascular wall cells; the mapping of cell types to specific effects is hidden.	Roles of fibroblasts, smooth muscle cells, and endothelial cells
R42844664	2	2	2	time-restricted feeding protect against accelerated cardiovascular ageing	The intervention and the direction of the effect are stated directly; the mediators remain to be identified.	Limosilactobacillus, acetate, GPR43, HDAC3, and NLRP3
R42853938	1	1	2	splicing-dependent mechanism enables resistance to CDK4/6 inhibition	Splicing and the class of therapy are given; the specific transcript and the resistance mechanism are hidden.	SUV39H2 exon 2, H3K9me3, and p21
R42858183	2	2	1	preserve lysosomal function and protein homeostasis during aging, thereby extending lifespan	The question specifies the sequence from lysosomal restoration through proteostasis to lifespan extension; the name of the intervention is hidden.	Rg3, phosphoinositides, TORC1-RSKS-1, and HLH-30
R42806945	1	1	2	metabolic regulator causally mitigates ageing-related cognitive impairment	The metabolic class of the regulator and the direction of the effect are named; the identity of the regulator and the cellular mechanism are hidden.	Ghrelin, microglia, and SHBG-JNK1-Beclin1
R42723144	2	2	1	equivalent heterogeneous nuclear backgrounds	An identical distribution of nuclear variants directs the search for a hereditary cause beyond the nuclear genome.	Mitochondrial haplotypes, TFAM import, and TOMM20
R42808804	1	1	0	blood-labyrinth barrier integrity	The search is directed towards damage to the cochlear vascular barrier; the specific cells and molecular causes are hidden.	Pericytes, IGF-1, SLC25A33, and TGF-β/Smad2
R42585340	1	1	2	mild cellular stress to preserve protein homeostasis	Mild stress, proteostasis, and lifespan extension are given; the type of stress and the protective programme are hidden.	Respiration suppression, ELT-2, and CPR-5/CPR-8 proteases
R42669067	2	2	2	SIRT1 regulate L1 retrotransposon activity	The question directly names two molecular participants from the central statement of the reference finding.	Direction of regulation, Lamin B1, KAP1, H3K9me3, and cGAS-STING
R42811065	1	1	2	stress-induced sympathetic activity to cellular senescence and impaired osteogenesis	A neural cause and intermediate cellular senescence are given; the local mediators and the mode of intervention are hidden.	Neuropeptide Y, Y1R, semaphorin 3A, and pulsed electromagnetic fields
R42841610	1	1	2	causal metabolic mechanism	The search is restricted to a metabolic explanation of mitochondrial dysfunction; the metabolite and the enzyme are hidden.	p38 MAPK, GLS1, urea, and CB-839
R42806003	1	1	0	intercellular mechanism	The intercellular nature of the cause is given; the cell types and the transmitted metabolic deficit are hidden.	Macrophages, IRF5, CD38, and NAD+ depletion in stromal cells
R42806572	2	2	2	dose-titratable immune engager safely eliminate senescent cells	The therapeutic construct, the mechanism of immune cell clearance, dosing, and translation of the effect from mice to primates are specified.	GFD-CD3, uPAR, endothelial toxicity, and aminotransferases
R42748238	1	1	2	vascular deterioration to promote systemic senescence	The direction from vascular dysfunction to systemic ageing is given; the enzymatic chain and the metabolite are hidden.	C/EBPβ, AEP, NAMPT cleavage, and NAD+ deficiency