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Wang et al. generate a single nucleus-resolved transcriptomic atlas of primate adrenal aging, with which they demonstrate regional changes in adrenal aging, and establish the role of LDLR in impeding cholesterol uptake and DHEA-S production in aging.
Pan et al. demonstrate that hearing loss promotes cognitive decline in an APP/PS1 mouse model of Alzheimer disease via inhibition of the GDF1 signaling pathway, unveiling GDF1 as a therapeutic target for Alzheimer disease.
Aging is a risk factor of Parkinson’s disease (PD). Adams, Song et al. present a multiomics analysis of the human midbrain showing age-induced changes in genes associated with glial function, with further alterations of oligodendrocytes in PD.
Older age is associated with worse outcomes for patients with melanoma, and the underlying mechanisms are incompletely understood. Here the authors show that the loss of HAPLN1 in aged skin fibroblasts drives melanoma progression by increasing ICAM1 and angiogenesis. Blocking ICAM1 shrinks tumors, suggesting potential for age-specific melanoma therapy.
Zhang et al. demonstrate that S6K suppression in the Drosophila fat body mediates the longevity effects of rapamycin and identify Syntaxin 13 as a conserved downstream effector regulating lysosome morphology and inflammation in a sex-specific manner.
Plasma membrane damage (PMD) can induce cell death or be repaired, whereas other cell fates are not well explored. In this study, the authors found that PMD induces senescence in yeast and human fibroblasts in a manner that is distinct from DNA damage-dependent senescence. They present transcriptomic data suggesting that this PMD response may explain the origins of senescent cells near cutaneous wounds.
Identifying individuals at risk of developing Alzheimer’s disease is an important task. Here Tang et al. leverage electronic health records to predict Alzheimer’s disease onset, and utilize knowledge networks to prioritize shared genes behind the clinical data as well as facilitate contextualization based on sex.
Large-scale proteomics data hold promise for individual disease risk prediction. Here the authors use data from more than 50,000 adults without dementia in the UK Biobank to predict the future risk of dementia and highlight GFAP as an important protein elevated in individuals more likely to develop dementia.
Using a multi-omics approach, Wang et al. explored sex-specific and region-specific patterns of intestinal aging in non-human primates, identifying regulators with conserved functions in Caenorhabditiselegans intestinal aging, in colitis in mice and in patient colorectal cancer samples.
The accumulation of senescent cells drives age-related diseases. In this study, the authors show that senolytic CAR T cells can rejuvenate metabolic function and fitness in old mice and that a single dose is sufficient to lead to long-term preventive effects.
An inflammatory profile is associated with aging and senescence. Here, Hao et al. show that TXNRD1 drives the senescence-associated secretory phenotype through the cGAS–STING pathway, independently of its enzymatic activity, during senescence and that the TXNRD1–cGAS interaction may be a target for selectively suppressing inflammaging.
The authors identify causality-enriched CpGs linked to aging using Mendelian randomization. They develop new epigenetic clocks, DamAge and AdaptAge, that more reliably track age-related changes, offering insights into aging mechanisms and interventions.
Cikes et al. report dysregulation of glycerophosphocholine (GPC) metabolism in aged mouse muscle, which they functionally link to severe glucose intolerance. Correspondingly, muscle GPC levels are altered in both older adults and patients with type 2 diabetes.
He et al. demonstrate a noncanonical role for the TRMT6–TRMT61A methyltransferase complex in hematopoietic stem cell (HSC) aging, where its enrichment activates necroptosis signaling. Blocking necroptosis counters features of HSC aging, suggesting a therapeutic strategy.
This study reveals that many previously reported changes in gene expression in aging hematopoietic stem cells (HSCs) may be linked to extraction stress rather than aging itself and has implications for future HSC aging research.
Isola, Ocañas et al. report age-related changes in the mouse ovarian transcriptome at single-cell resolution, demonstrating an increase in lymphocytes that corresponds to declines in collagen degradation and accumulation of multinucleated giant cells.
Griffin et al. present a versatile method for scalable and low-cost sequencing for the construction of epigenetic clocks. They assay 2,892 human or mouse samples, benchmark their method and assess diverse interventions.
Tijms et al. identify five molecular Alzheimer’s disease subtypes typified by hyperplasticity, impaired immune activation, RNA metabolism, and choroid plexus or blood–brain barrier function. Subtypes may need tailored cures.
Li and Guo et al. demonstrate that epigenetic dysregulation of the MLL complex at promoters of particular age-dependent genes results in their transcriptional downregulation and subsequent age-related dysfunction of neural stem and progenitor cells.
Yang et al. demonstrate that inhibition of early-acting autophagy genes in neurons extend C. elegans lifespan, improve neuronal proteostasis and increase exopher formation mediated by the autonomous WD40 domain-related function of ATG-16.2.