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Partial reprogramming to enhance regeneration and mitigate age-related phenotypes is limited by toxicity. Parras et al. report a transgenic reprogrammable mouse strain with attenuated toxicity, by avoiding OSKM expression in the liver and intestine.
Aging is associated with increased atherosclerosis risk and a changing immune landscape. In this study, the authors examined T cell changes in atherosclerotic plaques in mice with age and report an accumulation of clonally expanded effector and memory CD8+ T cells, including Gzmk+CD8+ T cells, which have cytotoxic transcriptomic signatures.
Aguado et al. show that SARS-CoV-2 induces senescence in human brain organoids and in the brains of COVID-19-infected mice and humans. They demonstrate the therapeutic potential of senolytic therapy in protection against COVID-19-induced brain aging.
Age impacts the effect of dietary health and longevity interventions but the underlying mechanisms are incompletely understood. Here the authors study fasting in killifish and find that older animals exhibit a metabolic shift resembling a fasting-like program, which is counteracted by boosting the activity of AMPKγ1, promoting health and longevity.
Chamoli et al. identified MIC, a benzocoumarin molecule, that promotes longevity in C. elegans by inducing mitophagy via DAF-12/FXR and HLH-30/TFEB, and they demonstrate a conserved MIC efficacy in mammalian cells, indicating potential broader relevance.
There is scant evidence for how intrinsic capacity (IC), the combination of an individual’s physical and mental capacities, varies throughout adulthood. In this study, the authors demonstrated a method to establish IC reference centile curves using data of individuals aged 20–102 years from the French INSPIRE-T cohort.
Using spatial and single-cell multiomics, Nikopoulou et al analyze how different cells within the mouse liver age, revealing zonation-specific aging trajectories and highlighting the importance of the local tissue microenvironment.
Guo et al. demonstrate that oral administration of chiral nanoparticles ameliorates Alzheimer’s disease-associated pathology and cognitive decline in mice via an increase in the gut metabolite, indole-3-acetic acid, potentially a therapeutic target.
Sun et al. identify a stem cell population of CD133+ endothelial-like cells (ELCs) that contribute to neovascularization. ELCs become dysfunctional with age, but ELC supplementation or pamidronate treatment to counter ELC aging promotes longevity.
CREB-regulated transcriptional coactivators (CRTCs) have an important role in modulating transcription in a context-dependent manner. Here the authors dissect the role of CRTC-1 in worm lifespan and show that the CRTC-1 transcriptional domain ensures longevity under specific histone marks.
Change in intercellular communication is an important but poorly characterized hallmark of aging. Here the authors provide a bioinformatics tool to infer changes in cell–cell signaling and an atlas of age-related communication changes in 23 mouse tissues.
Hong, Li and colleagues unveil a pivotal role of TET2 in heterochromatin relocalization, aberrant upregulation of endogenous retroviruses and overactivated innate immune response in hematopoietic stem and progenitor cells during aging.
Advanced age is a primary risk factor for female infertility due to declining oocyte quantity and quality. Here Yu Zhang et al. report that supplementation with spermidine rejuvenates the quality of oocytes from aged mice at least in part by enhancing mitophagy and mitochondrial function.
Unlike animals, plants prevent pathological polyQ aggregation through chloroplast proteostasis. Expression of the chloroplast protein SSP in human cell and nematode models prevents disease-related protein aggregation and neurodegeneration.
Ye et al. characterize the cardioprotective effect of SIRT2 in primates and reveal an important role for the SIRT2–STAT3–CDKN2B regulatory axis in primate cardiac aging, improving understanding of the epigenetic mechanism governing cardiac aging.
Ferrari-Souza et al. show that the APOEε4 allele potentiates the deleterious effects of Aβ on the longitudinal accumulation of tau tangles in neocortical brain regions, via tau phosphorylation, which coincides with brain atrophy and clinical decline.
A single-cell transcriptomic analysis by Lau et al. reveals a homeostatic–chemotactic–phagocytic state transition in microglia upon IL-33 stimulation, identifying VCAM1 as a key regulator of microglial chemotaxis by sensing Aβ plaque-associated ApoE.
Pereira, Kumar et al. identify cerebrospinal fluid DOPA decarboxylase as a promising biomarker for Parkinsonian disorders that may be used for early preclinical detection of Parkinsonian disorders as well as determining the risk of conversion to Lewy body disease.
Lamin A/C protects alveolar macrophages against nuclear envelope rupture and DNA damage, but it erodes during aging. Lack of lamin A/C leads to senescence and an aging signature, resulting in vulnerability to influenza virus and lung cancer growth.
Li et al. provide a transcriptional and epigenetic characterization of microglia in aging mice brain by developing a three-round depletion–repopulation (3xDR) model to study aged microglia in non-aged brain, giving insights into the molecular mechanism underlying microglia aging.