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Anerillas et al. provide a strategy to eliminate senescent cells that leverages on their secretory needs. Inhibiting YAP–TEAD triggers endoplasmic reticulum stress that eliminates senescent cells from several tissues, improving age-related fibrosis.
Urolithin A (UA) is a gut microbiome-derived metabolite that has been therapeutically explored in aging-related diseases and exerts its benefits in part through effects on mitochondria. Here Girotra, Chiang and colleagues show that UA administration boosts mitochondrial recycling in hematopoietic stem cells and reverses aging features in both the hematopoietic and immune systems.
Using multimodal MRI to delineate noradrenergic and dopaminergic nuclei in aging, Dahl et al. found differential associations with episodic and working memory, helping to disentangle the role of the neurotransmitter systems in age-related memory loss.
Risk stratification based on plasma p-tau217 can substantially reduce the need for invasive or expensive testing when screening for Aβ positivity in patients with cognitive impairment, offering a cost-effective strategy to support an Alzheimer’s disease diagnosis.
The intestinal barrier has an important role in organismal homeostasis; however, the mechanisms that mediate intestinal epithelial aging are incompletely understood. Here, Zhang et al. show that RAB-10 functionality is impaired in aging worms, affecting endocytic recycling and, thus, contributing to the age-related deterioration of adherens junctions.
The authors found that klotho, a longevity and cognition-enhancing factor, can increase the levels of multiple platelet factors in plasma, including PF4. PF4 treatment, which permeated the brain, in turn, enhanced cognition in young and old mice.
The authors report that a change to lysosome morphology, from vesicular to tubular form, supports lifespan extension upon dietary restriction and promotes heightened autophagy and healthy aging when stimulated artificially in well-fed animals.
This study identifies and characterizes evolutionarily conserved cytosine methylation patterns related to age across mammals and establishes pan-mammalian epigenetic clocks.
Using a multivariate genome-wide association study approach, the authors identified 52 genetic variants associated with aging-related traits, many of which are promising cardiometabolic targets that could promote healthy aging and inform future interventions.
Heterochronic parabiosis ameliorates age-related diseases in mice, but how it affects epigenetic aging and long-term health was not known. Here, the authors show that in mice exposure to young circulation leads to reduced epigenetic aging, an effect that persists for several months after removing the youthful circulation.
De-Souza, Thompson and Taylor demonstrate that pathogen-associated odorants can activate the UPR cell non-autonomously in C. elegans via neuronal TGF-β signaling, leading to extended lifespan and enhanced clearance of toxic proteins.
Adipose tissue has an important role in metabolic homeostasis and undergoes age-related changes contributing to metabolic decline, via mechanisms that remain incompletely explored. Here the authors show that Crtc2 deficiency in adipocytes protects against age-related hyperactivation of the BCAA–mTORC1 axis and metabolic alterations.
Many age-related disorders, such as neurodegenerative diseases, are associated with protein misfolding. Here, the authors identify LONRF2 as a protein quality control ubiquitin ligase that is expressed in neurons and ubiquitylates misfolded TDP-43 and hnRNP M1 and show that loss of Lonrf2 in mice results in late-onset motor neuron degeneration, whereas its ectopic expression partially rescued the phenotypes observed in motor neurons derived from patients with amyotrophic lateral sclerosis.
Yeo and Zhou et al. profile whole-genome chromatin accessibility in different cell types of the adult neurogenic niche, which reveals a reversible decrease in the migration of proliferative neural stem cells in aged mice.
Shen, Gao and Luo et al. show that the epigenetic regulator Cxxc1 plays an important role in maintaining homeostasis and function of group 3 innate lymphoid cells that are involved and key in regulating intestinal immunity during aging.
Delval, Hantute-Ghesquier, Sencio and colleagues demonstrate that depletion of age-associated senescent cells decreases pulmonary viral load and ameliorates early and late lung COVID-19 in a hamster model of aging.
Cognitive dysfunction in aging is a major biomedical challenge without medical therapies. Here, Castner et al. show that longevity factor klotho enhances cognition in aged nonhuman primates, increasing its relevance for a therapeutic path to humans.
Solá, Mereu and colleagues describe a chronic inflammatory state in the aging mouse skin that is characterized by IL-17 production by dermal lymphoid cells and demonstrate the potential of inhibition of IL-17 signaling in protection against skin aging.
Regulatory T (Treg) cells have an important role in age-related diseases and inflammation; however, the underlying mechanisms are not fully understood. Li et al. identify a Treg-specific long noncoding RNA, Altre, that binds Yin Yang 1 to regulate liver Treg mitochondrial function in old mice. Altre deletion accelerates aging-associated liver pathogenesis.
Seegren et al. demonstrate that the mitochondrial calcium uptake complex is a key molecular apparatus that links age-related changes in mitochondrial physiology to systemic macrophage-mediated age-associated inflammation.