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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.
Multiple lines of research show that NAD+ has an important role in ovarian aging; however, the role of NAD+ consumption during ovarian aging is incompletely understood. Here the authors study the role of the NADase CD38 to show that CD38 expression increases and NAD+ levels decrease with age in mice, and that CD38 deletion ameliorates ovarian aging.
To analyze neuronal aging in Huntington’s disease, Lee et al. perform direct neuronal reprogramming of longitudinally aged human fibroblasts, uncovering RCAN1 as a therapeutic target to promote neuronal resilience through chromatin reconfiguration.
Using C. elegans, Oleson et al. demonstrate that developmental exposure to reactive oxygen species protects against amyloid toxicity later in life, mediated by disruption of the H3K4me3 epigenetic machinery through HSF-1-dependent shifts in lipid metabolism.
The authors present the results of a phase 2 study of gosuranemab, a monoclonal antibody targeting N-terminal tau, in patients with early Alzheimer’s disease. Gosuranemab was safe and well tolerated, but the clinical efficacy endpoint was not met.
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.
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.
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.
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.
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.
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.
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.
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.
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.