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The Muscle Aging Cell Atlas presents approximately 200,000 single-cell and single-nuclei transcriptomes from 17 human donors across different ages, uncovering mechanisms of aging in muscle stem cells, myofibers and microenvironment cells, and demonstrates parallels in mouse muscle aging.
Lipid changes across the lifespan and their role in health and longevity are incompletely understood. Here, Tsugawa and colleagues conduct untargeted lipidomics across 13 sample types and four ages in mice, considering sex and microbiome dependencies. This study provides a comprehensive resource of lipid changes with aging and highlights regulatory metabolic components, such as the enzyme UGT8, as potentially responsible for male-specific glycolipid biosynthesis in the kidney.
Todorov-Völgyi, González-Gallego et al. provide a proteomic profiling of brain endothelium during aging to unveil changes undetected in transcriptomic studies, identifying a dysregulation of proteins involved in vesicle-mediated transport pathways, most prominently Arf6.
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.
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.
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.
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.
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.
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.
This study identifies and characterizes evolutionarily conserved cytosine methylation patterns related to age across mammals and establishes pan-mammalian epigenetic clocks.
Microglia, the innate immune cells of the brain, exhibit diverse functions and can influence Alzheimer’s disease progression. This study explores human microglial diversity in Alzheimer’s disease, uncovering unique disease-associated microglial populations and predicting underlying gene regulatory networks.
Single-cell transcriptomic profiling of young and old mouse brains following heterochronic parabiosis shows regulation of several canonical hallmarks of aging by a shift in age-induced changes of the transcriptome in a cell-type-specific manner.
By applying quantitative chemical cross-linking technologies, the authors show that changes in the mitochondrial interactome of the skeletal muscle contribute to mitochondrial functional decline in female mice.
Zhao et al. find evolutionarily conserved astrocyte and microglia subpopulations shared across multiple brain regions and reveal similarities and differences between AD and PD glia and regional variance linked to AD pathology and neurodegeneration.
Single-cell transcriptomic data from a neurogenic region of the mouse brain were used to build aging clocks for specific neural cell types. These clocks showed that heterochronic parabiosis and exercise lead to distinct transcriptomic rejuvenation patterns across cell types.
This study identifies CSF proteins specifically dysregulated along the AD continuum that reflect the multifactorial nature of disease progression. Some of these CSF proteins were used to build biomarker panels with high diagnostic accuracies.
The hypothalamus controls homeostatic functions such as metabolism and sleep, which undergo age-related changes. Here the authors perform single-nuclei transcriptomics profiling of young and old hypothalamus from female mice and describe changes in gene expression with age, in particular increased expression of the X inactivation gene Xist.
Luo et al. report a single-cell landscape of human blood from newborn to frailty. Comprehensive profiling uncovers frailty-specific immune cells and gene expression signatures useful for formulating a clinically relevant screen for unhealthy aging.
The authors find extensive remodeling of the gut microbiome and blood metabolome in extremely long-lived individuals (94–105 years old) compared to their children (50–79 years old) and report distinct generation-specific and cross-generational associations with genetic and socioeconomic factors.
The authors measured blood cell telomere length in 474,074 participants of UK Biobank providing a major resource for assessing the role of this proposed marker of biological age in human health and disease.