Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Somatic mutations accumulate with age; however, the role they have in cardiac aging is unclear. Here Choudhury et al. describe the somatic mutation landscape of human heart muscle cells by single-cell whole-genome sequencing and report mutational signatures indicative of increased oxidative DNA damage and failed repair.
A new population of dysfunctional astrocytes in the aging mouse hippocampus called autophagy-dysregulated astrocytes (APDAs) show impaired protein homeostasis and defective regulation of synapse formation and elimination and appear early in a mouse model of Alzheimer’s disease.
Measuring the rate of aging holds potential for capturing heterogeneity in aging. Here, the authors use longitudinal trajectories of aging phenotypes in the Baltimore Longitudinal Study of Aging and create a longitudinal phenotypic score that is associated with accelerated decline in health and physical and cognitive function.
This study finds that sST2 is a disease-causing factor for Alzheimer’s disease. Higher sST2 levels impair microglial Aβ clearance in APOE4+ female individuals. A genetic variant, rs1921622, is associated with a reduction in sST2 level and protects against AD in APOE4+ female individuals.
Epigenetic clocks are widely used aging biomarkers, but their utility is limited by technical noise. The authors report a method for producing high-reliability clocks for applications such as longitudinal studies and intervention trials.
Senescent cells accumulate with age and contribute to the functional decline of many tissues; however, their role in skeletal muscle is not well understood. Here the authors comprehensively assess cellular senescence in skeletal muscle of young and old mice and detail senescence features in subpopulations of p16+ fibroadipogenic progenitors and p21+ myofibers.
Aging is associated with a decline in stem cell function and impaired tissue homeostasis; however, the mechanisms that lead to the loss of stem cells are incompletely understood. Here the authors show that aging-associated skin vasculature atrophy causes dermal stiffening that leads to epidermal stem cell dysregulation.
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.
Transcription factors control cell identity and function in health, disease and aging. Here the authors identify age-associated changes of transcriptional regulatory networks in single cells, revealing cell-type and tissue-type-independent patterns in key pathways, including circadian rhythm, antigen processing, collagen processing and inflammation.
This study shows that during the first wave of SARS-CoV-2 infection in England, residents of long-term care facilities who survived infection developed a robust and stable immunity against the virus that did not negatively impact responses to other seasonal viruses.
Epigenetic clocks can measure biological aging, but the relationship between epigenetic age and other hallmarks of aging is incompletely understood. Here the authors show that epigenetic age is associated with nutrient sensing, mitochondria activity and stem cell depletion but distinct from cellular senescence, telomere attrition and genomic instability.
This study shows that the cellular pathway that removes dysfunctional mitochondria, mitophagy, becomes impaired in the aged fly brain. Inducing mitophagy in the aging brain prolongs health and lifespan, while slowing both muscle aging and gut aging.
The authors developed a deep learning-based model to estimate the brain age gap based on metabolic and structural imaging data in cognitively normal individuals and in patients with dementia. An older brain age was associated with Alzheimer’s disease biomarkers and was predictive of future cognitive decline.
The authors show that FOXM1 transcription factor transgene induction in Hutchison–Gilford progeria and naturally aged mice significantly extends their lifespan via restoring the loss of Foxm1 function with age that contributes to the aging phenotypes.
Change in sleep patterns is an important feature of the aging process. This study shows that sleep duration is nonlinearly associated with mental health and cognition measures in the 38- to 73-year-old population, with underlying brain and genetic mechanisms.
This study shows that body mass indexes (BMIs) in the overweight or mild obesity range are associated with a decreased risk of mortality in the oldest old in China, supporting the notion that optimal BMIs are age dependent and challenging national and international guidelines on healthy BMI.
The authors used PET imaging to stage individuals according to the Braak neuropathological system for Alzheimer’s disease. PET stage was associated with biomarker and cognitive changes, highlighting the potential to stage Alzheimer’s disease in living people.
Using single-cell and spatial transcriptomics, the authors identified several aging-associated and oxidized phosphatidylcholine-associated changes in microglia in the spinal cord, including an increase in osteopontin that contributed to neurodegeneration and neuroinflammation.
This study investigated trajectories of depressive symptoms associated with several health conditions using a sample of over 19,000 older adults. The presence of depressive symptoms was associated with poor health prognosis and increased mortality.
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.