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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.
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.
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.
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.
The authors show that pink1-mutant flies display intestinal dysfunction and that suppression of Relish, an innate immune response mediator, in the gut rescues mitochondrial dysfunction and cell death in the brain.
Apolipoprotein E (APOE) is a lipoprotein particle component and is genetically linked to human longevity and Alzheimer’s disease; however, the mechanisms that link APOE and aging are incompletely understood. Here, Zhao et al. show that APOE drives cellular senescence in aged human mesenchymal progenitor cells by destabilizing heterochromatin.
Immune function decreases with age, leading to increased risk of infectious disease. The authors show that N-glycan branching increases with age in females more than in males as a result of a sex-dimorphic increase in N-acetylglucosamine and interleukin-7 signaling. Reversing elevated branching reduced infection severity in aged female mice.
In vivo partial reprogramming by expression of Oct4, Sox2, Klf4 and c-Myc has been shown to have rejuvenating effects in a mouse model of premature aging. Here, the authors report that longer-term partial reprogramming regimens are safe and effective in delaying age-related changes in physiologically aged mice.
The authors compared muscle metabolomes of young and older adults with different muscle health and physical activity levels. They found that aging was characterized by lower levels of NAD+ that were correlated with activity levels and muscle function.
The molecular mechanisms that regulate senescence are incompletely understood. Here the authors couple high-throughput mapping of disease-associated functional SNPs (fSNPs) with proteomics analysis of fSNP-binding proteins to identify the transcription factor CUX1 as an activator of p16 expression and a regulator of senescence.
Osteoarthritis (OA) leads to joint degeneration, including the progressive loss of articular cartilage. Here the authors show that kindlin-2 expression is decreased in degenerate cartilage and that its overexpression decelerates the progression of OA in mice.
During aging, the ability of skeletal muscle to repair itself declines, in part due to a decrease in muscle stem cells. Here, the authors report that muscle stem cells that accumulate mitochondrial damage fuse with existing muscle fibers in a manner that depends on the induction of Scinderin.
Many aging-related phenotypes share a common genetic component, but to disentangle disease-specific variants from aging-specific ones has been challenging. Here Timmers et al. combined several genetics studies of aging-related traits to identify common underlying genetic factors that contribute to aging.