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This study demonstrates that the burden of protein-truncating variants identified through population-scale exome sequencing impacts how long we live. The authors report four distinct human lifespan genes with roles in cancer and clonal hematopoiesis.
Age-related cataracts are characterized by clouding of the eye’s lens and cause vision impairment or loss. Here the authors develop a retinal photograph-based deep-leaning method to detect visually significant cataracts and report that it detects cataracts with similar accuracy to ophthalmologists.
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.
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.
Using more than 100 independent iPSC lines derived from patients with Alzheimer’s disease, the authors discovered loci associated with the neuronal production of amyloid β and confirmed their influence using RNA interference.
The authors show that eye-drop administration of an NAD+ precursor ameliorates age-associated meibomian gland dysfunction, a leading cause of dry eye in older individuals, by (re)activating intracrine steroidogenic activity.
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.
This study shows that SARS-CoV-2 infection induces paracrine senescence in adjacent uninfected cells via virus-induced cytokine secretion. This resulted in a persistent inflammatory response associated with senescence even after SARS-CoV-2 disappearance.
Life expectancy gains have prompted a planned rise in state pension ages in a number of countries but may not be matched by an extension in healthy working lives. Here the authors project healthy working life expectancy in England to the year 2035 and forecast a lesser increase than the projected gains in life expectancy.
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.