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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 used limited proteolysis–mass spectrometry to assess changes in protein structures in mouse CSF with aging. They identified changes in proteins that correlated with cognition and Alzheimer’s disease in humans, including Cd5l/AIM and 14-3-3 proteins.
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.
The authors find that higher adherence to a healthful plant-based diet is associated with a decreased risk of mortality among older adults in China, whereas unhealthful plant-based dietary patterns are associated with increased mortality risk.
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.
In a cerebral amyloid angiopathy rat model, the authors show that spinal fluid moves more rapidly but partly bypasses the brain, thereby reducing and delaying waste removal via the glymphatic and lymphatic systems.
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.