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A metagenomic study of gut, oral and skin microbiota describes a pattern of microbial dysbiosis in more frail institutionalized older adults and identifies the skin as the major reservoir of pathogenicity.
Splicing dysfunction has been observed in Alzheimer’s disease but it remains unclear whether splicing defects have a causal role. Here the authors generate a mouse model with perturbed U1 snRNP activity, recapitulating RNA splicing defects, neuron hyperexcitability, neurodegeneration and synergy with the amyloid cascade when crossed with 5xFAD mice.
Skin thickness and bone density decrease with age; however, the interactions between skin and bone during aging are unclear. Here the authors show that cystatin-A is a skin-derived protein that decreases with age and causes age-related bone loss. Further, topical application of calcipotriol stimulates cystatin-A production in the skin and alleviates bone loss.
One in ten older adults in Canada are victims of elder abuse each year. Older adults with lower physical, mental or cognitive health or history of child maltreatment have elevated risk, while greater social support is protective against this issue.
In this multi-omics study, the authors identified C1q-dependent synapse elimination by both astrocytes and microglia in Alzheimer’s mouse models. While astrocytes preferentially removed excitatory synapses, microglia preferred inhibitory synapses.
RNA splicing has a role in aging and longevity, but the mechanisms involved are incompletely understood. Here the authors show that mRNA splicing components, RNP-6 and RBM-39, act in concert to regulate intron retention, inhibit mTORC1 signaling and prolong life in Caenorhabditis elegans.
Sexual interactions with males shorten the lifespan of the opposite sex in several species, including Caenorhabditis elegans, but the mechanisms are not fully understood. Here the authors use transcriptomic profiling in C.elegans to systematically identify the genetic pathways involved in male-induced demise, which include upregulation of a conserved ion channel that regulates fat metabolism.
With age, muscle stem cells have been reported to undergo a quiescence-to-senescence switch, thus reducing regenerative capacity. Here, using in vitro and mouse models, Guerrero et al. report that treatment with 3-deazaadenosine alleviates senescence and preserves the regenerative potential of muscle and hematopoietic stem cells.
A key challenge for repurposing the licensed drug rapamycin for geroprotection is to avoid side effects from chronic dosing regimens. The authors show in model organisms that a brief administration of the drug early in adulthood has long-lasting beneficial effects that are similar to lifelong treatment.
Goldman et al. demonstrate that meningeal lymphatic vessels play a role in sickness behavior. The authors also find that age-related lymphatic dysfunction increases susceptibility to sickness and that enhancement of meningeal lymphatic function improves movement in sick, aged mice.
The authors introduce a high-throughput machine-learning-based visual frailty index for mice that operates on video data from an open-field assay. The machine-vision-based approach extracts various morphometric and behavioral features from video to model frailty score and age.
Senescent cells are typically identified by a combination of senescence-associated markers, and the phenotype is heterogeneous. Here, using deep neural networks, Heckenbach et al. show that nuclear morphology can be used to predict cellular senescence in images of tissues and cell cultures.
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.