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A systematic review examining evidence from 32 studies across five countries on associations between care home ownership and COVID-19 found that for-profit care homes were linked to worse COVID-19 outcomes (infections and mortality) compared to non-profit and public sector homes.
Using live imaging, the study shows, in mice, that epithelial cells escape from the hair follicle stem cell compartment during aging. Stem cell escape is associated with reduced cell adhesion and extracellular matrix gene expression and leads to hair follicle miniaturization.
Transient expression of the pluripotency factors Oct4, Sox2, Klf4 and c-Myc can mitigate the effects of stem cell aging on tissue health. Neumann and colleagues show that Myc expression alone converts aged oligodendrocyte progenitor cells into neonatal-like cells, and is sufficient to enhance central nervous system regeneration in an otherwise aged environment.
Aging is the most important risk factor for breast cancer in women without genetic mutations. Shalabi and colleagues now show that histologically normal mammary epithelial cells genetically predisposed to cancer exhibit features of accelerated aging, such as the loss of cell lineage markers, differentiation defects and transcriptome-wide enrichment of expression of genes related to aging and inflammation.
As part of Myeloid Cells in Neurodegenerative Disease (MyND) initiative, the authors profiled the transcriptome of primary monocytes and microglia from patients with Parkinson’s disease and controls, revealing the pathways and genes that are altered in the immune system of patients with Parkinson’s disease.
Aged mesenchymal stem cells exhibit decreased osteogenesis. Pouikli et al. link impaired MSC differentiation to histone hypoacetylation caused by lower mitochondrial acetyl-CoA export due to enhanced lysosomal degradation of the citrate carrier Slc25a1. Restoring histone acetylation to youthful levels rescues osteogenesis.
In this whole-exome sequencing study of the largest centenarian cohort to date, Lin et al. demonstrate that conserved pathways—for example, IIS and AMPK signaling—are as relevant to human longevity and healthy aging as they are in worms, flies and mice.
Changes in hair and skin can be the most obvious and earliest signs of aging. The authors report that skin and hair follicle stem cell (HFSC) aging is driven by stress-induced upregulation of miR-31, which targets Clock to activate MAPK/ERK and deplete HFSCs via transepidermal elimination. Blocking the pathway with MAPK/ERK inhibitors protects against skin aging.
The gut microbiome can change with age and influence aging-related diseases systemically, including in the brain. The authors show that rejuvenation of the gut microbiome by fecal microbiota transplantation from young mice reverses aging-induced deficits in the hippocampal immune system, metabolome and transcriptome, and rescues selective cognitive deficits.
The authors report whole-blood RNA-seq for 4,871 samples from 1,570 participants in the Parkinson Progression Marker Initiative. This Resource documents blood-based transcriptomic changes associated with PD, including early increases in neutrophil gene expression with a decrease in lymphocytes.
A cognitive intervention study for communicating information about COVID-19 transmission risk found that older adults tended to forget numerical information but reported increased perceived risk after imagining a personalized scenario with social consequences.
In a mouse model of atherosclerosis, Childs and colleagues show that senescent cells inhibit the promigratory phenotype switching of vascular smooth muscle cells by secreting IGFBP3 and that senolysis promotes the repair of fibrous caps in advanced lesions.
The authors show that aged mammalian stem cells produce aberrant transcripts due to profound yet characteristic changes to chromatin during aging, a phenomenon only previously known to occur in simple invertebrate models, limiting their lifespan.
Lu and colleagues generated a transcriptomic, lipidomic and metabolomic atlas of primary bone-marrow mouse neutrophils with organismal aging and across biological sexes, revealing lifelong sex-dimorphic neutrophil functional regulation.
From the blood immunome of 1,001 individuals aged 8–96 years, the authors used deep learning to develop an inflammatory clock of aging (iAge) that tracks with multimorbidity, immunosenescence, frailty and cardiovascular aging, and is also associated with exceptional longevity in centenarians. The main contributor to iAge is the chemokine CXCL9, which is shown to control endothelial cell senescence and function.
The authors show that glial AP1 is initially protective after traumatic brain injury (TBI) but remains active chronically, driving tau pathology and degeneration. Glial AP1 similarly activates with normal aging, suggesting this may be accelerated by TBI.
An economic analysis suggests that targeting aging offers potentially larger economic gains than eradicating individual diseases. Slowing aging to increase life expectancy by 1 year is worth US$38 trillion, and by 10 years, US$367 trillion.
Facility-level factors associated with increased mortality rates among nursing home residents in Spain during the COVID-19 pandemic included a higher proportion of patients with complex diseases, lower scores on pandemic preparedness measures and higher COVID-19 incidence levels in the surrounding neighborhood.
Morshed et al. analyzed the proteome and phosphoproteome of brain tissue from patients with Alzheimer’s disease. The analysis of patient heterogeneity links glia pathologies and signaling pathways to stages of disease progression.
The authors present the results of a 24-month phase 2 study of AADvac1, a tau vaccine against Alzheimer’s disease. AADvac1 was safe and induced high levels of antibodies. In the whole study sample, there were no significant changes on clinical outcomes.