Volume 1 Issue 8, August 2021

Older adults are at high risk of suffering debilitating health effects from COVID-19. Effective communication of associated risks is therefore paramount. A new study finds that imagining a personalized disease transmission event amplifies perceived risk and bolsters risk-related information seeking in older age.

Cellular senescence and smooth muscle cells are key features of the atherosclerotic plaque; however, how senescent cells regulate smooth muscle cells is largely unknown. Herein, a new study in Nature Aging illuminates this interplay, providing insights into plaque dynamics and stability with potentially profound implications for heart attack and stroke.

This Review synthesizes recent research on the mechanisms and roles of autophagy in health, aging and disease and discusses how drugs that modulate the process of autophagy could be used to suppress age-associated diseases.

Rockwood and colleagues discuss how measuring the degree of frailty helps us understand how aging gives rise to the diseases of aging, and aids translation from comprehensive geriatric assessment and individual care plans to geroscience and back.

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.

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.

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.

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.

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.

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.