Volume 2 Issue 2, February 2022

Plasma biomarkers pertaining to the underlying pathophysiology of Alzheimer’s disease have recently become available (for example, amyloid beta and phosphorylated tau). The utility of these markers poses a question for clinicians (now and in the future): are plasma biomarkers for Alzheimer’s disease are ready for clinical use at this time?

As the elderly population continues to grow exponentially, dry eye disease is becoming increasingly common. In this issue, Sasaki and colleagues identified a NAD⁺-regulated steroidogenic pathway in the eye that supports the normal function of meibomian glands, and show that increasing the availability of NAD⁺ can alleviate the dry eye phenotype of aged mice.

Vascular senescence has been implicated in atherosclerosis. By characterizing SNPs in the p16-encoding CDKN2A/B locus, a new study in Nature Aging identifies CUX1 as a binding protein of an atherosclerosis-associated functional SNP, which activates CDKN2A expression and senescence in endothelial cells, thus providing a mechanism of transcriptional senescence regulation.

Telomeres, the caps of chromosomes, shorten with age. Using qPCR, Nilhesh Samani, Veryan Codd and colleagues measured leukocyte telomere length in close to half a million individuals from the UK Biobank, confirming several previous associations. This dataset offers many new opportunities to explore associations between leukocyte telomere length and other traits relevant to human aging and health.

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.

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.

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 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.

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.

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.