Three links in aging and longevity #3

Grandmothers, longevity, proximity; three cheers for Grandmothers!

‘Grandmother effect’ helps explain human longevity

Two new studies, both published in Current Biology, strengthen this notion. An analysis of church birth and death records in Finland for individuals born between 1731 and 1890 showed that having a maternal grandmother between 50 and 75 years of age while a grandchild was 5 years old or younger increased the child’s survival. The effect disappeared for grandmothers older than 75 years of age, possibly because they may not have been be able to help with child rearing. The effect on longevity was seen mostly with maternal grandmothers and not paternal grandmothers.

The second study drills down into this effect, showing that it is not just the existence of a grandmother, but her proximity that matters. The shorter the distance between grandmother and grandchild, the more involved the grandmother can be and the more benefits that accrue to her daughter and grandchildren.

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What can be learned from a single-cell RNA-seq and shotgun proteomics study on the aging lung? Single-cell RNA-seq on n=15 mice, k= 14,813 cells (7672 young, 7141 old), ~30 distinct cell types. Shotgun proteomics data of 4 replicates of young (3 months) & old mice (24 months).

An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics

Aging promotes lung function decline and susceptibility to chronic lung diseases, which are the third leading cause of death worldwide. Here, we use single cell transcriptomics and mass spectrometry-based proteomics to quantify changes in cellular activity states across 30 cell types and chart the lung proteome of young and old mice. We show that aging leads to increased transcriptional noise, indicating deregulated epigenetic control. We observe cell type-specific effects of aging, uncovering increased cholesterol biosynthesis in type-2 pneumocytes and lipofibroblasts and altered relative frequency of airway epithelial cells as hallmarks of lung aging. Proteomic profiling reveals extracellular matrix remodeling in old mice, including increased collagen IV and XVI and decreased Fraser syndrome complex proteins and collagen XIV. Computational integration of the aging proteome with the single cell transcriptomes predicts the cellular source of regulated proteins and creates an unbiased reference map of the aging lung.


Another mouse study suggesting in plain English that brain stem cells can be rescued  from being eliminated with age by staying molecularly quiet and go under the radar. This way they can still be triggered to take up the old posts again and regenerate. Good news.

Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain

  • Time-dependent stem cell depletion levels off in the old brain via increased quiescence
  • Age minimally changes the neural stem cell transcriptome
  • Once-activated neural stem cells perform similar in the old and young brain
  • The old niche keeps stem cells quiescent via inflammation and Wnt activity regulation