We don’t exactly know why we age; we know what aging looks like —the “symptoms”, so to speak— but the root causes remain foggy. One leading hypothesis is that the changes associated with old age, both external and internal, are a result of accumulating DNA damage. As this damage builds, cellular functions begin to break down and important pathways start going haywire.

One of the most extreme forms of DNA damage is the double-strand break, which happens when a strand of DNA snaps in half, leaving two separate slivers floating around. Left unfixed, these strands can snag at and break chromosomes, leading to diseases like cancer and other disorders. But how the body repairs this kind of wreckage has been a source of mystery. Now, scientists at the Dresden University of Technology have managed to shine a light on the process. Published in Cell, their work offers important new insights that may eventually help treat, and possibly reverse, DNA damage.

The capacity of intestinal stem cells to maintain cellular balance in the gut decreases upon ageing. Researchers at the University of Helsinki have discovered a new mechanism of action between the nutrient adaptation of intestinal stem cells and ageing. The finding may make a difference when seeking ways to maintain the functional capacity of the ageing gut.

The cellular balance of the intestine is carefully regulated, and it is influenced, among other things, by nutrition: ample nutrition increases the total number of cells in the gut, whereas fasting decreases their number.

The relative number of different types of cells also changes according to nutrient status.

Endothelial cells line at the most inner layer of blood vessels. They act to control hemostasis, arterial tone/reactivity, wound healing, tissue oxygen, and nutrient supply. With age, endothelial cells become senescent, characterized by reduced regeneration capacity, inflammation, and abnormal secretory profile. Endothelial senescence represents one of the earliest features of arterial ageing and contributes to many age-related diseases. Compared to those in arteries and veins, endothelial cells of the microcirculation exhibit a greater extent of heterogeneity. Microcirculatory endothelial senescence leads to a declined capillary density, reduced angiogenic potentials, decreased blood flow, impaired barrier properties, and hypoperfusion in a tissue or organ-dependent manner.