top of page
Voltaire Staff

Our immunity may be the reason behind ageing




Anything that doesn’t kill me, makes me stronger. He may be right about several things, but Nietzsche was wrong here. The very thing that protects us, may be responsible for our slow decline into senescence.


A recent research studying the impact of our immune system on ageing shows that a key mechanism that fires up our immune system against outside pathogens may be responsible for inflammation of our organs –operationally defined as ageing by biologists.


Researchers at Ecole Polytechnique Federale De Lausanne studied the impact of cGAS–STING pathway – a key mechanism that fires up immune response in our brain – by blocking its reception in mice and in vitro to conclude that the blockade resulted in a scaling down in inflammation in organs and improved tissue function -- in short, a moratorium on ageing.

"Blockade of STING suppresses the inflammatory phenotypes of senescent human cells and tissues, attenuates ageing-related inflammation in multiple peripheral organs and the brain in mice, and leads to an improvement in tissue function," read the paper published in Nature.


"In parallel to the reduction in inflammatory cytokines, STING-inhibited animals showed reduced inflammatory cell accumulation in the kidneys, associated with reduced levels of kidney damage markers (creatinine, urea) and reduced numbers of macrophages in white adipose tissue…," it read.


The paper also shows that experiment conducted on naturally ageing mice that activation of cGAS–STING signalling is an essential contributor to the ageing-related type I IFN response in microglia to direct neuronal loss and cognitive impairment, which may lead to brain conditions such as Alzheimer’s and dementia.


"Our findings establish the cGAS–STING pathway as a driver of ageing-related inflammation in peripheral organs and the brain, and reveal blockade of cGAS–STING signalling as a potential strategy to halt neurodegenerative processes during old age," the researchers said.

Comments


bottom of page