Washington: In a new study, researchers have shown that cells that do not have the ability to divide like neurons in the brain, follow the same molecular pathway that reacts to cell damage and stems the cell’s ability to divide – known as cell senescence.
The ageing process has its roots deep within the cells and molecules that make up our bodies.
This new finding by a team of scientists at Newcastle University, led by Professor Thomas von Zglinicki challenges previous assumptions on cell senescence and opens new areas to explore in terms of treatments for conditions such as dementia, motor neuron disease or age-related hearing loss.
“We want to continue our work looking at the pathways in human brains as this study provides us with a new concept as to how damage can spread from the first affected area to the whole brain,” Professor Zglinicki said.
Working with the University’s special colony of aged mice, the scientists have discovered that ageing in neurons follows exactly the same rules as in senescing fibroblasts, the cells which divide in the skin to repair wounds.
DNA damage responses essentially re-program senescent fibroblasts to produce and secrete a host of dangerous substances including oxygen free radicals or reactive oxygen species (ROS) and pro-inflammatory signaling molecules.
This makes senescent cells the ‘rotten apple in a basket’ that can damage and spoil the intact cells in their neighborhood. However, so far it was always thought that ageing in cells that can’t divide - post-mitotic, non-proliferating cells - like neurons would follow a completely different pathway.
Now, this research explains that in fact ageing in neurons follows exactly the same rules as in senescing fibroblasts.
“We will now need to find out whether the same mechanisms we detected in mouse brains are also associated with brain ageing and cognitive loss in humans. We might have opened up a short-cut towards understanding brain ageing, should that be the case,” Professor Zglinicki added.