But, Monsonego found in tests on mice that a set of white blood cells, named cytotoxic T helpers, can identify and destroy these senescent cells.
The team's research focused on the longevity of 'super centenarians' in Japan (Getty Images)Getty Images
He told The Times of Israel: "The immune system deteriorates with time, and that process may dictate the pace of ageing.
"We know that with ageing, you get more inflammation and a less capable immune system. We were curious to know why.
“We found these cytotoxic T helper cells can be very effective in reducing the burden of senescent cells, allowing tissues to regenerate and recover
"No one ever did that before, we were pioneers in identifying, in detail, the dynamic changes of cytotoxic T helper cells in ageing mice.
"This is when we realised the surprising and significant accumulation of these cells, without these cells, the mice lived shorter lives.
"We hope this research will lead to diagnostic tools and then therapy treatments to track and improve healthy ageing."
However, Monsonego emphasised that this breakthrough is no silver bullet.
"For most of us, it depends on how we live. Increasing your lifespan means being aware that you need to work hard at it. You need to make sure that you have a good diet and exercise," he said.
"People need to change their lifestyle early enough, before they develop a chronic disease. Medicine alone can’t do magic.”
Instead of thinking only of lifespan, he encouraged people to consider their “health span” when it comes to ensuring a more fulfilling later life.
He went on: “When you say ‘ageing,’ people think of their seventies, but it actually starts much earlier.
"If you want to preserve health span, you need to start early.
"It’s not enough to live to 90 with five different diseases. We need to think about living healthy, not just living long."
The findings have been published in Natural Ageing, a peer-reviewed journal, by Monsonego’s lead researcher, Dr Yehezqel Elyahu, in collaboration with Professor Esti Yeger-Lotem, also from Ben-Gurion, and Professor Valery Krizhanovsky of the Weizmann Institute of Science.
Asya Rolls, a professor of neuroscience at Tel Aviv University, who was not involved in the study, told The Times of Israel that the conclusions suggest that “ageing might be more controllable than we thought”.
"Strengthening this natural immune mechanism could eventually open new ways to slow down age-related decline and keep tissues healthier for longer.”
Professor Eran Perlson (C) of Tel Aviv University (Tel Aviv University)[Missing Credit]
It comes after a team at Tel Aviv University, working jointly with Ben-Gurion University and the Weizmann Institute, recorded a potentially major breakthrough in the treatment of Motor Neurone Disease (MND), also known as amyotrophic lateral sclerosis (ALS).
The team was able to identify a particular strand of Ribonucleic acid (RNA), a vital molecule used in most of the body’s biological functions, that can combat the degenerative effects of MND/ALS, specifically the damage it causes to nerve cells, which leads to loss of motor function in patients.
"When we added a specific RNA molecule to human cells and animal models for ALS, the nerve cells stopped degenerating and even regenerated”, Professor Eran Perlson told The Times of Israel.
The team’s previous work had identified a protein, known as TDP-43, which forms toxic clusters on nerve cells in MND patients, but helps to regulate protein-making in healthy people.
This most recent study identified the agent that causes TDP-43 to go rogue, a different molecule called microRNA-126. When there is not enough microRNA-126 in the body, too much TDP-43 is produced, which can cause debilitating symptoms
The researchers found that adding extra microRNA-126 to tissues from MND patients and to mice injected with the disease was able to mitigate and even reverse the neurodegenerative effects.
Next, they want to take their findings and apply them to clinical trials. If successful, it would represent remarkable headway for a disease that has historically been extremely difficult to treat.
"We wanted to get to the root of the matter of what causes ALS to enable the development of effective drugs for this incurable disease,” Perlson added.
