Blog , Health and Wellness

We Are Living Longer Than Ever. Medical Science Might Help Us Enjoy The Extra Years

Posted on Monday, December 20, 2021
by AMAC, John Grimaldi

WASHINGTON, DC, Dec 20 – Do you want to live to the ripe old age of 150?  According to the Statista Website, the average human lifespan in the U.S. these days is 78.9 years, thanks to modern medicine. Some scientists who focus on aging will tell you that future treatment breakthroughs might help us to live well beyond 150. 

Sergey Young, the founder of the Longevity Vision Fund, is not a physician; he’s an investor who bets on the notion that there is a market for longer lifespans.  As he puts it, “My mission is to help one billion people around the world to extend their healthy lifespans … For the time being, due to wear and tear, the human body doesn’t typically last much beyond 100 years. However, revolutionary approaches in medicine will push boundaries of what was previously thought possible and offer solutions to renew and replace our body parts.”

In fact, medical scientists may have already discovered one such revolutionary approach – a way to stop what is known as “zombie cells” in our bodies. They are scientifically known as senescent cells – “normal cells that have stopped multiplying but don’t die.  Instead, they stick around like ‘undead zombies’ and release chemicals that can trigger inflammation in surrounding healthy cells.  Senescence can be caused by a number of factors, including the general wear and tear of the cell’s genetic material that occurs with each successive division, as well as wider DNA damage.  A 2011 study found that eliminating these senescent cells delays age-related illnesses and later studies confirmed that removing them can alleviate, and perhaps even prevent, certain illnesses,” according to the science Website IFL Science.

A team of Japanese researchers may have found a way to eliminate those nasty zombie cells; they say they’ve developed a vaccine that targets the zombie cells that accrue in our bodies as we age and are responsible for a variety of age-related illnesses such as arterial stiffening and diabetes.  They tested their experimental vaccine on mice with a similar type of arterial thickening that occurs in aging humans, and it not only improved the stiffening, but it also “prolonged the lifespan of mice with premature aging.”

It is interesting to note that research on cellular senescence is an avenue of study of perhaps one of the most dreaded age-related illnesses, Alzheimer’s Disease.  In a recent paper entitled, Cellular senescence at the crossroads of inflammation and Alzheimer’s disease [AD], by Drs. Ana Guerrero, Bart De Strooper, and I. Lorena Arancibia-Cárcamo at the UK Dementia Research Institute, noted that: “Senescence emerges as a pivotal player in the complex cellular landscape of Alzheimer’s disease.  The senescence secretome constitutes a promising therapeutic target to balance neuroinflammation during AD progression. Aging is a key risk factor for Alzheimer’s disease, but the reasons for this association are not well understood. Senescent cells accumulate in aged tissues and have been shown to play causal roles in age-related pathologies through their proinflammatory secretome. The question arises whether senescence-induced inflammation might contribute to AD and bridge the gap between aging and AD.”

Meanwhile, researchers at the University of Texas Health Science Center at San Antonio report that there is a link between cellular senescence and 20 types of human brain diseases – most notably Alzheimer’s.  They used middle-aged Alzheimer’s mice to test a combination of drugs to clear senescent cells from their brains.

Research health scientist Miranda E. Orr, Ph.D., reported that “The mice were 20 months old and had advanced brain disease when we started the therapy.  After clearing the senescent cells, we saw improvements in brain structure and function. This was observed on brain MRI studies (magnetic resonance imaging) and postmortem histology studies of cell structure. The treatment seems to have stopped the disease in its tracks.”

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