Aging happens gradually, impacting our organs at different times, causing tissues to progressively wear down.
While aging is not a disease itself, it is a risk factor for Age-Related Diseases (ARDs) such as cardiovascular disease, osteoporosis, osteoarthritis, Alzheimer’s and Parkinson’s Disease, among others.
There is growing scientific opinion that studying the aging process, and how it works on the cellular level, can lead to benefits to our lifespan.
Just as importantly, understanding how aging works by studying cells, could benefit a longer healthspan, the time in our lives before ARDs when we are at optimal health.
How can studying the cellular process of aging benefit us all?
Cells are just like all of us. They are born, they age, and they die. When a cell comes to the end of its own cellular lifespan, it goes through a process of a cellular death, which we call apoptosis.
At the time of apoptosis, a cell has specific proteins that are released to ultimately destroy the DNA found in the cell’s nucleus.
The cell then reduces in size and activates the immune system by sending out distress signals.
This process summons macrophages, which act a little like the Pac Man character from video games—in effect gobbling up the former cells so that nothing is left behind.
However, that’s not what always happens.
Senescent or “Zombie” Cells
Our cells are dividing constantly, renewing our muscles, blood vessels, and especially skin and blood cells that turn over rapidly.
But in the process, chromosomes in cells lose their telomeres, the top portion of chromosomes that helps keep your genetic material protected and functioning.
When chromosomes have telomeres that are too short, a cell becomes “senescent.”
These senescent cells can’t perform the functions they once did when they were healthy, but for reasons scientists are currently studying, they do not go through apoptosis.
Our bodies can’t really get rid of them on their own, and when fully senescent they can’t divide and make new cells, so they start to impact the healthy cells around them, creating more senescent cells.
This is the reason senescent cells have earned the nickname “Zombie” cells—neither dead nor alive, but still causing cellular mayhem.
Zombie cells are in a sense frozen, making damaged or dysfunctional cells unable to pass on their genes to another generation. In balance, although biologically necessary, it may also come at a cost.
Because they don’t go away, these zombies continue to make trouble for the body by releasing SASP, a mixture of chemicals that gives rise to inflammatory signals that increase as we age.
Zombie Cells Infographic
For this reason, we call these signals “inflammaging” cytokines. The inflammaging signals can lead to oxidative stress, which impacts several biological functions that have been directly linked to more senescent cells accumulating as we age.
The intersection of cellular senescence and inflammaging cytokines has recently emerged as a crucial mechanism for slowing and one day possibly reversing the aging process.
There is increasing evidence that the clearance of senescent cells in animal models can possibly impact the progression of age-related disorders.
Clearing senescent cells, learning how to reprogram them, or better regulating inflammaging signaling, are potential strategies for combating ARDs and expanding the healthspan of humans.
Scientists are developing future drugs that can one day target and remove senescent cells.
But there are problems with this approach—we do not know yet the full health ramifications of complete removal of senescent cells, and the drug approval process is long, expensive, and far from assured.
So what can be done now?
Mammalian studies conducted at the Buck Institute for Research of Aging and the National University of Singapore suggest taking Calcium Alpha-Ketoglutarate (Ca-AKG) can in effect, help block the inflammaging signals of senescent cells.
Also, better lifestyle choices, such as cessation of smoking, increasing your level of activity/exercise and adopting a healthy diet and limiting exposure to external stressors (e.g., radiations, pollutants, and stress itself) can be the first line of defense against senescent cells, SASP, and inflammaging.
So, the next time you tune into your favorite cable TV show and watch how zombies are on the loose, remember that your body has its own armies of “undead cells” we need to combat as well.