For today’s video, I’ve scoured the latest news coming out of the field of longevity
and rejuvenation biotechnology, and these are the stories that I’ve curated, especially
for you.
So stay tuned, I’ll be right back.
Today, we’ll start out by taking a look at a resource that’s already present in
our own tissue that could be co-opted for use as a senolytic.
We’ll also examine a new gene sequencing technique that has challenged the theory that
cellular mutations are driven by cell division.
And finally, and I’m really excited about this, we’ll be taking a close look at resilience,
a new biomarker for aging that can be measured and tracked over time, and a new app that
will do just that.
Let’s get started.
A new study that was just published in May provides an interesting take on cellular senescence.
As you know, cellular senescence is responsible for many age-related, chronic diseases, and
clearing them out using senolytics is a major form of longevity therapy.
Usually, the senolytic does this by inducing apoptosis, or programmed cell death, forcing
the senescent cell to die and be cleared out by the immune system.
Researchers reported that, in mice at least, reawakened immune cells do the same thing.
They found that activation of invariant natural killer T-cells, also known as iNKT cells,
will eliminate senescent cells.
Now, scientist have known for a while now that the failure of immune surveillance mechanisms
to identify and remove senescent cells is what drives the progression of disease.
But the identity of the surveillance mechanism that mediated the clearance of senescent cells
wasn’t evident.
They didn’t know what it was.
So the researchers used “lipid antigen presentation,” whatever that is, to activate iNKT cells.
And they found that this can constitute an immunosurveillance system capable of being
manipulated to clear senescent cells.
In two different senescent-cell disease models, activation of these iNKT cells was sufficient
to both clear out senescent cells and to confer disease improvement.
In obese mice, they found that the removal of senescent cell by iNKT cells improved glucose
control.
In the other disease model, removal of senescent cells also decreased lung fibrosis and improved
survival.
The also found that human iNKT cells were “preferentially cytotoxic to senescent lung
fibrosis.”
Meaning that they cleared those puppies right out.
This is really interesting news, because it means that we may house powerful senolytics
in our own bodies since iNKT cells are already present in most tissue…all we have to do
is activate them.
A lot more research is required, but these results should pave the way for senolytic
therapies that target these cells and their method of activation.
Scientists and researchers have known for some time now that genetic changes, known
as somatic mutations, occur in our cells as we age.
But the current level in technology has not been accurate enough to examine new mutations
in non-dividing cells, which constitute the majority of cells in our bodies.
This means that it’s been impossible to observe somatic mutations accurately.
So, researchers at the Wellcome Sanger Institute developed a new method of genetic sequencing,
called nonorate sequencing, or NanoSeq, that makes it possible to examine changes to our
genome with accuracy that was previously unattainable.
They were able to improve accuracy down to less than 5 errors per billion letters of
DNA.
They then applied this new technology to the study of somatic mutations, and they discovered
something unexpected.
They studied samples of blood, colon, brain and muscle tissue, and they compared the rates
and patterns of mutation in these non-dividing, somatic cells to the same rates and patterns
of mutation in stem cells, which do divide.
They looked at slowly dividing stem cells in blood, and at more rapidly dividing progenitor
cells.
They looked at non-dividing neurons and at rarely dividing muscle cells.
And they were surprised by what they found.
The number of mutations across all these different types of cells were about the same, and they
discovered that mutation can accumulate throughout the life of a cell, even without cell division.
So, if genetic mutations happen equally across all types of cells, even those that don’t
divide at all or rarely divide, that challenges the idea that cell division is the primary
mechanism driving genetic mutations.
Now, I’m sure that this study is going to drive a lot more research, and if true, it’ll
mean some changes in theory of genomic instability.
Alright, I’m pretty excited about this last story and it’s about a new biomarker for
aging called resilience.
Russian researchers from a Singapore-based company called Gero recently published a paper
in Nature Communications.
They conducted a longitudinal study, which is one where they take repeated observations,
or measurements, of the same variables over an extended period of time.
And they found that resilience, or the ability to recover in response to stress, can be accurately
measured and that it’s linked to the development of chronic disease and elevated risk for all-cause
mortality.
Now, leading scientists in the field of longevity have hailed this new study, scientists like
Brian Kennedy and David Sinclair, who said, “The investigation shows that recovery rate
is an important signature of aging that can guide the development of drugs to slow the
process and extend healthspan.”
Think of it like this: The older we get, the more time it takes to recover after we experience
some form of stress.
This can be called our resilience, and a decline in resilience has long been associated with
the aging process.
But this new research seems to show that resilience is a quantifiable, measurable biomarker for
aging.
And that this biomarker might hold the key to the development of strategies designed
to increase human lifespans…dramatically.
After studying several thousand subjects, they found that, on average, the time that
it takes for our bodies to return to the “equilibrium baseline level” after stress, is about 2
weeks.
Now, that’s in 40 year old, healthy adults.
By the time we reach our 80’s, that time to recovery has grown to about 6 weeks.
Now, if this trend holds throughout our lives, then they can extrapolate a complete loss
of human body resilience by around the age of 120 to 150 years.
And THAT, is an indication of the current limit of the human lifespan.
This reduced resilience was observed even in individuals who were not suffering from
any chronic disease.
This predictable loss of resilience in even the healthiest people might explain why we
haven’t seen any evidence of an increase in the maximum lifespan of humans.
And this in spite of the fact that the average lifespan has been on the rise over recent
decades.
The company also suggests that strategies that don’t target this decline in resilience
will probably only result in incremental increases in human longevity.
However, please keep in mind that there are no laws of nature that prohibit such strategies.
OK, so the researchers confirmed this characterization of resilience on two different datasets based
on two kinds of biological measurements.
Parameters taken from blood tests and physical activity levels recorded by wearable devices.
The first parameter is often referred to as “biological age,” and it’s exemplified
by what the researchers called the Dynamic Organism State Index, or DOSI.
This measurement is associated with stresses, lifestyles and chronic diseases, and it can
be computed from a standard blood test.
The second parameter, which they called resilience, is new.
This parameter reflects how quickly the DOSI value returns to normal, or equilibrium baseline
levels, in response to stresses.
Physiological measurements will naturally fluctuate around some equilibrium level.
After you eat a meal, your glucose levels will rise, and then return to normal.
You get a different amount of sleep each night.
In order to calculate resilience, you need to know exactly when recovery was achieved,
and that requires repeated measurements.
And that’s the basis for a longitudinal dataset.
As a rule of thumb, the period of observation that you need to calculate your biological
age should include multiple stress and recovery events.
Now, for even the healthiest individuals, this observation period would amount to several
months, and it would get longer the older that you are.
And it would require, at a minimum, the same measurements on a daily basis, if not even
more frequently than that.
That’s where wearable technology comes in.
The only practical way to collect daily samples is to use a mobile, wearable sensor of some
kind.
Now, in another paper, the researchers have focused on wearable, mobile sensor data, and
they have developed an app that records DOSI sensor data, called GeroSense.
And GeroSense can calculate resilience.
It uses Person-generated Health Data, including data from commercial wearables to create individual,
longitudinal profiles of health.
GeroSense is free and it’s available for smartphones and smartwatches.
Now, I’m not exactly sure just how all this works yet, but I’ve downloaded the app,
and I will be investigating this further.
And I’ll be back in a few weeks with more information.
OK, that wraps up another edition of longevity news.
Check out this playlist to watch other editions of the news.
That’s it for me, I’ll catch you guys later.