May 27, 2025 • 14 mins
What if solving the puzzle of brain aging isn't about adding something new to our bodies, but removing what's already there? This groundbreaking discussion explores the startling reality that neurodegeneration—vividly termed "unbraining" by researchers—begins as early as our twenties, long before symptoms appear.
The conversation delves into fascinating experimental evidence showing how simply diluting old blood plasma can trigger remarkable rejuvenation effects. When researchers performed neutral blood exchange in aged mice, they witnessed an astonishing eightfold increase in new neuron growth after just one treatment. Even more exciting, the human equivalent—therapeutic plasma exchange—is already FDA-approved and showing promising results in early studies.
We explore the paradigm-shifting theory behind these findings: that aging may be driven less by the absence of youth factors and more by the accumulation of inhibitory factors that act like brakes on our body's natural repair systems. By diluting these factors, we might effectively release those brakes, allowing our inherent regenerative abilities to function properly again across multiple tissues—muscle, liver, brain, and possibly even immune function.
This represents a fundamental shift in how we approach aging biology. Rather than searching for miracle compounds or complex interventions, the key to better tissue resilience and function might involve leveraging an existing medical procedure to simply clear the way for our bodies to do what they're designed to do. With clinical trials now in development, these findings could transform how we address age-related decline and cognitive health in the coming years.
Disclaimer:
The information provided in this podcast is for educational purposes only and is not intended as medical advice. Always consult with a qualified healthcare professional before making changes to your supplement regimen or health routine. Individual needs and reactions vary, so it’s important to make informed decisions with the guidance of your physician.
Connect with Us:
If you enjoyed today’s episode, be sure to subscribe, leave us a review, and share it with someone who might benefit. For more insights and updates, visit our website at Lifewellmd.com.
Stay Informed, Stay Healthy:
Remember, informed choices lead to better health. Until next time, be well and take care of yourself.
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Okay, so let's unpack this.
We're diving deep today intosomething that well, it feels
pretty personal, maybe even abit scary for a lot of us.
Speaker 2 (00:09):
Yeah.
Speaker 1 (00:09):
We're talking about health decline as we age and
specifically brain health andmemory.
It's something people often,you know, prefer not to think
about too much.
Speaker 2 (00:19):
It really is and you know the scale of this challenge
which comes up in the sourceswe looked at.
It's quite sobering.
Speaker 1 (00:26):
How sobering are we talking?
Speaker 2 (00:27):
Well, think about this Over 6 million people just
in the United States arecurrently living with dementia 6
million.
Speaker 1 (00:35):
Wow, that's a huge number, and the trend is
worrying too, isn't it?
Speaker 2 (00:40):
It is.
While we're getting better attackling other diseases, things
like heart disease the rates fordementia and Alzheimer's are
actually climbing.
Speaker 1 (00:47):
Partly because we're living longer, I suppose.
Speaker 2 (00:49):
Exactly.
Longer lifespans mean morepeople reach the ages where
dementia becomes more common,but it definitely signals a
really persistent and growingproblem.
Speaker 1 (00:57):
And the process itself, neurodegeneration.
One source called it unbraining.
That's quite a term.
Speaker 2 (01:02):
It is vivid, isn't it ?
It describes this progressivemultifactorial process.
Speaker 1 (01:10):
Multifactorial meaning lots of causes.
Speaker 2 (01:12):
Yeah, not just one thing.
It's about losing thosecritical connections between
neurons, and it's described asrelentless, unfortunately.
Speaker 1 (01:20):
Okay, here's the part that really caught my attention
and it's kind of mind-blowing.
This whole process, thisunbrainingining, starts way
earlier than most people think.
Speaker 2 (01:28):
That's right.
The source suggests it couldbegin around your 20s.
Your 20s.
Speaker 1 (01:32):
Yep.
So by the time someone gets anactual Alzheimer's diagnosis,
which is often much later inlife, they might have already
lost, say, over 40 percent ofthose neuron connections.
Speaker 2 (01:43):
Wow, so the damage is just quietly building up for
decades.
Speaker 1 (01:46):
Right, that long sort of hidden lead up time is a
major challenge, but there's abit of hope.
Mentioned too Definitely andit's crucial.
The sources emphasize thatgetting older doesn't
automatically mean you'll getdementia.
Aging doesn't equal dementia.
Speaker 2 (02:00):
Okay.
Speaker 1 (02:00):
Not everyone who lives to be 80, 90, or even 100
develops it.
Speaker 2 (02:04):
So there are other factors at play, variables
beyond just counting birthdaysExactly, and that opens the door
suggesting there might be waysto intervene, things we can
influence.
Speaker 1 (02:13):
Right.
So if it's not just about age,where did scientists start
looking for potential answers?
Our sources point back to asurprisingly old idea, actually.
Speaker 2 (02:23):
Yeah, messing with the blood, basically the
systemic environment.
Speaker 1 (02:27):
Sounds a bit sci-fi, but it has real history, doesn't
it?
Parabiosis.
Speaker 2 (02:31):
Yes, heteroconic parabiosis, it goes back decades
.
It's this technique whereresearchers surgically connected
the circulatory systems of labanimals, usually an old one and
a young one.
Speaker 1 (02:44):
So they ended up sharing blood and tissues.
Speaker 2 (02:46):
Correct.
It sounds pretty wild, I know.
Speaker 1 (02:48):
And what happened?
What did they see?
Speaker 2 (02:50):
Well, the findings are really consistent and,
frankly, compelling.
The older animals often showedreal improvements.
Their cartilage, muscles, liver, even brain tissues seemed
rejuvenated in some ways.
Speaker 1 (03:01):
Okay, so the old partners got a boost.
What about the young ones?
Speaker 2 (03:04):
Ah, that's the flip side.
The young partners, when hookedup to the old ones, often
showed signs of premature agingnegative effects.
Speaker 1 (03:12):
Interesting so that strongly suggested there was
something in the blood driving.
These age effects both good andbad.
Exactly.
Speaker 2 (03:18):
It led researchers to think okay, maybe we don't need
to connect whole animals, Maybeit's just about the blood
itself or components within it.
Speaker 1 (03:26):
Which leads to just exchanging blood or plasma,
right, yep.
What did those studies show?
Speaker 2 (03:32):
So those initial blood exchange studies, swapping
plasma between old and youngmice, they did show some similar
things.
The old mice gained somerejuvenation in muscle and liver
and the young mice, exposed toold blood, declined quickly.
Speaker 1 (03:44):
Like with the parabiosis.
Speaker 2 (03:45):
Right, but there was a really interesting twist,
especially concerning the brain.
Oh, hippocampal neurogenesis,that's the growth of new neurons
in the hippocampus, which iskey for learning and memory.
Yeah, that didn't reallyimprove much in the old mice
just by getting young bloodplasma.
Speaker 1 (04:00):
Huh, okay.
So just adding young stuffwasn't the magic bullet, at
least not for the brain.
Speaker 2 (04:05):
In that context, Precisely it suggested the
problem wasn't just a lack ofyouthful factors, maybe.
Maybe there was something inthe old blood actively blocking
or inhibiting brain health andrepair.
Speaker 1 (04:18):
Like old factors, gum stuff from the old and that
question sets the stage for thereally key research we're
looking at today neutral bloodexchange NB.
Speaker 2 (04:37):
Exactly.
Nb was designed to test exactlythat question.
Speaker 1 (04:41):
How did it work?
Speaker 2 (04:42):
So they took old mice again, but instead of giving
them young plasma, they replacedabout half of their existing
blood plasma with the neutralsolution.
Speaker 1 (04:50):
Neutral meaning.
Speaker 2 (04:50):
Just saline Pretty much.
Speaker 1 (04:52):
Saline with a bit of albumin added, which is a common
protein in blood.
But, crucially, no youngfactors were deliberately added.
Speaker 2 (04:58):
The goal was just dilution, reducing the
concentration of whatever wasalready in that old plasma.
Speaker 1 (05:03):
That was the core idea Dilute the old environment.
And the results, even from asingle NBE procedure, were well,
they were, pretty remarkable.
Okay, tell me what happened inthese mice.
Speaker 2 (05:14):
In muscle tissue they saw better repair, less
fibrosis that's scarring,getting close to levels seen in
young mice, and the new musclefibers that grew were actually
bigger.
Speaker 1 (05:24):
Okay, muscle improved .
What else?
Speaker 2 (05:26):
Liver, significant reduction in fat buildup,
adiposity, and also lessfibrosis there too.
Speaker 1 (05:32):
All right, but the big question is the brain right,
Since the young blood didn'tseem to help there before, this
is where it got really dramaticIn the hippocampus, specifically
the dentate gyrus, that areavital for new neuron growth.
Yeah.
Speaker 2 (05:45):
A single NBE treatment led to a huge increase
in neurogenesis, like aneightfold increase in the growth
of new neural precursor cells.
Speaker 1 (05:53):
Wait, say that again.
Eightfold from one dilutiontreatment.
Speaker 2 (05:57):
Eightfold.
It was massive.
Actually, it was even more ofan increase than they had seen
in the old mice connected toyoung mice through parabiosis.
Speaker 1 (06:04):
That's incredible.
What about the young mice?
Did diluting their plasma hurtthem?
Speaker 2 (06:08):
That's important too.
A single NBE didn't seem tosignificantly worsen things for
the young mice based on theparameters they checked.
Maybe a bit more variability inthe results compared to young
mice who had nothing done, butno major negative impact
reported from one go.
Speaker 1 (06:23):
So the big takeaway from the mouse study seems to be
just swapping out old plasmafor a neutral fluid is enough
Enough to cause significantrejuvenation in muscle, liver
and the brain.
Speaker 2 (06:35):
That's the powerful conclusion.
Yes, it really bolsters theidea that the aged systemic
environment itself is inhibitory.
It's actively suppressingtissue health and repair.
Speaker 1 (06:46):
Less about needing young factors and more about the
old factors getting in the way.
Speaker 2 (06:50):
That's the hypothesis this work strongly supports.
Speaker 1 (06:52):
Okay, fascinating mouse work, but how does this
connect to us, to humans?
The sources talk about aprocedure already in use.
Speaker 2 (07:00):
Right, and this is where it gets really practical
and exciting.
The procedure is calledtherapeutic plasma exchange, or
TPE.
Speaker 1 (07:06):
TPE and this isn't some future tech.
Speaker 2 (07:08):
Not at all.
Tpe is a standard, fda-approvedmedical procedure.
It's been used routinely inclinics for decades for various
autoimmune diseases and otherconditions.
It's basically the humanclinical equivalent of the MBE
they did in mice.
Speaker 1 (07:22):
So researchers could actually study people who'd had
this procedure.
Speaker 2 (07:26):
Yes, they analyzed blood samples from older adults
around 65 to 70 years old whounderwent a single TPE session
for existing medical reasons.
They looked at samples takenbefore the TPE and then again
about a month after.
Speaker 1 (07:40):
And what did they find in the human blood?
Did it mirror the mouse results?
Speaker 2 (07:44):
It really seemed to.
Functionally they saw signs ofrejuvenation.
For example, blood serum fromthese older individuals before
TPE tended to inhibit the growthof muscle stem cells in a lab
dish, but serum taken after TPEthat inhibition was gone.
The muscle progenitor cellscould grow robustly, much like
they would if exposed to serumfrom a younger person.
Speaker 1 (08:04):
So the TPE effectively cleaned up the
inhibitory effect of the olderblood on muscle regeneration, at
least in this test.
Speaker 2 (08:10):
That's what it looked like, and they saw molecular
changes too.
Speaker 1 (08:13):
Like changes in proteins.
Speaker 2 (08:14):
Exactly A single TPE treatment caused significant,
widespread changes in the mix ofproteins circulating in the
blood, and these changes werestill measurable a month later.
Speaker 1 (08:24):
What kinds of proteins changed?
Speaker 2 (08:26):
They did proteomic analysis, looking at the whole
protein landscape.
They found changes in proteinsinvolved in forming new blood
vessels, angiogenic regulatorscontrolling the immune system,
immune regulators and promotingcell growth and repair growth
factors.
Speaker 1 (08:41):
And did the levels go up or down?
Speaker 2 (08:43):
Interestingly, many important proteins were actually
upregulated.
After TPE.
Their levels increased.
Speaker 1 (08:52):
Which fits perfectly with that idea of removing
inhibitors.
Right, if something was holdingback their production?
Diluting it would let thelevels rise.
Speaker 2 (08:57):
Precisely.
It aligns beautifully with themouse data and the core
hypothesis.
The researchers concluded thatTPE seems to promote molecular
and functional rejuvenation inthe blood of older people,
supporting processes likemyogenesis muscle building.
Speaker 1 (09:11):
So, bringing this all together, what's the main
theory for how this dilutionactually works?
How does simply reducing theconcentration of stuff in old
plasma trigger theserejuvenation effects?
Speaker 2 (09:22):
The leading model based on this research is
centered on that idea ofdilution, specifically diluting
age-elevated inhibitory factorsand maybe some auto-regulatory
proteins that have built up.
Speaker 1 (09:34):
Okay, inhibitory factors like those breaks we
talked about.
Speaker 2 (09:37):
Exactly.
Think of it like your body hasall these natural pathways for
maintenance, repair,regeneration, but as we age,
certain molecules accumulate inthe blood that act like
suppressors or brakes on thesepathways.
Speaker 1 (09:50):
They slow things down , stop repairs from happening
effectively.
Speaker 2 (09:54):
Right.
So TPE, by diluting theconcentration of these braking
molecules, essentially takes thepressure off those brakes.
Speaker 1 (10:01):
Ah, so you're not necessarily adding rocket fuel,
you're just letting the enginerun properly again by easing off
the brakes.
Speaker 2 (10:08):
That's a great analogy.
The body's inherentregenerative capacity seems to
still be there, it's just beingheld back.
Dilution lets it work better.
Speaker 1 (10:15):
And the protein data seeing levels increase after TPE
supports that suggesting theirproduction was being suppressed
before.
Speaker 2 (10:22):
Exactly, the system seems primed to work.
It just needs the inhibitionlifted.
Speaker 1 (10:27):
What about the albumin you mentioned?
It was in the replacement fluid.
Does that play a major roleitself?
Speaker 2 (10:31):
That's a fair question.
Albumin was used and some labtests, like in vitro tests,
showed it could help neuralprecursor cells grow.
But the overall conclusion forthe main study was that albumin
likely isn't the main driver ofthe broad effects seen from NBE
or TPE.
Speaker 1 (10:48):
So it helps maybe, but it's not the whole story.
Speaker 2 (10:57):
Probably not In TPE.
Adding albumin is often justabout replacing what's lost
during the procedure to maintainnormal levels.
It's not necessarily aboutboosting it way up, and
interestingly, trying todirectly infuse albumin into the
brain in other studies hassometimes been harmful.
So it seems the key really isthe dilution of those other
inhibitory factors.
Speaker 1 (11:11):
OK, that makes sense.
So stepping back.
What are the biggerimplications here?
If this dilution approach holdsup, what could it mean for
aging and health?
Speaker 2 (11:20):
Well, the potential is quite broad.
It suggests we might be able touse a procedure like TPE, which
we already know how to dosafely, to improve the health
and repair capacity of multipleorgan systems simultaneously in
older people.
Speaker 1 (11:31):
Muscle, liver, brain, maybe more.
Speaker 2 (11:35):
Potentially, yes, improving overall tissue
function, making tissues moreresilient, maybe even helping
with cognitive health.
It's quite a shift in thinking.
Speaker 1 (11:44):
And you mentioned something earlier, an anecdotal
link to the immune system.
Speaker 2 (11:48):
Yes, that was interesting.
An observation noted in thesources was that patients
receiving TPE for other reasonsseem to get fewer viral
infections.
Speaker 1 (11:57):
Really Fewer colds, fewer flu episodes, that sort of
thing.
Speaker 2 (12:01):
That was the anecdotal report.
It's not definitive proof froma controlled trial yet, but it's
intriguing.
It hints at potential benefitsfor immune function.
Speaker 1 (12:09):
Which could be huge for older adults, who are often
more vulnerable to infections.
Speaker 2 (12:13):
Absolutely Better recovery from illnesses, maybe
even better responses tovaccines.
It could tie back to thosechanges we saw in immune
regulators and growth factorsand just generally improve
tissue health, allowing theimmune system to function better
.
Speaker 1 (12:27):
So the really significant thing here is using
an existing, safe clinical toolto potentially address
widespread age-related decline.
Speaker 2 (12:35):
That's the crux of it , and the sources mentioned that
further clinical trials, likephase 2b and phase 3 studies,
are being developed to reallynail down these effects in
humans.
Speaker 1 (12:45):
Exciting times for this research, then, so let's
try to summarize the coreinsight from this deep dive.
Speaker 2 (12:51):
I think the key takeaway is that the evidence is
pointing towards plasmaexchange, like TPE, having this
potential to kind of reset thebody's internal environment.
Speaker 1 (13:02):
Not by adding miracle youth factors, but by diluting
the aging factors, thoseinhibitory signals that build up
over time in our blood.
Speaker 2 (13:09):
Right, and by doing that it seems to unleash the
body's own ability to repair andrejuvenate tissues, leading to
tangible benefits we can see inmuscle, liver and even
potentially promoting new neurongrowth in the brain.
Speaker 1 (13:22):
It really flips the script, doesn't it?
The focus shifts from findingsomething new to add to maybe
just needing to clear out theold stuff that's hindering our
natural resilience.
Speaker 2 (13:31):
It's a profound shift in perspective on aging biology
.
Speaker 1 (13:34):
So the final thought for you listening to this what
if a powerful key to betterhealth, to improved function in
our tissues, better resilienceas we age?
What if it's not about findingsome revolutionary new pill or
injection?
Speaker 2 (13:49):
What if, instead, it's about leveraging a way to
simply reduce the burden of whattime allows to accumulate
within us?
Speaker 1 (13:56):
Clearing the way, perhaps, for our own bodies to
do what they're designed to domaintain and repair themselves
more effectively, even as theyears pass.
Speaker 2 (14:03):
It's a compelling idea and definitely makes this
area of longevity research oneto keep a very close eye on.
Okay, so let's unpack this.
We're diving deep today intosomething that well, it feels
pretty personal, maybe even abit scary for a lot of us.
Speaker 2 (00:09):
Yeah.
Speaker 1 (00:09):
We're talking about health decline as we age and
specifically brain health andmemory.
It's something people often,you know, prefer not to think
about too much.
Speaker 2 (00:19):
It really is and you know the scale of this challenge
which comes up in the sourceswe looked at.
It's quite sobering.
Speaker 1 (00:26):
How sobering are we talking?
Speaker 2 (00:27):
Well, think about this Over 6 million people just
in the United States arecurrently living with dementia 6
million.
Speaker 1 (00:35):
Wow, that's a huge number, and the trend is
worrying too, isn't it?
Speaker 2 (00:40):
It is.
While we're getting better attackling other diseases, things
like heart disease the rates fordementia and Alzheimer's are
actually climbing.
Speaker 1 (00:47):
Partly because we're living longer, I suppose.
Speaker 2 (00:49):
Exactly.
Longer lifespans mean morepeople reach the ages where
dementia becomes more common,but it definitely signals a
really persistent and growingproblem.
Speaker 1 (00:57):
And the process itself, neurodegeneration.
One source called it unbraining.
That's quite a term.
Speaker 2 (01:02):
It is vivid, isn't it ?
It describes this progressivemultifactorial process.
Speaker 1 (01:10):
Multifactorial meaning lots of causes.
Speaker 2 (01:12):
Yeah, not just one thing.
It's about losing thosecritical connections between
neurons, and it's described asrelentless, unfortunately.
Speaker 1 (01:20):
Okay, here's the part that really caught my attention
and it's kind of mind-blowing.
This whole process, thisunbrainingining, starts way
earlier than most people think.
Speaker 2 (01:28):
That's right.
The source suggests it couldbegin around your 20s.
Your 20s.
Speaker 1 (01:32):
Yep.
So by the time someone gets anactual Alzheimer's diagnosis,
which is often much later inlife, they might have already
lost, say, over 40 percent ofthose neuron connections.
Speaker 2 (01:43):
Wow, so the damage is just quietly building up for
decades.
Speaker 1 (01:46):
Right, that long sort of hidden lead up time is a
major challenge, but there's abit of hope.
Mentioned too Definitely andit's crucial.
The sources emphasize thatgetting older doesn't
automatically mean you'll getdementia.
Aging doesn't equal dementia.
Speaker 2 (02:00):
Okay.
Speaker 1 (02:00):
Not everyone who lives to be 80, 90, or even 100
develops it.
Speaker 2 (02:04):
So there are other factors at play, variables
beyond just counting birthdaysExactly, and that opens the door
suggesting there might be waysto intervene, things we can
influence.
Speaker 1 (02:13):
Right.
So if it's not just about age,where did scientists start
looking for potential answers?
Our sources point back to asurprisingly old idea, actually.
Speaker 2 (02:23):
Yeah, messing with the blood, basically the
systemic environment.
Speaker 1 (02:27):
Sounds a bit sci-fi, but it has real history, doesn't
it?
Parabiosis.
Speaker 2 (02:31):
Yes, heteroconic parabiosis, it goes back decades
.
It's this technique whereresearchers surgically connected
the circulatory systems of labanimals, usually an old one and
a young one.
Speaker 1 (02:44):
So they ended up sharing blood and tissues.
Speaker 2 (02:46):
Correct.
It sounds pretty wild, I know.
Speaker 1 (02:48):
And what happened?
What did they see?
Speaker 2 (02:50):
Well, the findings are really consistent and,
frankly, compelling.
The older animals often showedreal improvements.
Their cartilage, muscles, liver, even brain tissues seemed
rejuvenated in some ways.
Speaker 1 (03:01):
Okay, so the old partners got a boost.
What about the young ones?
Speaker 2 (03:04):
Ah, that's the flip side.
The young partners, when hookedup to the old ones, often
showed signs of premature agingnegative effects.
Speaker 1 (03:12):
Interesting so that strongly suggested there was
something in the blood driving.
These age effects both good andbad.
Exactly.
Speaker 2 (03:18):
It led researchers to think okay, maybe we don't need
to connect whole animals, Maybeit's just about the blood
itself or components within it.
Speaker 1 (03:26):
Which leads to just exchanging blood or plasma,
right, yep.
What did those studies show?
Speaker 2 (03:32):
So those initial blood exchange studies, swapping
plasma between old and youngmice, they did show some similar
things.
The old mice gained somerejuvenation in muscle and liver
and the young mice, exposed toold blood, declined quickly.
Speaker 1 (03:44):
Like with the parabiosis.
Speaker 2 (03:45):
Right, but there was a really interesting twist,
especially concerning the brain.
Oh, hippocampal neurogenesis,that's the growth of new neurons
in the hippocampus, which iskey for learning and memory.
Yeah, that didn't reallyimprove much in the old mice
just by getting young bloodplasma.
Speaker 1 (04:00):
Huh, okay.
So just adding young stuffwasn't the magic bullet, at
least not for the brain.
Speaker 2 (04:05):
In that context, Precisely it suggested the
problem wasn't just a lack ofyouthful factors, maybe.
Maybe there was something inthe old blood actively blocking
or inhibiting brain health andrepair.
Speaker 1 (04:18):
Like old factors, gum stuff from the old and that
question sets the stage for thereally key research we're
looking at today neutral bloodexchange NB.
Speaker 2 (04:37):
Exactly.
Nb was designed to test exactlythat question.
Speaker 1 (04:41):
How did it work?
Speaker 2 (04:42):
So they took old mice again, but instead of giving
them young plasma, they replacedabout half of their existing
blood plasma with the neutralsolution.
Speaker 1 (04:50):
Neutral meaning.
Speaker 2 (04:50):
Just saline Pretty much.
Speaker 1 (04:52):
Saline with a bit of albumin added, which is a common
protein in blood.
But, crucially, no youngfactors were deliberately added.
Speaker 2 (04:58):
The goal was just dilution, reducing the
concentration of whatever wasalready in that old plasma.
Speaker 1 (05:03):
That was the core idea Dilute the old environment.
And the results, even from asingle NBE procedure, were well,
they were, pretty remarkable.
Okay, tell me what happened inthese mice.
Speaker 2 (05:14):
In muscle tissue they saw better repair, less
fibrosis that's scarring,getting close to levels seen in
young mice, and the new musclefibers that grew were actually
bigger.
Speaker 1 (05:24):
Okay, muscle improved .
What else?
Speaker 2 (05:26):
Liver, significant reduction in fat buildup,
adiposity, and also lessfibrosis there too.
Speaker 1 (05:32):
All right, but the big question is the brain right,
Since the young blood didn'tseem to help there before, this
is where it got really dramaticIn the hippocampus, specifically
the dentate gyrus, that areavital for new neuron growth.
Yeah.
Speaker 2 (05:45):
A single NBE treatment led to a huge increase
in neurogenesis, like aneightfold increase in the growth
of new neural precursor cells.
Speaker 1 (05:53):
Wait, say that again.
Eightfold from one dilutiontreatment.
Speaker 2 (05:57):
Eightfold.
It was massive.
Actually, it was even more ofan increase than they had seen
in the old mice connected toyoung mice through parabiosis.
Speaker 1 (06:04):
That's incredible.
What about the young mice?
Did diluting their plasma hurtthem?
Speaker 2 (06:08):
That's important too.
A single NBE didn't seem tosignificantly worsen things for
the young mice based on theparameters they checked.
Maybe a bit more variability inthe results compared to young
mice who had nothing done, butno major negative impact
reported from one go.
Speaker 1 (06:23):
So the big takeaway from the mouse study seems to be
just swapping out old plasmafor a neutral fluid is enough
Enough to cause significantrejuvenation in muscle, liver
and the brain.
Speaker 2 (06:35):
That's the powerful conclusion.
Yes, it really bolsters theidea that the aged systemic
environment itself is inhibitory.
It's actively suppressingtissue health and repair.
Speaker 1 (06:46):
Less about needing young factors and more about the
old factors getting in the way.
Speaker 2 (06:50):
That's the hypothesis this work strongly supports.
Speaker 1 (06:52):
Okay, fascinating mouse work, but how does this
connect to us, to humans?
The sources talk about aprocedure already in use.
Speaker 2 (07:00):
Right, and this is where it gets really practical
and exciting.
The procedure is calledtherapeutic plasma exchange, or
TPE.
Speaker 1 (07:06):
TPE and this isn't some future tech.
Speaker 2 (07:08):
Not at all.
Tpe is a standard, fda-approvedmedical procedure.
It's been used routinely inclinics for decades for various
autoimmune diseases and otherconditions.
It's basically the humanclinical equivalent of the MBE
they did in mice.
Speaker 1 (07:22):
So researchers could actually study people who'd had
this procedure.
Speaker 2 (07:26):
Yes, they analyzed blood samples from older adults
around 65 to 70 years old whounderwent a single TPE session
for existing medical reasons.
They looked at samples takenbefore the TPE and then again
about a month after.
Speaker 1 (07:40):
And what did they find in the human blood?
Did it mirror the mouse results?
Speaker 2 (07:44):
It really seemed to.
Functionally they saw signs ofrejuvenation.
For example, blood serum fromthese older individuals before
TPE tended to inhibit the growthof muscle stem cells in a lab
dish, but serum taken after TPEthat inhibition was gone.
The muscle progenitor cellscould grow robustly, much like
they would if exposed to serumfrom a younger person.
Speaker 1 (08:04):
So the TPE effectively cleaned up the
inhibitory effect of the olderblood on muscle regeneration, at
least in this test.
Speaker 2 (08:10):
That's what it looked like, and they saw molecular
changes too.
Speaker 1 (08:13):
Like changes in proteins.
Speaker 2 (08:14):
Exactly A single TPE treatment caused significant,
widespread changes in the mix ofproteins circulating in the
blood, and these changes werestill measurable a month later.
Speaker 1 (08:24):
What kinds of proteins changed?
Speaker 2 (08:26):
They did proteomic analysis, looking at the whole
protein landscape.
They found changes in proteinsinvolved in forming new blood
vessels, angiogenic regulatorscontrolling the immune system,
immune regulators and promotingcell growth and repair growth
factors.
Speaker 1 (08:41):
And did the levels go up or down?
Speaker 2 (08:43):
Interestingly, many important proteins were actually
upregulated.
After TPE.
Their levels increased.
Speaker 1 (08:52):
Which fits perfectly with that idea of removing
inhibitors.
Right, if something was holdingback their production?
Diluting it would let thelevels rise.
Speaker 2 (08:57):
Precisely.
It aligns beautifully with themouse data and the core
hypothesis.
The researchers concluded thatTPE seems to promote molecular
and functional rejuvenation inthe blood of older people,
supporting processes likemyogenesis muscle building.
Speaker 1 (09:11):
So, bringing this all together, what's the main
theory for how this dilutionactually works?
How does simply reducing theconcentration of stuff in old
plasma trigger theserejuvenation effects?
Speaker 2 (09:22):
The leading model based on this research is
centered on that idea ofdilution, specifically diluting
age-elevated inhibitory factorsand maybe some auto-regulatory
proteins that have built up.
Speaker 1 (09:34):
Okay, inhibitory factors like those breaks we
talked about.
Speaker 2 (09:37):
Exactly.
Think of it like your body hasall these natural pathways for
maintenance, repair,regeneration, but as we age,
certain molecules accumulate inthe blood that act like
suppressors or brakes on thesepathways.
Speaker 1 (09:50):
They slow things down , stop repairs from happening
effectively.
Speaker 2 (09:54):
Right.
So TPE, by diluting theconcentration of these braking
molecules, essentially takes thepressure off those brakes.
Speaker 1 (10:01):
Ah, so you're not necessarily adding rocket fuel,
you're just letting the enginerun properly again by easing off
the brakes.
Speaker 2 (10:08):
That's a great analogy.
The body's inherentregenerative capacity seems to
still be there, it's just beingheld back.
Dilution lets it work better.
Speaker 1 (10:15):
And the protein data seeing levels increase after TPE
supports that suggesting theirproduction was being suppressed
before.
Speaker 2 (10:22):
Exactly, the system seems primed to work.
It just needs the inhibitionlifted.
Speaker 1 (10:27):
What about the albumin you mentioned?
It was in the replacement fluid.
Does that play a major roleitself?
Speaker 2 (10:31):
That's a fair question.
Albumin was used and some labtests, like in vitro tests,
showed it could help neuralprecursor cells grow.
But the overall conclusion forthe main study was that albumin
likely isn't the main driver ofthe broad effects seen from NBE
or TPE.
Speaker 1 (10:48):
So it helps maybe, but it's not the whole story.
Speaker 2 (10:57):
Probably not In TPE.
Adding albumin is often justabout replacing what's lost
during the procedure to maintainnormal levels.
It's not necessarily aboutboosting it way up, and
interestingly, trying todirectly infuse albumin into the
brain in other studies hassometimes been harmful.
So it seems the key really isthe dilution of those other
inhibitory factors.
Speaker 1 (11:11):
OK, that makes sense.
So stepping back.
What are the biggerimplications here?
If this dilution approach holdsup, what could it mean for
aging and health?
Speaker 2 (11:20):
Well, the potential is quite broad.
It suggests we might be able touse a procedure like TPE, which
we already know how to dosafely, to improve the health
and repair capacity of multipleorgan systems simultaneously in
older people.
Speaker 1 (11:31):
Muscle, liver, brain, maybe more.
Speaker 2 (11:35):
Potentially, yes, improving overall tissue
function, making tissues moreresilient, maybe even helping
with cognitive health.
It's quite a shift in thinking.
Speaker 1 (11:44):
And you mentioned something earlier, an anecdotal
link to the immune system.
Speaker 2 (11:48):
Yes, that was interesting.
An observation noted in thesources was that patients
receiving TPE for other reasonsseem to get fewer viral
infections.
Speaker 1 (11:57):
Really Fewer colds, fewer flu episodes, that sort of
thing.
Speaker 2 (12:01):
That was the anecdotal report.
It's not definitive proof froma controlled trial yet, but it's
intriguing.
It hints at potential benefitsfor immune function.
Speaker 1 (12:09):
Which could be huge for older adults, who are often
more vulnerable to infections.
Speaker 2 (12:13):
Absolutely Better recovery from illnesses, maybe
even better responses tovaccines.
It could tie back to thosechanges we saw in immune
regulators and growth factorsand just generally improve
tissue health, allowing theimmune system to function better
.
Speaker 1 (12:27):
So the really significant thing here is using
an existing, safe clinical toolto potentially address
widespread age-related decline.
Speaker 2 (12:35):
That's the crux of it , and the sources mentioned that
further clinical trials, likephase 2b and phase 3 studies,
are being developed to reallynail down these effects in
humans.
Speaker 1 (12:45):
Exciting times for this research, then, so let's
try to summarize the coreinsight from this deep dive.
Speaker 2 (12:51):
I think the key takeaway is that the evidence is
pointing towards plasmaexchange, like TPE, having this
potential to kind of reset thebody's internal environment.
Speaker 1 (13:02):
Not by adding miracle youth factors, but by diluting
the aging factors, thoseinhibitory signals that build up
over time in our blood.
Speaker 2 (13:09):
Right, and by doing that it seems to unleash the
body's own ability to repair andrejuvenate tissues, leading to
tangible benefits we can see inmuscle, liver and even
potentially promoting new neurongrowth in the brain.
Speaker 1 (13:22):
It really flips the script, doesn't it?
The focus shifts from findingsomething new to add to maybe
just needing to clear out theold stuff that's hindering our
natural resilience.
Speaker 2 (13:31):
It's a profound shift in perspective on aging biology
.
Speaker 1 (13:34):
So the final thought for you listening to this what
if a powerful key to betterhealth, to improved function in
our tissues, better resilienceas we age?
What if it's not about findingsome revolutionary new pill or
injection?
Speaker 2 (13:49):
What if, instead, it's about leveraging a way to
simply reduce the burden of whattime allows to accumulate
within us?
Speaker 1 (13:56):
Clearing the way, perhaps, for our own bodies to
do what they're designed to domaintain and repair themselves
more effectively, even as theyears pass.
Speaker 2 (14:03):
It's a compelling idea and definitely makes this
area of longevity research oneto keep a very close eye on.
Popular Podcasts
United States of Kennedy
United States of Kennedy is a podcast about our cultural fascination with the Kennedy dynasty. Every week, hosts Lyra Smith and George Civeris go into one aspect of the Kennedy story.
Stuff You Should Know
If you've ever wanted to know about champagne, satanism, the Stonewall Uprising, chaos theory, LSD, El Nino, true crime and Rosa Parks, then look no further. Josh and Chuck have you covered.
Dateline NBC
Current and classic episodes, featuring compelling true-crime mysteries, powerful documentaries and in-depth investigations. Follow now to get the latest episodes of Dateline NBC completely free, or subscribe to Dateline Premium for ad-free listening and exclusive bonus content: DatelinePremium.com