October 15, 2025 • 28 mins
Dr. Reza Bolouri, a memory expert, joins Dr. Michael Koren to discuss Alzheimer’s, what it is, the risks, how it differs from other forms of dementia. The doctors also explore how treatment of dementia has evolved and progressed over the years from symptomatic treatments to new, disease-modifying medications that can slow the progression of Alzheimer’s. They also talk about how clinical trials are exploring the next generation of Alzheimer’s medications and tests which may provide preventative solutions to stop the disease before it even starts.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Announcer (00:00):
Welcome to MedEvidence!, where we help you
navigate the truth behindmedical research with unbiased,
evidence-proven facts, hosted bycardiologist and top medical
researcher, Dr.
Michael Koren.
Dr. Michael Koren (00:11):
Hello, I'm Dr.
Michael Koren, the executiveeditor for MedEvidence! And we
get a lot of questions here atMedEvidence, and one of the
things that comes up all thetime is about memory issues.
And I'm so fortunate to have anexpert in memory issues, Dr.
Reza Bolouri, who's joining mehere in the studio.
And we're going to have anexciting conversation about
(00:33):
memory issues and also talkabout clinical research in the
memory area.
So, Reza, thank you so much forbeing part of our MedEvidence
family.
Dr. Reza Bolouri (00:42):
Thank you so much for inviting me.
Great to have you.
Dr. Michael Koren (00:45):
Yeah, so let's just start.
We like to start by justgetting to know each other, you,
me, and the audience.
So tell us a little bit aboutyour background.
You had a little bit of anon-traditional way that you
became a memory physician.
So why don't you let everybodyknow how you got there?
And and and by the way, uh Rezais one of really the national
experts in memory and inresearch in the memory area.
(01:06):
So again, thank you for that.
But how'd you get there?
Dr. Reza Bolouri (01:09):
Thank you.
Actually, after medical school,I um was uh studying for my
boards, being a foreign medicalgraduate.
So I was looking for a job andI stumbled into this um um
neurology practice that was uh ageneral practice, but they were
they had started doing someclinical trials on Alzheimer's
(01:30):
disease.
So I was hired as a researchcoordinator.
Dr. Michael Koren (01:33):
Wow.
Dr. Reza Bolouri (01:33):
And um I that's how I got my feet wet and
started looking at studies uhwhen we really didn't have much
uh knowledge about what wasgoing on with Alzheimer's
disease, what was happening,even the amyloid hypothesis was
just growing.
And eventually uh through theyears, after uh several hundred
studies uh began to understandAlzheimer's disease, became very
(01:58):
interested in Alzheimer'sdisease and therapeutic areas.
And uh at some point I startedmy residencies after passing my
boards, did uh uh psychiatry anduh subsequently neurology, and
uh settled down in Charlotte,North Carolina, opened up my own
practice after working for ahospital for about two years,
(02:22):
then started a general practiceand eventually cognitive
neurology, and then subsequentlywent back to clinical trials
and doing research.
Dr. Michael Koren (02:31):
So interesting.
So you really started from theground up Even before you were
a practicing physician in theUnited States, you were actually
learning research.
Dr. Reza Bolouri (02:40):
That's correct.
Dr. Michael Koren (02:40):
That's really, really cool.
I love that.
Great story.
So tell us a little bit moreabout how your practice
developed.
I know that you have a uniquemodel of reaching out into the
community to help people thatmay have concerns about the
memory.
Dr. Reza Bolouri (02:53):
Well, actually, given my background in
Alzheimer's, I became extremelyinterested in geriatric
neurology and specifically in uhcognitive neurology.
And um we do know that themajority of the cases of
dementia happen to beAlzheimer's disease.
That's why a lot of folks uhinterchangeably use Alzheimer's
(03:14):
and dementia, whereas they'renot exactly the same thing.
So I um um focused on uhcognitive neurology.
Dementia established uh a majorpopulation of folks in the
Charlotte area who had memorydisorders, and then uh my
practice began to focus more inthe dementia area, and then my
(03:35):
background in research, wedecided to go ahead and restart
our clinical trials.
So we've been very successfulover the past 20 years in not
only the general practice, butalso our uh research grew uh uh
rather rapidly.
And um uh we've done over 200studies just in the past two
years, uh 20 years, sorry.
(03:57):
And um uh we we are I'm proudto be um uh one of the uh
investigators involved in allthe drugs out there for
Alzheimer's disease, startingfrom the symptomatic therapies
and newly approved uh diseasemodifying drugs.
And we continue uh that pathand um we are introduced to uh
much better, new and improveddrugs, which we are working on
(04:20):
right now.
Dr. Michael Koren (04:20):
Yeah, and that's so satisfying.
Actually, one of the great joysI get as a clinical
investigator is to be part ofthese programs that result in
products that help people'slives.
So there's nothing better thanthat.
Yes.
So let's let's break downmemory issues for the public.
As you mentioned, you alludedto the fact that Alzheimer's is
(04:41):
a subset of dementia issues andmemory issues, but there's a lot
of confusion out there.
So let's start with a patientthat's concerned about his or
her memory.
They come to you, how do youbreak down this particular
person's uh concerns fromsomething that's either real or
not so real, quote unquote.
And how do you figure out ifit's Alzheimer's versus another
(05:01):
form of dementia?
Dr. Reza Bolouri (05:03):
Well, the best way I usually explain that
to my patients and theirfamilies is um dementia is not a
disease, it's a syndrome.
And uh basically what thatmeans is, for example, we have
heart failure, we have liverfailure, kidney failure, and so
on.
And dementia is nothing but abrain failure.
So if you could just uh um Idescribe it that way, it's a
(05:27):
brain failure.
So when someone comes to mewith any kind of a cognitive
issues, the first thing I wantto do is get a good history, do
a good physical examination, dosome preliminary workup to
distinguish uh the type ofdementia we are dealing with.
For example, someone who isdrinking 20 years every day, all
(05:48):
day, that's alcoholic dementia.
Okay.
When you do an MRI of the brainand you see a bunch of strokes,
that's vascular dementia.
If somebody is exhibiting someParkinsonism, it could be a
Parkinsonian dementia or Lewybody dementia.
A patient starting with thelanguage problem, behavioral
problems, it could befrontemporal dementia.
(06:08):
Through some assessments andgood clinical work, we determine
exactly what kind of dementiathat is.
Dr. Michael Koren (06:16):
Interesting.
So just to help people, you youyou threw out a lot of stuff
there, which is great.
But for example, uhParkinsonian dementia would be
associated with other elementsof the Parkinsonian syndrome or
disease, including likestiffness.
Maybe mention some other thingsthat would be associated with
so people can understand thedifference between that and
Alzheimer's.
Dr. Reza Bolouri (06:36):
Well, you know, uh once once you begin to
learn about the dementias, isyou you're able to distinguish
the differences.
However, uh uh, for example,Parkinsonian dementias, uh there
are two types.
Uh there are several types ofParkinsonian dementias.
For example, there are folkswho have established diagnosis
of Parkinson's disease, andlater in the course of their
(06:58):
disease, they develop dementia.
That's called Parkinson'sdisease-related dementia.
Whereas other types ofParkinsonian dementias, the
Parkinsonism and dementia comeat the same time or within a
year from each other.
So that's different than awell-established Parkinson's
disease, whereas uh Parkinsoniandementias that are not
(07:19):
Parkinson's disease-relateddementia, they do not exhibit
all the signs and symptoms of atypical Parkinson's disease.
Dr. Michael Koren (07:26):
Got it, got it.
So taking a step back, becausethis is a common question that I
get, even in my cardiologypractice, is when people are
having difficulty with theirmemory, how do you distinguish
changes in your memory and maybeyour mental acuity as you get
older versus an actual disease?
Dr. Reza Bolouri (07:46):
Well, I'm asked about this question a lot.
Uh, there is a phenomenon uh uhcalled age-associated memory
impairment.
In the old days, we used tocall them senile dementia,
presenility, hardening of thearteries, and a whole host of
things.
We no longer use thosederogatory terms.
Uh so we call it age-relatedmemory problem.
(08:06):
How do we distinguish theage-related memory problem from
Alzheimer's disease?
Is as we age, just likeeverything else, we slow down
mentally and physically.
Age-associated memory problem,the folks begin to have some
short-term memory problem.
They go to a room wonderingwhat they went there for, and
then uh slow down in manyrespects in their responses, in
(08:29):
their activities.
However, they do not progress.
They remain the same and fullyfunctional.
They're 90-year-olds,100-year-olds who are still
doing their things, but yes,they have lapses of memory, the
senior moments.
Whereas with Alzheimer's, thefolks who are transitioning to
Alzheimer's, they begin to losethe ability of the learned
(08:52):
processes, learned uh habits,learned activities.
That's why we call it a greatunlearning.
And these are the folks whohave learned, they have raised
families, they've educated, theyworked, and eventually they
lose the ability to drive, tomake decisions, to pay
bills, and that's why you cantell the difference versus
(09:15):
progressive o r stable form ofmemory impairment.
And that's that's that that'show we can tell the difference.
Dr. Michael Koren (09:22):
Got it.
Is there something you canlearn about that difference by
doing mental status testing?
How good is mental statustesting at determining who has
this more ominous progressiveform versus people that may just
be getting a little slowerbecause of age?
Dr. Reza Bolouri (09:40):
Well, I mean, the science has advanced.
I mean, now we have ways toreally tell if someone is
developing Alzheimer's disease,which we can go to when we talk
about research.
But generally, uh, a goodclinical practice, a good uh
practitioner observes thepatients for a while to see who
is declining and who is not.
The best source of informationis patients' family.
(10:02):
Okay.
They tell you he or she is notthe same.
He forgot, uh he got lostdriving, he forgot to pay a
bill, he made a bad decision, hegot scammed uh online.
Uh those are the things thatraise the flag of something else
is going on.
And besides, when we talk aboutdementia, when we talk about
memory memory, it's not justmemory.
(10:23):
It's memory, problem solving,decision making, planning,
organizing.
Everything is affected.
It's not just memory.
Memory is the first thing wenotice, but everything else uh
happens.
Dr. Michael Koren (10:34):
So interviews with family and the patient you
think is more valuable thansome of the formal cognitive
testing, or there's a role forboth?
Dr. Reza Bolouri (10:42):
It's a combination.
There's a role for both.
Of course, we we do rely onsome of the testing, but there's
there's nothing best betterthan a good history from the
patients, from their families.
They tell you everything that'sgoing on.
And you know, if you'reexperienced, you can catch on as
to what's going on.
And then, of course, you know,you order your general uh
(11:03):
workup, MRI, blood work, and awhole host of things.
But basically, I personallyrely on that history and
physical exam before anythingelse.
Dr. Michael Koren (11:12):
Fascinating.
Interesting.
So tell us a little bit moreabout Alzheimer's as a
percentage of all forms ofdementia, and then uh walk us
through what the definitive testis for Alzheimer's.
Dr. Reza Bolouri (11:25):
Well, like I said earlier, the reason folks
use the Alzheimer's and dementiainterchangeably because 60 to
80% of the dementias happen tobe Alzheimer's disease.
And for that reason, besidesthe good history and physical
exam and some of the initialassessments, now we have
sophisticated methods, uh, brainPET scan, amyloid PET scan, Tau
(11:47):
PET scan, blood biomarkers, anduh and a genetic test to check
for susceptibility gene forAlzheimer's disease.
Now we have become much more uhsophisticated in uh actually
identifying the Alzheimer'sversus non-Alzheimer types of
dementia.
In fact, now uh most of theresearch is focusing on
(12:09):
prevention to identify thepatients who are at risk of
developing Alzheimer's disease20 years from now.
Dr. Michael Koren (12:16):
Interesting.
So that's that's that's how wehave uh advanced, whereas we are
identifying folks who will bedeveloping Alzheimer's disease
20 years from now.
The changes in the brain havestarted, but they're functioning
normally.
They're working, they'reraising family, they're making
decisions without any problems.
So fascinating.
(12:36):
So tell us a little bit aboutum the definitive test that gets
people involved in a clinicaltrial.
What you usually have to findfor people to be able to enroll
in a clinical trial.
Dr. Reza Bolouri (12:48):
Well, for the longest time, you know, I'm
sure a lot of folks have heardthat we used to say, you know,
after uh a patient passes, youknow, you do the pathological
evaluation of their brain.
We no longer do that.
So the the the evolve uhevolving um uh diagnostic workup
initially was uh brain PETscan, just a FTG PET scan to
(13:12):
distinguish between Alzheimer's,frontotemporal dementia, Lewy
body dementia, and so on.
But with the advent of theamyloid scans, now we can do
amyloid PET scans where we canactually see the amyloid that
lights up in those images.
We can tell.
Dr. Michael Koren (13:28):
That's interesting.
Dr. Reza Bolouri (13:29):
However, unfortunately, amyloid PET's uh
are very expensive.
And a lot of insurancecompanies, even Medicare, was
not on board with that, $10,000,$15,000.
So then they we resorted tospinal fluid analysis, where if
the theory, the theory goes ifthose proteins are sitting on
the brain, there's not enough ofthem drained in the spinal
(13:49):
fluid.
So by those measurements, wecould come to a fairly close
approximation of the developmentof Alzheimer's disease.
Over the past five years, nowwe have blood biomarkers.
Uh recently, uh Lumi pulse uhis the most sophisticated blood
test that uh can accuratelydiagnose Alzheimer's bit uh 90
(14:13):
uh uh percent sensitivity andspecificity.
So, with that in mind, nowrather than the PET scan or
spinal fluid, where a lot ofpatients don't like it because
of the pain and so on involved.
So, with a simple blood test,we can actually determine if
somebody uh is developingAlzheimer's.
Dr. Michael Koren (14:32):
Interesting.
So, how does that blood test at90% accuracy compare with an
FDG, FDG PET, which is lookingat glucose metabolism in the
brain for people that are notfamiliar with the terminology?
Dr. Reza Bolouri (14:43):
Well, you know, uh understanding
Alzheimer's, uh we do know thatthe folks with diabetes are at
highest risk of developingAlzheimer's simply because their
glucose dysmetabolism is one ofthe biggest culprits in
Alzheimer's disease.
For for the longest time, thethe metabolism of glucose
through the FDG PET, we wereable to determine if there is a
(15:05):
metal decreased metabolism inthe temporal areas, in parietal
areas.
If it was temporal and frontal,they would be frontotemporal.
Dr. Michael Koren (15:13):
If it was occipital, and frontal here and
temporal here, just for peoplethat-
-frontal, temporal-
-use to these terms.
Dr. Reza Bolouri (15:20):
Occipital, which is uh basically the Lewy
body.
But what happened is that wasnonspecific.
It was giving us some ideas,Just like MRI shows some
atrophy, for example.
However, with the with theamyloid, now we can actually uh
inject a tracer where theamyloid lights up.
Dr. Michael Koren (15:39):
Interesting.
And that's what we know.
Yes, that's amyloid that'ssitting there.
Uh now with the tau, we cantell that the tau protein is
sitting in the brain.
So those are the markers thatare over above a 95-96%.
Fascinating.
Okay, so we diagnosed somebodywith Alzheimer's dementia.
Tell us about the therapy.
(16:00):
I know there are some oldschool drugs that we've used.
Are they still being used?
I know there's some reallyinteresting research findings
that have led to new approvals.
So why don't you break thatdown for everybody?
Dr. Reza Bolouri (16:10):
Yeah, I I remember when I was a research
coordinator um uh in um Miami,initial uh medications were
focusing on um cholinesteraseinhibitors.
And uh because the cholinergicuh theory was out there, we we
did know that cholinergicdeficiency caused Alzheimer's
disease.
And it's interesting how itcame about.
(16:32):
The folks who are usingscopolamine patch for the
seasickness, they were beginningto become forgetful.
That's how it all came about.
They realized the cholinergictherapy.
So a lot of companies, a lot ofthe science, scientific
community began to focus oncholinergic uh therapy.
So um the body cannot uhmetabolize choline.
(16:53):
So they found indirect ways offinding how we can increase the
acetylcholine.
So indirectly, by inhibitingthe enzyme acetylcholinesterase,
we were able to increase theamount of choline in the body.
So that's whenanticholinesterase inhibitors
like donepezil, rivastigmine,galantamine came about.
(17:14):
And eventually, uh the firstone uh which was tacrine in
1994, that was approved, and thedonepezil in 1996.
Those were the symptomatictherapy.
They were providing somesymptoms for uh a year or two,
or maximum of three years, andthen they would become less
efficient because there was lesscells to uh you know uh rescue.
(17:37):
Right.
So eventually uh memantine wasapproved.
We did work on the 90s in 1996,it was approved in 97, it's a
different class of drug, it's anNMDA receptor antagonist.
So we had nothing until about2020, 2020, 2021, where the
anti-amyloid antibodies began togain popularity.
Dr. Michael Koren (17:57):
It's about 20 years of not a whole lot of
activity.
Dr. Reza Bolouri (18:00):
There was nothing.
So in the clinical practice, wecouldn't really offer anything
beyond those symptomatictherapy.
One of the things I loved aboutmy research and practice is
beyond the symptomatic therapy,I was able to offer
disease-modifying drugs to mypatients.
And that's where the researchcomes, and it makes it much more
interesting because you know,once you have done what you
(18:22):
could with symptomatic, thenyou're able to offer your
patients clinical trials,research uh uh medicines which
are beyond the symptomatic,those called disease-modifying
drugs.
Dr. Michael Koren (18:34):
Absolutely.
So, where do we stand withanti-amyloid drugs and disease
modifying drugs?
Do we have do we have the magicbullet yet?
Or what what should we lookingfor?
What what is yourrecommendation in terms of what
people should ask for at thispoint in terms of how far we've
progressed?
Dr. Reza Bolouri (18:50):
Well, definitely we we uh have been
able to slow the progression ofthe disease.
I think that's a that's a majorvictory as far as I'm
concerned.
And um uh there there was fourthat that that was uh uh came
out, and the first one,unfortunately, because of some
potential side effects, did notpan out.
However, right now the two mostsuccessful anti-amyloid
(19:12):
antibodies are Leqembi orLecanemab or Kisunla or
Donanemab.
Those two drugs are available.
So physicians, not only theresearchers, not only the
neurologists, a lot ofphysicians can offer it, but
they do require very carefulmonitoring because of potential
side effects.
So, having said that, rightnow, the drugs that we are
(19:35):
testing are the new and improvedanti-amyloid and anti-Tau
antibodies that we are workingon, which I believe within the
next uh few years, we're gonnahave a combination of
anti-amyloid and anti-Tauantibodies to really put a dent
in the course of the disease.
However, a lot of people askme, when are you gonna find the
cure?
(19:55):
Uh uh, my the best answer I cangive is in order to find a cure
for a disease, you have to finda single etiology for that
disease to be able to tackle.
Alzheimer's is not caused byone thing.
Alzheimer's disease is causedby a whole host of bad things
that happens in the brain.
So are we gonna be able totackle every single one?
(20:17):
Probably no, but I anticipate acocktail of medicines are
eventually really going to put auh stop to the progression of
the disease because just likeHIV, right?
You know, in the beginning,when I was in medical school in
the 80s,
Dr. Michael Koren (20:33):
It was a death sentence.
Death sentence.
But now people are living witha good cocktail, normal lives.
So I'm hoping for that forAlzheimer's medicine.
Interesting, very, very interesting.
So, what's the next chapter foryou?
I I know that uh we talked alittle bit about the fact that
you've been doing this for awhile and you're really
interested in helping the nextgeneration become great
researchers.
So tell us a little bit aboutthat.
Dr. Reza Bolouri (20:54):
Well, actually, uh my philosophy in
medicine has always been uh Ithere's a lot I don't know.
But what I do know, I wouldlike to go ahead and pass it on
to the next generation, to thestudents, to the residents, to
the new neurologists, newpsychiatrists, new physicians
who have an interest in tacklingthis devastating disease that's
(21:14):
uh really affecting it's it'snot only national, it's an
international uh uh catastrophethat uh I would like to go ahead
and pass on the knowledge anddo the best I can to contribute.
Dr. Michael Koren (21:25):
Absolutely.
So you have a bunch of uhmentees lined up to follow your
in your footsteps as Iunderstand it.
Yes, yes,
That's exciting.
Reza, that was fascinating.
That was a great, great summaryof Alzheimer's dementia and a
great summary of some of theresearch that has led to some
affected products and reallyhope for the future in terms of
(21:46):
potentially a cocktail that willturn Alzheimer's dementia into
something that's verymanageable, like HIV disease, as
you pointed out.
So those are really, reallyexciting things.
Any final words you want toshare with our audience with
regard to uh your approach orwhat they should do if they're
concerned about memory issues?
Dr. Reza Bolouri (22:03):
I mean, the the the best advice I can give
to healthcare providers is uh beaware of memory issues.
Don't just discount it, don'tsweep it under the rug.
Uh get some help, do someassessments.
If you don't feel comfortableabout doing that, send them to
the memory specialists, sendthem to the memory centers, have
them worked up because thesefolks deserve better than just,
(22:24):
you know, it's just aging, whatdo you expect?
I think I think that's uh whenI do uh my talks to the primary
care physicians and otherneurologists, I I emphasize the
fact that it's very importantfor us to be able to establish
some kind of a criteria as partof the annual workup of
Medicare, you know, wellness uhprograms.
And I think that's that'sextremely important.
(22:46):
I think uh I need to uhemphasize that we are doing some
prevention trials right now.
Prevention trials are forpeople who do not have memory
problems, but they have themarkers of Alzheimer's disease.
Uh and uh one of the studiesjust got uh uh uh okay to
continue, uh, which is veryexciting.
If that drug pans out and it'sis approved, I think I'll be the
(23:09):
first one to say after the ageof 50, everybody should be
screened for Alzheimer's diseaseto catch it early on before the
symptoms begin.
Dr. Michael Koren (23:16):
Makes sense.
Dr. Reza Bolouri (23:17):
Because by the time you come with symptoms,
several years has alreadypassed.
Dr. Michael Koren (23:20):
Right.
Dr. Reza Bolouri (23:20):
So catch it early, that's the key.
Dr. Michael Koren (23:23):
Absolutely.
Well, that's that's greatinsight.
So thank you very much forsharing that.
Dr. Reza Bolouri (23:27):
Welcome.
Dr. Michael Koren (23:27):
So, Reza, give us an example of a patient
that's been helped by theadvances in pharmacotherapy for
Alzheimer's.
Dr. Reza Bolouri (23:36):
Well, you know, the disease, the new
disease-modifying drugs actuallyuh do dissolve these proteins
in the brain.
For example, the the newlydiagnosed uh uh newly approved
drugs that Kisunla and Leqembi,uh, we can actually measure the
amount of protein that's been uhcleared uh by these drugs.
And by that, in fact, at somepoint within a year and a half
(24:00):
to two years, you can actuallystop those because the clearance
has been completed, where thebrain almost has no more amyloid
or tau protein.
So that's quite impressive.
That I I believe that with newand improved therapies with less
potential side effects, weshould be able to get this.
I have many patients that havebeen following that in the past
(24:21):
they would not survive beyondfive or six years, ten years on,
they're still communicating,they're interacting.
So that's that's quiterewarding for me as a
researcher.
Dr. Michael Koren (24:31):
And you see people that respond clinically
that actually get better.
Yes.
Isn't that great?
Dr. Reza Bolouri (24:36):
Yes, yes.
There are some authorities thatactually believe Alzheimer's is
a type 3 diabetes, simplybecause we do know that brain
uses glucose as a metabol, as afuel.
So when there's not enoughglucose or there is a disruption
of the glucose delivery to thebrain, brain is affected.
Dr. Michael Koren (24:55):
Right.
Dr. Reza Bolouri (24:56):
There are two types of Alzheimer's disease.
There's an old onset, there's ayoung onset.
Fortunately, young onset is aminority of the cases, and they
happen to run in families almostin a form of autosomal dominant
inheritance.
There's a group in Colombia,everybody has Alzheimer's
disease.
Even children have Alzheimer'sdisease.
(25:17):
Fortunately, young onsetAlzheimer's disease is rare
simply because it's a moremalignant form of Alzheimer's
disease.
It happens in a youngerpopulation with significant
behavioral disturbances.
Um, but uh majority of thecases are the are the older type
Alzheimer's.
So if I'm gonna developAlzheimer's disease, I don't
mind in my 50s and 60s, I mindin my 80s.
(25:40):
Got it.
What happens is uhstatistically, uh the Hispanics
are at the highest risk ofAlzheimer's disease.
Dr. Michael Koren (25:47):
Interesting,
-followed by the AfricanAmericans uh and then
Caucasians.
Okay.
So uh why do why don't we havemore uh Hispanics or African
Americans simply because of thethe uh availability of the
healthcare uh and educationalbackground to seek help?
I think that's been amazing.
Are there any theories as to why Hispanics
(26:08):
are at higher risk?
Dr. Reza Bolouri (26:10):
Well, um my theory is uh the folks in the
minority community do not getthe medical attention that they
deserve for hypertension, fordiabetes, for high cholesterol.
And we know at the end of theday, all these brain disorders
are vascular.
Dr. Michael Koren (26:26):
Yeah.
It gets into somethinginteresting, which is called the
Hispanic paradox.
So people of Hispanic ethnicityactually live three years
longer on average than whitepeople.
And uh that's always aninteresting little tidbit in the
United States that we don'ttalk that much about.
So there's some things thatHispanic populations are doing
really well.
They have a closer familyties, having a Hispanic as a
(26:50):
wife.
Well, that can be or they eat better or
they are more physically active,but it's it's a it's an
interesting paradox.
Dr. Reza Bolouri (26:56):
Yes.
Dr. Michael Koren (26:56):
So, Reza, a lot of my patients come to me
and ask me, I'm really concernedI have Old Timers disease.
So is it Old Timers or is itAlzheimer's?
And why do we call itAlzheimer's?
Dr. Reza Bolouri (27:08):
Actually, uh a lot of folks uh since uh age
happens to be the biggest riskfactor for Alzheimer's disease,
a lot of older folks developAlzheimer's.
So it's just, you know, somefolks say it's Old timers
disease or All Timers disease.
In fact, the term comes fromDr.
Alois Alzheimer, who was aGerman pathologist and had seen
(27:30):
a patient uh uh who was a veryyoung woman uh in her 50s.
Uh the initial description ofAlzheimer's change was a young
onset Alzheimer's patient, um,which uh uh that's how the name
came about.
Uh Alzheimer's
So it's a relatively moderndisease, only about 100 years
old.
That's right.
Dr. Michael Koren (27:51):
Reza, it's been a delightful conversation.
Thank you for being part ofMedEvidence!
Welcome.
Thank you so much for havingme.
Announcer (27:57):
Thanks for joining the MedEvidence Podcast.
To learn more, head over toMedevidence.com or subscribe to
our podcast on your favoritepodcast platform.
Welcome to MedEvidence!, where we help you
navigate the truth behindmedical research with unbiased,
evidence-proven facts, hosted bycardiologist and top medical
researcher, Dr.
Michael Koren.
Dr. Michael Koren (00:11):
Hello, I'm Dr.
Michael Koren, the executiveeditor for MedEvidence! And we
get a lot of questions here atMedEvidence, and one of the
things that comes up all thetime is about memory issues.
And I'm so fortunate to have anexpert in memory issues, Dr.
Reza Bolouri, who's joining mehere in the studio.
And we're going to have anexciting conversation about
(00:33):
memory issues and also talkabout clinical research in the
memory area.
So, Reza, thank you so much forbeing part of our MedEvidence
family.
Dr. Reza Bolouri (00:42):
Thank you so much for inviting me.
Great to have you.
Dr. Michael Koren (00:45):
Yeah, so let's just start.
We like to start by justgetting to know each other, you,
me, and the audience.
So tell us a little bit aboutyour background.
You had a little bit of anon-traditional way that you
became a memory physician.
So why don't you let everybodyknow how you got there?
And and and by the way, uh Rezais one of really the national
experts in memory and inresearch in the memory area.
(01:06):
So again, thank you for that.
But how'd you get there?
Dr. Reza Bolouri (01:09):
Thank you.
Actually, after medical school,I um was uh studying for my
boards, being a foreign medicalgraduate.
So I was looking for a job andI stumbled into this um um
neurology practice that was uh ageneral practice, but they were
they had started doing someclinical trials on Alzheimer's
(01:30):
disease.
So I was hired as a researchcoordinator.
Dr. Michael Koren (01:33):
Wow.
Dr. Reza Bolouri (01:33):
And um I that's how I got my feet wet and
started looking at studies uhwhen we really didn't have much
uh knowledge about what wasgoing on with Alzheimer's
disease, what was happening,even the amyloid hypothesis was
just growing.
And eventually uh through theyears, after uh several hundred
studies uh began to understandAlzheimer's disease, became very
(01:58):
interested in Alzheimer'sdisease and therapeutic areas.
And uh at some point I startedmy residencies after passing my
boards, did uh uh psychiatry anduh subsequently neurology, and
uh settled down in Charlotte,North Carolina, opened up my own
practice after working for ahospital for about two years,
(02:22):
then started a general practiceand eventually cognitive
neurology, and then subsequentlywent back to clinical trials
and doing research.
Dr. Michael Koren (02:31):
So interesting.
So you really started from theground up Even before you were
a practicing physician in theUnited States, you were actually
learning research.
Dr. Reza Bolouri (02:40):
That's correct.
Dr. Michael Koren (02:40):
That's really, really cool.
I love that.
Great story.
So tell us a little bit moreabout how your practice
developed.
I know that you have a uniquemodel of reaching out into the
community to help people thatmay have concerns about the
memory.
Dr. Reza Bolouri (02:53):
Well, actually, given my background in
Alzheimer's, I became extremelyinterested in geriatric
neurology and specifically in uhcognitive neurology.
And um we do know that themajority of the cases of
dementia happen to beAlzheimer's disease.
That's why a lot of folks uhinterchangeably use Alzheimer's
(03:14):
and dementia, whereas they'renot exactly the same thing.
So I um um focused on uhcognitive neurology.
Dementia established uh a majorpopulation of folks in the
Charlotte area who had memorydisorders, and then uh my
practice began to focus more inthe dementia area, and then my
(03:35):
background in research, wedecided to go ahead and restart
our clinical trials.
So we've been very successfulover the past 20 years in not
only the general practice, butalso our uh research grew uh uh
rather rapidly.
And um uh we've done over 200studies just in the past two
years, uh 20 years, sorry.
(03:57):
And um uh we we are I'm proudto be um uh one of the uh
investigators involved in allthe drugs out there for
Alzheimer's disease, startingfrom the symptomatic therapies
and newly approved uh diseasemodifying drugs.
And we continue uh that pathand um we are introduced to uh
much better, new and improveddrugs, which we are working on
(04:20):
right now.
Dr. Michael Koren (04:20):
Yeah, and that's so satisfying.
Actually, one of the great joysI get as a clinical
investigator is to be part ofthese programs that result in
products that help people'slives.
So there's nothing better thanthat.
Yes.
So let's let's break downmemory issues for the public.
As you mentioned, you alludedto the fact that Alzheimer's is
(04:41):
a subset of dementia issues andmemory issues, but there's a lot
of confusion out there.
So let's start with a patientthat's concerned about his or
her memory.
They come to you, how do youbreak down this particular
person's uh concerns fromsomething that's either real or
not so real, quote unquote.
And how do you figure out ifit's Alzheimer's versus another
(05:01):
form of dementia?
Dr. Reza Bolouri (05:03):
Well, the best way I usually explain that
to my patients and theirfamilies is um dementia is not a
disease, it's a syndrome.
And uh basically what thatmeans is, for example, we have
heart failure, we have liverfailure, kidney failure, and so
on.
And dementia is nothing but abrain failure.
So if you could just uh um Idescribe it that way, it's a
(05:27):
brain failure.
So when someone comes to mewith any kind of a cognitive
issues, the first thing I wantto do is get a good history, do
a good physical examination, dosome preliminary workup to
distinguish uh the type ofdementia we are dealing with.
For example, someone who isdrinking 20 years every day, all
(05:48):
day, that's alcoholic dementia.
Okay.
When you do an MRI of the brainand you see a bunch of strokes,
that's vascular dementia.
If somebody is exhibiting someParkinsonism, it could be a
Parkinsonian dementia or Lewybody dementia.
A patient starting with thelanguage problem, behavioral
problems, it could befrontemporal dementia.
(06:08):
Through some assessments andgood clinical work, we determine
exactly what kind of dementiathat is.
Dr. Michael Koren (06:16):
Interesting.
So just to help people, you youyou threw out a lot of stuff
there, which is great.
But for example, uhParkinsonian dementia would be
associated with other elementsof the Parkinsonian syndrome or
disease, including likestiffness.
Maybe mention some other thingsthat would be associated with
so people can understand thedifference between that and
Alzheimer's.
Dr. Reza Bolouri (06:36):
Well, you know, uh once once you begin to
learn about the dementias, isyou you're able to distinguish
the differences.
However, uh uh, for example,Parkinsonian dementias, uh there
are two types.
Uh there are several types ofParkinsonian dementias.
For example, there are folkswho have established diagnosis
of Parkinson's disease, andlater in the course of their
(06:58):
disease, they develop dementia.
That's called Parkinson'sdisease-related dementia.
Whereas other types ofParkinsonian dementias, the
Parkinsonism and dementia comeat the same time or within a
year from each other.
So that's different than awell-established Parkinson's
disease, whereas uh Parkinsoniandementias that are not
(07:19):
Parkinson's disease-relateddementia, they do not exhibit
all the signs and symptoms of atypical Parkinson's disease.
Dr. Michael Koren (07:26):
Got it, got it.
So taking a step back, becausethis is a common question that I
get, even in my cardiologypractice, is when people are
having difficulty with theirmemory, how do you distinguish
changes in your memory and maybeyour mental acuity as you get
older versus an actual disease?
Dr. Reza Bolouri (07:46):
Well, I'm asked about this question a lot.
Uh, there is a phenomenon uh uhcalled age-associated memory
impairment.
In the old days, we used tocall them senile dementia,
presenility, hardening of thearteries, and a whole host of
things.
We no longer use thosederogatory terms.
Uh so we call it age-relatedmemory problem.
(08:06):
How do we distinguish theage-related memory problem from
Alzheimer's disease?
Is as we age, just likeeverything else, we slow down
mentally and physically.
Age-associated memory problem,the folks begin to have some
short-term memory problem.
They go to a room wonderingwhat they went there for, and
then uh slow down in manyrespects in their responses, in
(08:29):
their activities.
However, they do not progress.
They remain the same and fullyfunctional.
They're 90-year-olds,100-year-olds who are still
doing their things, but yes,they have lapses of memory, the
senior moments.
Whereas with Alzheimer's, thefolks who are transitioning to
Alzheimer's, they begin to losethe ability of the learned
(08:52):
processes, learned uh habits,learned activities.
That's why we call it a greatunlearning.
And these are the folks whohave learned, they have raised
families, they've educated, theyworked, and eventually they
lose the ability to drive, tomake decisions, to pay
bills, and that's why you cantell the difference versus
(09:15):
progressive o r stable form ofmemory impairment.
And that's that's that that'show we can tell the difference.
Dr. Michael Koren (09:22):
Got it.
Is there something you canlearn about that difference by
doing mental status testing?
How good is mental statustesting at determining who has
this more ominous progressiveform versus people that may just
be getting a little slowerbecause of age?
Dr. Reza Bolouri (09:40):
Well, I mean, the science has advanced.
I mean, now we have ways toreally tell if someone is
developing Alzheimer's disease,which we can go to when we talk
about research.
But generally, uh, a goodclinical practice, a good uh
practitioner observes thepatients for a while to see who
is declining and who is not.
The best source of informationis patients' family.
(10:02):
Okay.
They tell you he or she is notthe same.
He forgot, uh he got lostdriving, he forgot to pay a
bill, he made a bad decision, hegot scammed uh online.
Uh those are the things thatraise the flag of something else
is going on.
And besides, when we talk aboutdementia, when we talk about
memory memory, it's not justmemory.
(10:23):
It's memory, problem solving,decision making, planning,
organizing.
Everything is affected.
It's not just memory.
Memory is the first thing wenotice, but everything else uh
happens.
Dr. Michael Koren (10:34):
So interviews with family and the patient you
think is more valuable thansome of the formal cognitive
testing, or there's a role forboth?
Dr. Reza Bolouri (10:42):
It's a combination.
There's a role for both.
Of course, we we do rely onsome of the testing, but there's
there's nothing best betterthan a good history from the
patients, from their families.
They tell you everything that'sgoing on.
And you know, if you'reexperienced, you can catch on as
to what's going on.
And then, of course, you know,you order your general uh
(11:03):
workup, MRI, blood work, and awhole host of things.
But basically, I personallyrely on that history and
physical exam before anythingelse.
Dr. Michael Koren (11:12):
Fascinating.
Interesting.
So tell us a little bit moreabout Alzheimer's as a
percentage of all forms ofdementia, and then uh walk us
through what the definitive testis for Alzheimer's.
Dr. Reza Bolouri (11:25):
Well, like I said earlier, the reason folks
use the Alzheimer's and dementiainterchangeably because 60 to
80% of the dementias happen tobe Alzheimer's disease.
And for that reason, besidesthe good history and physical
exam and some of the initialassessments, now we have
sophisticated methods, uh, brainPET scan, amyloid PET scan, Tau
(11:47):
PET scan, blood biomarkers, anduh and a genetic test to check
for susceptibility gene forAlzheimer's disease.
Now we have become much more uhsophisticated in uh actually
identifying the Alzheimer'sversus non-Alzheimer types of
dementia.
In fact, now uh most of theresearch is focusing on
(12:09):
prevention to identify thepatients who are at risk of
developing Alzheimer's disease20 years from now.
Dr. Michael Koren (12:16):
Interesting.
So that's that's that's how wehave uh advanced, whereas we are
identifying folks who will bedeveloping Alzheimer's disease
20 years from now.
The changes in the brain havestarted, but they're functioning
normally.
They're working, they'reraising family, they're making
decisions without any problems.
So fascinating.
(12:36):
So tell us a little bit aboutum the definitive test that gets
people involved in a clinicaltrial.
What you usually have to findfor people to be able to enroll
in a clinical trial.
Dr. Reza Bolouri (12:48):
Well, for the longest time, you know, I'm
sure a lot of folks have heardthat we used to say, you know,
after uh a patient passes, youknow, you do the pathological
evaluation of their brain.
We no longer do that.
So the the the evolve uhevolving um uh diagnostic workup
initially was uh brain PETscan, just a FTG PET scan to
(13:12):
distinguish between Alzheimer's,frontotemporal dementia, Lewy
body dementia, and so on.
But with the advent of theamyloid scans, now we can do
amyloid PET scans where we canactually see the amyloid that
lights up in those images.
We can tell.
Dr. Michael Koren (13:28):
That's interesting.
Dr. Reza Bolouri (13:29):
However, unfortunately, amyloid PET's uh
are very expensive.
And a lot of insurancecompanies, even Medicare, was
not on board with that, $10,000,$15,000.
So then they we resorted tospinal fluid analysis, where if
the theory, the theory goes ifthose proteins are sitting on
the brain, there's not enough ofthem drained in the spinal
(13:49):
fluid.
So by those measurements, wecould come to a fairly close
approximation of the developmentof Alzheimer's disease.
Over the past five years, nowwe have blood biomarkers.
Uh recently, uh Lumi pulse uhis the most sophisticated blood
test that uh can accuratelydiagnose Alzheimer's bit uh 90
(14:13):
uh uh percent sensitivity andspecificity.
So, with that in mind, nowrather than the PET scan or
spinal fluid, where a lot ofpatients don't like it because
of the pain and so on involved.
So, with a simple blood test,we can actually determine if
somebody uh is developingAlzheimer's.
Dr. Michael Koren (14:32):
Interesting.
So, how does that blood test at90% accuracy compare with an
FDG, FDG PET, which is lookingat glucose metabolism in the
brain for people that are notfamiliar with the terminology?
Dr. Reza Bolouri (14:43):
Well, you know, uh understanding
Alzheimer's, uh we do know thatthe folks with diabetes are at
highest risk of developingAlzheimer's simply because their
glucose dysmetabolism is one ofthe biggest culprits in
Alzheimer's disease.
For for the longest time, thethe metabolism of glucose
through the FDG PET, we wereable to determine if there is a
(15:05):
metal decreased metabolism inthe temporal areas, in parietal
areas.
If it was temporal and frontal,they would be frontotemporal.
Dr. Michael Koren (15:13):
If it was occipital, and frontal here and
temporal here, just for peoplethat-
-frontal, temporal-
-use to these terms.
Dr. Reza Bolouri (15:20):
Occipital, which is uh basically the Lewy
body.
But what happened is that wasnonspecific.
It was giving us some ideas,Just like MRI shows some
atrophy, for example.
However, with the with theamyloid, now we can actually uh
inject a tracer where theamyloid lights up.
Dr. Michael Koren (15:39):
Interesting.
And that's what we know.
Yes, that's amyloid that'ssitting there.
Uh now with the tau, we cantell that the tau protein is
sitting in the brain.
So those are the markers thatare over above a 95-96%.
Fascinating.
Okay, so we diagnosed somebodywith Alzheimer's dementia.
Tell us about the therapy.
(16:00):
I know there are some oldschool drugs that we've used.
Are they still being used?
I know there's some reallyinteresting research findings
that have led to new approvals.
So why don't you break thatdown for everybody?
Dr. Reza Bolouri (16:10):
Yeah, I I remember when I was a research
coordinator um uh in um Miami,initial uh medications were
focusing on um cholinesteraseinhibitors.
And uh because the cholinergicuh theory was out there, we we
did know that cholinergicdeficiency caused Alzheimer's
disease.
And it's interesting how itcame about.
(16:32):
The folks who are usingscopolamine patch for the
seasickness, they were beginningto become forgetful.
That's how it all came about.
They realized the cholinergictherapy.
So a lot of companies, a lot ofthe science, scientific
community began to focus oncholinergic uh therapy.
So um the body cannot uhmetabolize choline.
(16:53):
So they found indirect ways offinding how we can increase the
acetylcholine.
So indirectly, by inhibitingthe enzyme acetylcholinesterase,
we were able to increase theamount of choline in the body.
So that's whenanticholinesterase inhibitors
like donepezil, rivastigmine,galantamine came about.
(17:14):
And eventually, uh the firstone uh which was tacrine in
1994, that was approved, and thedonepezil in 1996.
Those were the symptomatictherapy.
They were providing somesymptoms for uh a year or two,
or maximum of three years, andthen they would become less
efficient because there was lesscells to uh you know uh rescue.
(17:37):
Right.
So eventually uh memantine wasapproved.
We did work on the 90s in 1996,it was approved in 97, it's a
different class of drug, it's anNMDA receptor antagonist.
So we had nothing until about2020, 2020, 2021, where the
anti-amyloid antibodies began togain popularity.
Dr. Michael Koren (17:57):
It's about 20 years of not a whole lot of
activity.
Dr. Reza Bolouri (18:00):
There was nothing.
So in the clinical practice, wecouldn't really offer anything
beyond those symptomatictherapy.
One of the things I loved aboutmy research and practice is
beyond the symptomatic therapy,I was able to offer
disease-modifying drugs to mypatients.
And that's where the researchcomes, and it makes it much more
interesting because you know,once you have done what you
(18:22):
could with symptomatic, thenyou're able to offer your
patients clinical trials,research uh uh medicines which
are beyond the symptomatic,those called disease-modifying
drugs.
Dr. Michael Koren (18:34):
Absolutely.
So, where do we stand withanti-amyloid drugs and disease
modifying drugs?
Do we have do we have the magicbullet yet?
Or what what should we lookingfor?
What what is yourrecommendation in terms of what
people should ask for at thispoint in terms of how far we've
progressed?
Dr. Reza Bolouri (18:50):
Well, definitely we we uh have been
able to slow the progression ofthe disease.
I think that's a that's a majorvictory as far as I'm
concerned.
And um uh there there was fourthat that that was uh uh came
out, and the first one,unfortunately, because of some
potential side effects, did notpan out.
However, right now the two mostsuccessful anti-amyloid
(19:12):
antibodies are Leqembi orLecanemab or Kisunla or
Donanemab.
Those two drugs are available.
So physicians, not only theresearchers, not only the
neurologists, a lot ofphysicians can offer it, but
they do require very carefulmonitoring because of potential
side effects.
So, having said that, rightnow, the drugs that we are
(19:35):
testing are the new and improvedanti-amyloid and anti-Tau
antibodies that we are workingon, which I believe within the
next uh few years, we're gonnahave a combination of
anti-amyloid and anti-Tauantibodies to really put a dent
in the course of the disease.
However, a lot of people askme, when are you gonna find the
cure?
(19:55):
Uh uh, my the best answer I cangive is in order to find a cure
for a disease, you have to finda single etiology for that
disease to be able to tackle.
Alzheimer's is not caused byone thing.
Alzheimer's disease is causedby a whole host of bad things
that happens in the brain.
So are we gonna be able totackle every single one?
(20:17):
Probably no, but I anticipate acocktail of medicines are
eventually really going to put auh stop to the progression of
the disease because just likeHIV, right?
You know, in the beginning,when I was in medical school in
the 80s,
Dr. Michael Koren (20:33):
It was a death sentence.
Death sentence.
But now people are living witha good cocktail, normal lives.
So I'm hoping for that forAlzheimer's medicine.
Interesting, very, very interesting.
So, what's the next chapter foryou?
I I know that uh we talked alittle bit about the fact that
you've been doing this for awhile and you're really
interested in helping the nextgeneration become great
researchers.
So tell us a little bit aboutthat.
Dr. Reza Bolouri (20:54):
Well, actually, uh my philosophy in
medicine has always been uh Ithere's a lot I don't know.
But what I do know, I wouldlike to go ahead and pass it on
to the next generation, to thestudents, to the residents, to
the new neurologists, newpsychiatrists, new physicians
who have an interest in tacklingthis devastating disease that's
(21:14):
uh really affecting it's it'snot only national, it's an
international uh uh catastrophethat uh I would like to go ahead
and pass on the knowledge anddo the best I can to contribute.
Dr. Michael Koren (21:25):
Absolutely.
So you have a bunch of uhmentees lined up to follow your
in your footsteps as Iunderstand it.
Yes, yes,
That's exciting.
Reza, that was fascinating.
That was a great, great summaryof Alzheimer's dementia and a
great summary of some of theresearch that has led to some
affected products and reallyhope for the future in terms of
(21:46):
potentially a cocktail that willturn Alzheimer's dementia into
something that's verymanageable, like HIV disease, as
you pointed out.
So those are really, reallyexciting things.
Any final words you want toshare with our audience with
regard to uh your approach orwhat they should do if they're
concerned about memory issues?
Dr. Reza Bolouri (22:03):
I mean, the the the best advice I can give
to healthcare providers is uh beaware of memory issues.
Don't just discount it, don'tsweep it under the rug.
Uh get some help, do someassessments.
If you don't feel comfortableabout doing that, send them to
the memory specialists, sendthem to the memory centers, have
them worked up because thesefolks deserve better than just,
(22:24):
you know, it's just aging, whatdo you expect?
I think I think that's uh whenI do uh my talks to the primary
care physicians and otherneurologists, I I emphasize the
fact that it's very importantfor us to be able to establish
some kind of a criteria as partof the annual workup of
Medicare, you know, wellness uhprograms.
And I think that's that'sextremely important.
(22:46):
I think uh I need to uhemphasize that we are doing some
prevention trials right now.
Prevention trials are forpeople who do not have memory
problems, but they have themarkers of Alzheimer's disease.
Uh and uh one of the studiesjust got uh uh uh okay to
continue, uh, which is veryexciting.
If that drug pans out and it'sis approved, I think I'll be the
(23:09):
first one to say after the ageof 50, everybody should be
screened for Alzheimer's diseaseto catch it early on before the
symptoms begin.
Dr. Michael Koren (23:16):
Makes sense.
Dr. Reza Bolouri (23:17):
Because by the time you come with symptoms,
several years has alreadypassed.
Dr. Michael Koren (23:20):
Right.
Dr. Reza Bolouri (23:20):
So catch it early, that's the key.
Dr. Michael Koren (23:23):
Absolutely.
Well, that's that's greatinsight.
So thank you very much forsharing that.
Dr. Reza Bolouri (23:27):
Welcome.
Dr. Michael Koren (23:27):
So, Reza, give us an example of a patient
that's been helped by theadvances in pharmacotherapy for
Alzheimer's.
Dr. Reza Bolouri (23:36):
Well, you know, the disease, the new
disease-modifying drugs actuallyuh do dissolve these proteins
in the brain.
For example, the the newlydiagnosed uh uh newly approved
drugs that Kisunla and Leqembi,uh, we can actually measure the
amount of protein that's been uhcleared uh by these drugs.
And by that, in fact, at somepoint within a year and a half
(24:00):
to two years, you can actuallystop those because the clearance
has been completed, where thebrain almost has no more amyloid
or tau protein.
So that's quite impressive.
That I I believe that with newand improved therapies with less
potential side effects, weshould be able to get this.
I have many patients that havebeen following that in the past
(24:21):
they would not survive beyondfive or six years, ten years on,
they're still communicating,they're interacting.
So that's that's quiterewarding for me as a
researcher.
Dr. Michael Koren (24:31):
And you see people that respond clinically
that actually get better.
Yes.
Isn't that great?
Dr. Reza Bolouri (24:36):
Yes, yes.
There are some authorities thatactually believe Alzheimer's is
a type 3 diabetes, simplybecause we do know that brain
uses glucose as a metabol, as afuel.
So when there's not enoughglucose or there is a disruption
of the glucose delivery to thebrain, brain is affected.
Dr. Michael Koren (24:55):
Right.
Dr. Reza Bolouri (24:56):
There are two types of Alzheimer's disease.
There's an old onset, there's ayoung onset.
Fortunately, young onset is aminority of the cases, and they
happen to run in families almostin a form of autosomal dominant
inheritance.
There's a group in Colombia,everybody has Alzheimer's
disease.
Even children have Alzheimer'sdisease.
(25:17):
Fortunately, young onsetAlzheimer's disease is rare
simply because it's a moremalignant form of Alzheimer's
disease.
It happens in a youngerpopulation with significant
behavioral disturbances.
Um, but uh majority of thecases are the are the older type
Alzheimer's.
So if I'm gonna developAlzheimer's disease, I don't
mind in my 50s and 60s, I mindin my 80s.
(25:40):
Got it.
What happens is uhstatistically, uh the Hispanics
are at the highest risk ofAlzheimer's disease.
Dr. Michael Koren (25:47):
Interesting,
-followed by the AfricanAmericans uh and then
Caucasians.
Okay.
So uh why do why don't we havemore uh Hispanics or African
Americans simply because of thethe uh availability of the
healthcare uh and educationalbackground to seek help?
I think that's been amazing.
Are there any theories as to why Hispanics
(26:08):
are at higher risk?
Dr. Reza Bolouri (26:10):
Well, um my theory is uh the folks in the
minority community do not getthe medical attention that they
deserve for hypertension, fordiabetes, for high cholesterol.
And we know at the end of theday, all these brain disorders
are vascular.
Dr. Michael Koren (26:26):
Yeah.
It gets into somethinginteresting, which is called the
Hispanic paradox.
So people of Hispanic ethnicityactually live three years
longer on average than whitepeople.
And uh that's always aninteresting little tidbit in the
United States that we don'ttalk that much about.
So there's some things thatHispanic populations are doing
really well.
They have a closer familyties, having a Hispanic as a
(26:50):
wife.
Well, that can be or they eat better or
they are more physically active,but it's it's a it's an
interesting paradox.
Dr. Reza Bolouri (26:56):
Yes.
Dr. Michael Koren (26:56):
So, Reza, a lot of my patients come to me
and ask me, I'm really concernedI have Old Timers disease.
So is it Old Timers or is itAlzheimer's?
And why do we call itAlzheimer's?
Dr. Reza Bolouri (27:08):
Actually, uh a lot of folks uh since uh age
happens to be the biggest riskfactor for Alzheimer's disease,
a lot of older folks developAlzheimer's.
So it's just, you know, somefolks say it's Old timers
disease or All Timers disease.
In fact, the term comes fromDr.
Alois Alzheimer, who was aGerman pathologist and had seen
(27:30):
a patient uh uh who was a veryyoung woman uh in her 50s.
Uh the initial description ofAlzheimer's change was a young
onset Alzheimer's patient, um,which uh uh that's how the name
came about.
Uh Alzheimer's
So it's a relatively moderndisease, only about 100 years
old.
That's right.
Dr. Michael Koren (27:51):
Reza, it's been a delightful conversation.
Thank you for being part ofMedEvidence!
Welcome.
Thank you so much for havingme.
Announcer (27:57):
Thanks for joining the MedEvidence Podcast.
To learn more, head over toMedevidence.com or subscribe to
our podcast on your favoritepodcast platform.
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