January 21, 2025 • 26 mins
Welcome back for part three of our interview with
Dr. Todd Levine from CND LifeSciences to share with us all information about the new syn-one skin test that can help in diagnosing LBD.
Our good friend Wendy Cogan joined us to help ask the right questions so we get a better understanding of this new test.
This is a three part recording because our interview was well over an hour and a half but we had lots of questions to ask the doctor.
Enjoy part three
Link for CNDLifeSciences is
https://cndlifesciences.com/
A shout out to all out supporters including Vickie Setterberg, Kristen Medica, Tiffany Hanna, Janice Prochaska, Kara Biller, Don Pinkos, Dee Richert, Marcia Treffman, The Geraci's and everyone else who has been with us from day one.
We are doing this for all of us and we thank you from the bottom of our hearts.
Should you wish to bless us with your support you can use links below.
Copy and paste link, if needed
https://patreon.com/lewybodyrollercoasterpodcast
the GoFundMe page at
https://gofund.me/c416ecb6
Thank you for listening each week.
Don't forget to join our Lewy Body Roller Coaster Podcast Facebook page.
If you have a topic you would like us to discuss or wish to share your thoughts on any episode, please email us at lewybodyrollercoaster@gmail.com
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:03):
Hello and welcome to our podcast about living on the
Lewy Body Roller Coaster apodcast for Lewy Body Dementia
patients and their families.
Presented by Lewy Body patientsand their families.
Speaker 2 (00:13):
You will hear firsthand the ups and downs and
twists and turns of Lewy BodyDementia From families directly
affected.
We'll share our support andexperiences on all things Lewy
Body.
Speaker 1 (00:25):
We're your hosts, Linda and Curry.
I have a loved one with LewyBody Dementia.
Speaker 2 (00:30):
And I am living with Lewy Body Dementia.
Speaker 1 (00:33):
Let's get started.
Welcome back podcast family.
Speaker 2 (00:42):
Please welcome back to the podcast Dr Ted Levine and
also a guest helper, wendyCogan, whose husband has Lewy
body dementia.
Speaker 1 (00:50):
Dr Levine, I think you mentioned earlier about the
NIH.
Can you update us on theprogress of a synuclein-1 study
funded by the NIH and when willthe findings be available?
Because we noticed that it'sbeing offered in 20 by 25
clinical sites and I guess themost important question is are
(01:11):
you still accepting people inthe study and how can our
listeners become a part of it?
Speaker 3 (01:16):
Yep.
So the study was designed to bethe largest kind of prospective
study to say does the skinbiopsy help?
Now what we've done in thestudy is to say we're taking
people with the force ofnucleonopathy, so not REM
behavior disorder, soParkinson's, msa, dlb and pure
(01:36):
autonomic failure who areclinically definite, so the ones
that the doctor says I'm assure, sure, sure as I can be,
because we're not going toobviously do autopsies, so short
of autopsies, it has to be thedoctor going.
I'm really, really, really surethat that's what this patient
has.
And then we're doing the skinbiopsies on them.
So previous studies, our work,the Italians published last year
(01:59):
, you know big studies are 50,60 patients.
This will be 500 patients.
So it should be the definitiveword on how, what is the
sensitivity and the specificityof the SYN1 test.
We hope to complete by Decemberenrollment and then, you know,
we probably have the data bythis time next year.
(02:21):
So, figure 12 months, we shouldhave all the data.
The other thing that we'redoing in that study, as we have
talked about, I think, before,is that because myself and Dr
Gibbons, who are the blindedpathologists, so we won't really
know what the patient has,we're trying to say can what we
see help say this is more likelyParkinson's or more likely DLB
(02:44):
or more likely MSA?
So we're going to do all ofthat.
So we should have that within ayear, wow.
And then, if people want toparticipate.
So we had, as I said, the fourdifferent diseases.
Some of those diseases haveclosed already.
So, for example, parkinson'sdisease, we filled up very
quickly, as you can imagine, butwe are still looking for DLB
(03:12):
patients.
So I know the last half of thisyear we would welcome anyone to
do that.
The sites are on our website.
I think there's, as you said,25, maybe 28 at this point, and
you can also go toclinicaltrialsgov, look for our
study and then you could seewhich centers are enrolling and
then hopefully there's a centerthat's near you.
So someone who wanted toparticipate would have to go to
(03:33):
the doctor at that center.
It's about a three-hour visitto do all the clinical
information, do the biopsy.
It's just a single visit andthat's it.
So we would definitely welcomeDLB folks.
Speaker 1 (03:45):
Now, are you looking for people just with MCI, or are
you looking for people alreadydiagnosed with LBD?
Speaker 3 (03:54):
So in the SYN1 study we want people that are already
diagnosed and again the onesthat the doctor says this is
textbook case, no questionsasked kind of case.
This is, you know, textbookcase, no questions asked kind of
case.
We just were awarded anothergrant by the NIH to look at the
MCI folks.
So this was we're going tocompare mild cognitive
impairment of the Lewy body typeto mild cognitive impairment of
(04:17):
the Alzheimer's type.
We have not yet enrolled all ofthose sites.
We probably will have about 10sites in that study.
It'll be a little smaller studyand they'll probably be.
Some of them will be enrollingby the fall.
So definitely just keepwatching our website or
clinicaltrialsgov, and I woulddefinitely like to find those
(04:40):
people.
Speaker 1 (04:41):
Yeah, he's got a question.
Do you see his pen?
Speaker 2 (04:44):
Yeah, Doctor, let me ask you a question.
Just reiterate, if you will howfar in advance do you think
that your can recognizeillnesses like Lewy body
dementia?
Speaker 3 (05:00):
Yeah, it's a great question, so we don't really
know.
What I can tell you is that ourbest data is that REM behavior
disorder develops five or 10years before the other
conditions.
We can see the abnormal SYN1test in REM behavior disorder
(05:22):
about 85% of the time in REMbehavior disorder about 85% of
the time.
So that would mean in 85% ofthe patients we can probably see
the protein starting toaccumulate five to 10 years
before the full clinicalsymptoms begin.
It may be longer, but that'sthe best sort of comparison.
Because of that, there is agroup of very smart sleep
(05:43):
doctors neurologists mostlyacross the country that have
formed a group called NAPS,which is the best name for sleep
doctors to call.
Their group is NAPS.
I love it.
I'm very jealous that they cameup with that name, but it
stands for North AmericanProdromal Synucleinopathy Group,
so they are looking for theprodromal people, right, and so
(06:06):
this is where I get very excited.
I love the question because it'sone thing if we say, okay, I
can diagnose Lewy body much moredefinitively with this test,
but we know by the time thatthat's been diagnosed the
protein's been accumulating 5,10, 15, 20 years, and so the
(06:27):
ability to get that protein outof the brain and to save neurons
is going to be a challenge,right.
I mean that's going to be tough.
I think we'll get thereeventually, but that's going to
be tough.
On the other hand, if you coulddetect that 10 years before and
say this protein is starting toaccumulate in this person, now
let's give them that same drugand slow it down by 20 or 30%
(06:51):
Now maybe they don't get thedisease till they're 90 as
opposed to 60.
So that whole starting todiagnose this much earlier and
treat much earlier is actuallystarting to become a reality
because we can see it before theperson has all the symptoms of
the brain damage that occursfrom the protein accumulating.
Speaker 1 (07:13):
Thank you.
Yeah, that's big because we Ican't even tell you how many
people have come on the podcastand people who come into the
support groups.
Kari was a rare one.
He got a quicker diagnosis butthe wrong diagnosis, like Wendy
said, and sometimes up to fiveyears to get the proper
(07:34):
diagnosis, and that's a lot oftime that they could have been
living a better quality lifewith the right meds.
And one of the big things isbecause they're not diagnosed,
they get meds that make.
One of the big things isbecause they're not diagnosed,
they get meds that make the Lewybody worse.
So I'm very excited that thisis taking place and that you are
(07:55):
all working so hard towardsthis disease and I just pray
there's a cure someday in ourlifetime, but I guess this is a
start.
So, wendy, you want to jumpdown to your next question,
because he already answered mine.
Speaker 4 (08:13):
Yeah, yeah, and actually I just have.
When I was listening to thediscussion, a couple things
popped into my mind too was howimportant it is to understand
the pathology so that you areusing the right type of
medicines and you getting intothe right type of clinical
trials, and also a point thatwas made earlier about the
(08:36):
difference between pathologyversus a biomarker.
So my husband had the positiveDAT scan and at the time, um, I
thought that meant you know that, uh, synucleinopathy type of
thing like Parkinson's or MSA orLewy body.
But what I didn't realize atthe time is that it can also be
(08:59):
positive for cortical basalsyndrome, which is the disease
that, um, they suspected myhusband had.
And then ultimately, of course,the skin biopsy showed that he
has at least the alpha-synucleinpathology.
But I do think it's important tomention that probably a lot of
(09:19):
dementias are mixed and maybe,you know, at the time of the
autopsy or death, the mixeddementia has become pretty much
more likely than just a singledementia.
And I do wonder at times ifmaybe my husband has two type of
dementias.
We know that he doesn't havethe Alzheimer's because we can
(09:42):
tell by cerebral spinal fluidand scans, but we can't tell yet
other diseases that are causedby things like four-hour tau,
and so it's possible that maybemy husband has the four-hour tau
too.
But back to understanding thepathology and why it's so
important is that this Aricepreally works well for Lewy body
(10:06):
dementia patients.
It really helps with cognition.
But sometimes the doctors sayif you've got the wrong disease
and the person actually hascortical basal syndrome and you
give them something like Aricep,it can make psychiatric
conditions worse.
So that's why I think it'sreally important to know the
(10:27):
pathology and the disease so youcan treat it properly.
Speaker 1 (10:32):
Yeah.
Speaker 3 (10:35):
Sorry, I was just gonna sort of add to that.
I agree completely and I thinkin Lewy body it's unbelievably
important to think about themedications we choose, because
People with Lewy body dementiacan have behavioral problems.
They can be hospitalized orseen by psychiatrists and given
(10:55):
medications that will make theirdisease much worse.
If you don't know that it'sLewy body More so than the other
conditions Well, maybeParkinson's too, but usually
it's a little more clear.
But with behavioral problems,really understanding what
medicines are safe for a Lewybody patient to take and not is
critical, Because I mean, I'veseen, unfortunately,
(11:16):
circumstances where I think apatient's death was hastened
with Lewy body dementia becausethey were given the wrong
symptomatic medication.
So it is critical.
Speaker 4 (11:25):
Yeah, yeah, and that was definitely what happened to
my husband.
He was on lithium and he wasdoing okay, but it wasn't
impacting his cognition and madehim appear like he was having
tremors.
And then they put him on aurinary medicine that caused his
levels of lithium to go up andhe went into the full blown
(11:46):
delirium, and so it took a whileto get that all figured out and
sorted out, but he's able tohandle like the Aricep has
helped tremendously.
And so you got to experimentand you also have to know the
disease, what you're dealingwith.
So that's a really importantpoint.
(12:08):
I did notice and I think you'veaddressed this to some degree,
but I did hear that there's aSwiss biomarker or Swiss biotech
company that, during the March2022 International Conference on
Alzheimer's and Parkinson'sDisease, announced a potential
new pet tracer that candifferentiate MSA from
(12:32):
Parkinson's disease and Lewybody dementia in living patients
.
And initially I was going toask you if you guys were
evolving to be able to tell thedifferences between, like
Parkinson's and Lewy body andMSA.
But from what you explainedearlier, this NIH study might
(12:53):
help you actually get there.
You might actually come up witha conclusion that says, hey, we
can differentiate these four orfive different diseases.
So that's wonderful.
So the other thing is we talkabout clinical trials.
(13:15):
Um, one thing that's reallyimportant when you're looking at
the pathology or a biomarker isyou've got to be able to tell
if a certain intervention ordrug is actually working and
you've got to be able to have abiomarker to measure that and to
show improvement.
And right now, as you say, it'smore of kind of a yes, no, you
(13:39):
know whether they have the piecein or whether they don't.
This that maybe you can, but doyou think you'll be able to
evolve your test to be able totell disease progression or
severity so that it can beultimately used in clinical
(14:02):
trials?
Speaker 3 (14:04):
Yeah, so we're using it in clinical trials in just
that way now.
So we're working with threedifferent pharmaceutical
companies to do pre and postbiopsies and to see whether or
not the levels change.
Now what we know is that if youfollow at least Parkinson's
(14:24):
patients, you see about a 7%increase in the amount of
sunuclein per year, in theamount of synuclein per year.
So the hope would be then thatonce we have a drug that
decreases it, that we would beable to see that decrease or at
least that stabilization overtime.
So far those trials are stillongoing.
(14:45):
So far none of the drugs havebeen able to accomplish that yet
.
But the hope would be that oncethere's a drug that can reduce
the synuclein, that the SYN1test would be able to look that
yet.
But the hope would be that oncethere's a drug that can reduce
the synuclein that the SYN1 testwould be able to look at that.
Speaker 1 (15:00):
Yeah, this is.
I'm riveted.
That's why I'm just rivetedlistening to all this.
So, wendy, thank you forhelping us dig deeper into this,
but I, for time's sake, becausewe do a Zoom at 1030 on Mondays
central time, so it's 15minutes and I know I've got to
(15:22):
give my buddy Corey a rest.
Speaker 4 (15:27):
Do you?
Speaker 1 (15:27):
want me to ask my last question, if you go down to
page 10, because as a woman.
I'm asking this as a womanbecause the women in our groups
say how hard it is, that theyseem to have a harder time to
get diagnosed.
So has Sin 1 development testsbeen based on male symptoms?
(15:53):
I guess that's what I'm asking.
In your study, is it equalamount of male and female?
Because women with LBD seem tohave less REM sleep behavior
issues, could the test bemissing some differences in
(16:13):
females, like hormones or othervariables?
So I'm asking this for all thewomen out there who we have,
several that are struggling toget diagnosed and and it and
it's, it's bad.
It's bad where they say to themlike, oh, you're just going
through menopause or it's just awoman thing.
So I'm asking this for all thewomen out there trying to yeah.
Speaker 3 (16:39):
So it's a great, really, really complex question,
so I'll try to answer it a fewdifferent ways.
So first is, we don't see anysex difference in the pathology
and I have to get you the exactnumbers.
But if you look at the sex ofthe people that have gotten the
test done, there's not a hugedifference that we've seen so
far.
So if you look at the sex ofthe people that have gotten the
test done, there's not a hugedifference that we've seen so
far.
So I don't think the test wouldbe affected.
Now, could it be affected bythings like hormones and other
(17:02):
things?
I suppose it could, but so farwe haven't really seen that.
Then the second part of thequestion is why is it harder for
women to get diagnosed?
So that's really complicated,but I'll start by giving just
some facts.
We know, for example, thatwomen who have heart attacks are
much less likely to complain ofchest pain.
That's been well described for70, 100 years now.
(17:24):
We know that women are lesslikely to get seen for cognitive
complaints at the same time asmen.
Now one argument is that'sbecause if people have dementia,
it's usually the caregiver orthe spouse that brings that
person in.
It's very rare for a person tocome in and say I'm becoming
(17:47):
forgetful.
It's not impossible, but it'susually the spouse that says
they're becoming forgetful.
And one could argue that thefemale spouse is just more
observant than the male spouseand therefore men are brought in
much sooner than women.
My parents are both in their90s and I would say that applies
to them as well who both havesome cognitive issues.
(18:07):
So that is one issue.
It's sort of an observer bias,right?
So if the people closest tothem have to observe the
cognitive loss, that could be aproblem.
The second would be the patientbias, which is like the women
with the heart attack story.
Women just don't complain of itas often and that may be part
(18:30):
of the story of it as often, andthat may be part of the story
you were alluding to.
What I hope isn't the case, butwhich is a third possibility,
which is that women who presentcomplaining of cognitive
problems may be told more oftenthat it is something other than
cognitive problems, that it istheir depression, that it is the
divorce they're going through,the death of their whatever, and
(18:52):
that men don't seem to get thatresponse from doctors quite as
much.
I hope that's not the case.
But it's probably somecombination of all of those
things that lead to that.
Sometimes in our lab we talkabout the moonshot, right?
So what would happen with ourlab if we were JFK and we were
(19:16):
trying to get to the moon?
You know, kurt, your point.
My moon shot for what we'restarting to do here, and we'll
probably be long after I'm gone,would be kind of like the
colonoscopy.
So imagine, for example, we allat 50, we get colonoscopies, we
get mammograms because we'rescreening for cancer, right?
(19:36):
Imagine you could do one skinbiopsy at 50 and screen for
synuclein and tau and TDP43 andall of those proteins that are
going to build up in 20 or 30percent of the population as
they get older.
And then imagine that we've gotdrugs that now can block the
accumulation of those proteinsand you're starting them long
(19:57):
before you're symptomatic.
That's again my moonshot.
That's how you cure lewy bodyand alzheimer's.
You can't cure it once they'redemented.
It's just, it's just going tobe too hard.
Um, you've got to stop it fromever happening, and so to stop
it from happening.
You've got to stop it from everhappening, and so to stop it
from happening, you've got toidentify it, then get the drugs
(20:17):
and then treat the people.
So some of this may getresolved over time because we're
going to start screening forall of these neurodegenerative
diseases in a way that we havemedications for.
And that's sort of my you know,that'll be my dream.
Speaker 1 (20:35):
Keep dreaming.
Reach for the stars as teachersalways say Wendy has one.
Speaker 2 (20:39):
That was very good.
Go ahead.
Speaker 1 (20:41):
Yeah, wendy has one quick question and then we're
going to wrap up.
Speaker 4 (20:44):
That's an outstanding vision and that would be
awesome.
I think the question, one ofthe things they were trying to
figure out on that question is Ithink the question, one of the
things they were trying tofigure out on that question, is
is it possible that certainstrains of misfolded
alpha-synuclein are missing orthere's a missing pathology that
isn't being picked up in Lewybody dementia patients beyond
(21:06):
the PSIN, or maybe it's a dye orsomething like that.
Speaker 3 (21:18):
Could it be something that people are missing if
somebody thinks they have Lewybody dementia?
So there is a lot more herethat we don't know than we do
know, right?
So, for example, as best anyonehas been able to tell, it's the
same PSIN protein in all fiveof these diseases.
So why in Parkinson's diseasedoes that protein build up in
the substantia nigra and thelocus coeruleus?
Why in Lewy body patients doesit build up in the cortical
(21:39):
structures and affect theirmemory?
Why in multiple system diseasedoes it build up in many places?
And that's where people arereally getting to the concept
that you've introduced, which isare there different
conformations of the protein?
Does it fold differently andtherefore dictate which parts of
the nervous system it's goingto go to?
(21:59):
Are there additional proteinsthat fold with it that maybe
shuttle it to different parts ofthe nervous system?
Why do some people withParkinson's eventually develop a
terrible dementia, you know,and we call that Parkinson's
disease dementia, because theyhad Parkinson's for 10 years
first, and some people havedementia with Lewy bodies and
then eventually develop someParkinson's features later.
(22:22):
It all has to do with where theprotein is accumulating in the
brain, and I don't think anybodyhas any idea as to why that is.
Everyone's trying to study itand to figure that out.
Your theories are just as goodas anybody else's theories.
Which is?
Different shapes of theproteins, different other
proteins, sex differences?
(22:42):
Any of those things could betrue, but we just don't know.
Speaker 1 (22:47):
So I know I said that was the last question but, as
you're talking, I want to knowhow do neurologists out there
know that this test is available?
Because we're finding thatwe're telling our people in our
support groups and they're goingto the doctors and telling the
doctors about this test, and itshouldn't be that way Because
(23:08):
there's for the people thataren't attending our Zoom, like
it's.
It shouldn't be that way.
So how is this gettingdisseminated out to the medical?
Speaker 3 (23:17):
professionals.
We'll take some of the blamefor that, which is that we
launched two months before COVIDhit and so our first two years
really was spent just trying toemail some folks and you know,
patients weren't even cominginto doctor's offices for a year
and I mean, everybody remembersthe mask, right.
So we are a little behind,where we'd like to be for three
(23:40):
years, commercialized.
What I will say is I think weare now in 43 states, so
neurologists in 43 states haveused us.
I think we have over 500neurologists that are using us
across the country.
There are 13,000 neurologists.
So we have only really begun toreach out.
We advertise in journals, we doCME activities, we go to
(24:04):
national conferences, but we aredefinitely a little behind,
kind of where we'd like to be,and we do hear that patients
often go in and say, hey, couldyou do this test?
And the doctor's never heard ofus.
And we encourage, encouragethat.
So that's great, because thenthey call us and we get to talk
to them and we can usually getthem going.
Um, but we we do need to try toreach out a little more broadly
(24:26):
, um.
Speaker 1 (24:27):
So yeah, thank you for that.
Um, we're, trust me, we're.
We're kind of creating our ownlittle I don't know what.
What are we group of marchersthat are just shouting at the
rooftop to help one another?
But anyway, due to time, we'regoing to have to stop there.
But I really appreciate youanswering, especially that final
(24:49):
question regarding women versusmen getting a diagnosis,
because the person who sent thatquestion to us had valid
concerns in her struggles to getdiagnosed.
So thank you, wendy, for comingon and helping us with the more
(25:09):
technical questions and, drLevine, we can't thank you
enough for what you all aredoing to help get a diagnosis
for this disease.
Speaker 3 (25:20):
I appreciate it.
Thanks for having me on.
Speaker 1 (25:22):
Keep reaching for the stars, mister.
Please keep reaching, we willtry yeah.
Speaker 4 (25:28):
We appreciate what you're doing.
Definitely, yeah, we do,actually, both of you guys, all
three of you guys, thank you.
Speaker 2 (25:35):
Well, folks, that's all we have time for this week.
Thank you again to Dr Levineand to our guest helper, wendy
Kogan.
Remember you can email us withsuggestions on what you'd like
us to discuss on future episodes, or you can ask any questions
you have, and we'll sure do ourbest to help get you the best
answer possible.
Speaker 1 (26:02):
And remember that Curry sometimes remembers to put
to add the link to the to theweekly pod.
You're doing a good job, curry.
Yeah, you're slacking this weekbut most of the times, yeah, he
does remember to post the links.
Um, hey, I take blame too,because sometimes I forget to
push publish and I'm like afterit gets done and I'm like how
come you haven't posted?
But anyway, if you'reinterested in helping us as a
volunteer and advocate, pleasesend us an email at
louiebodyrollercoaster atgmailcom, because the more
(26:22):
people who reach out, the morepeople we can help.
Speaker 2 (26:26):
And if you'd like to learn how you can be a supporter
of the podcast, please see theepisode notes, as we post
information on that there.
Well, folks, thanks again forjoining us Until next week.
This is Linda and Curry signingoff.
Hello and welcome to our podcast about living on the
Lewy Body Roller Coaster apodcast for Lewy Body Dementia
patients and their families.
Presented by Lewy Body patientsand their families.
Speaker 2 (00:13):
You will hear firsthand the ups and downs and
twists and turns of Lewy BodyDementia From families directly
affected.
We'll share our support andexperiences on all things Lewy
Body.
Speaker 1 (00:25):
We're your hosts, Linda and Curry.
I have a loved one with LewyBody Dementia.
Speaker 2 (00:30):
And I am living with Lewy Body Dementia.
Speaker 1 (00:33):
Let's get started.
Welcome back podcast family.
Speaker 2 (00:42):
Please welcome back to the podcast Dr Ted Levine and
also a guest helper, wendyCogan, whose husband has Lewy
body dementia.
Speaker 1 (00:50):
Dr Levine, I think you mentioned earlier about the
NIH.
Can you update us on theprogress of a synuclein-1 study
funded by the NIH and when willthe findings be available?
Because we noticed that it'sbeing offered in 20 by 25
clinical sites and I guess themost important question is are
(01:11):
you still accepting people inthe study and how can our
listeners become a part of it?
Speaker 3 (01:16):
Yep.
So the study was designed to bethe largest kind of prospective
study to say does the skinbiopsy help?
Now what we've done in thestudy is to say we're taking
people with the force ofnucleonopathy, so not REM
behavior disorder, soParkinson's, msa, dlb and pure
(01:36):
autonomic failure who areclinically definite, so the ones
that the doctor says I'm assure, sure, sure as I can be,
because we're not going toobviously do autopsies, so short
of autopsies, it has to be thedoctor going.
I'm really, really, really surethat that's what this patient
has.
And then we're doing the skinbiopsies on them.
So previous studies, our work,the Italians published last year
(01:59):
, you know big studies are 50,60 patients.
This will be 500 patients.
So it should be the definitiveword on how, what is the
sensitivity and the specificityof the SYN1 test.
We hope to complete by Decemberenrollment and then, you know,
we probably have the data bythis time next year.
(02:21):
So, figure 12 months, we shouldhave all the data.
The other thing that we'redoing in that study, as we have
talked about, I think, before,is that because myself and Dr
Gibbons, who are the blindedpathologists, so we won't really
know what the patient has,we're trying to say can what we
see help say this is more likelyParkinson's or more likely DLB
(02:44):
or more likely MSA?
So we're going to do all ofthat.
So we should have that within ayear, wow.
And then, if people want toparticipate.
So we had, as I said, the fourdifferent diseases.
Some of those diseases haveclosed already.
So, for example, parkinson'sdisease, we filled up very
quickly, as you can imagine, butwe are still looking for DLB
(03:12):
patients.
So I know the last half of thisyear we would welcome anyone to
do that.
The sites are on our website.
I think there's, as you said,25, maybe 28 at this point, and
you can also go toclinicaltrialsgov, look for our
study and then you could seewhich centers are enrolling and
then hopefully there's a centerthat's near you.
So someone who wanted toparticipate would have to go to
(03:33):
the doctor at that center.
It's about a three-hour visitto do all the clinical
information, do the biopsy.
It's just a single visit andthat's it.
So we would definitely welcomeDLB folks.
Speaker 1 (03:45):
Now, are you looking for people just with MCI, or are
you looking for people alreadydiagnosed with LBD?
Speaker 3 (03:54):
So in the SYN1 study we want people that are already
diagnosed and again the onesthat the doctor says this is
textbook case, no questionsasked kind of case.
This is, you know, textbookcase, no questions asked kind of
case.
We just were awarded anothergrant by the NIH to look at the
MCI folks.
So this was we're going tocompare mild cognitive
impairment of the Lewy body typeto mild cognitive impairment of
(04:17):
the Alzheimer's type.
We have not yet enrolled all ofthose sites.
We probably will have about 10sites in that study.
It'll be a little smaller studyand they'll probably be.
Some of them will be enrollingby the fall.
So definitely just keepwatching our website or
clinicaltrialsgov, and I woulddefinitely like to find those
(04:40):
people.
Speaker 1 (04:41):
Yeah, he's got a question.
Do you see his pen?
Speaker 2 (04:44):
Yeah, Doctor, let me ask you a question.
Just reiterate, if you will howfar in advance do you think
that your can recognizeillnesses like Lewy body
dementia?
Speaker 3 (05:00):
Yeah, it's a great question, so we don't really
know.
What I can tell you is that ourbest data is that REM behavior
disorder develops five or 10years before the other
conditions.
We can see the abnormal SYN1test in REM behavior disorder
(05:22):
about 85% of the time in REMbehavior disorder about 85% of
the time.
So that would mean in 85% ofthe patients we can probably see
the protein starting toaccumulate five to 10 years
before the full clinicalsymptoms begin.
It may be longer, but that'sthe best sort of comparison.
Because of that, there is agroup of very smart sleep
(05:43):
doctors neurologists mostlyacross the country that have
formed a group called NAPS,which is the best name for sleep
doctors to call.
Their group is NAPS.
I love it.
I'm very jealous that they cameup with that name, but it
stands for North AmericanProdromal Synucleinopathy Group,
so they are looking for theprodromal people, right, and so
(06:06):
this is where I get very excited.
I love the question because it'sone thing if we say, okay, I
can diagnose Lewy body much moredefinitively with this test,
but we know by the time thatthat's been diagnosed the
protein's been accumulating 5,10, 15, 20 years, and so the
(06:27):
ability to get that protein outof the brain and to save neurons
is going to be a challenge,right.
I mean that's going to be tough.
I think we'll get thereeventually, but that's going to
be tough.
On the other hand, if you coulddetect that 10 years before and
say this protein is starting toaccumulate in this person, now
let's give them that same drugand slow it down by 20 or 30%
(06:51):
Now maybe they don't get thedisease till they're 90 as
opposed to 60.
So that whole starting todiagnose this much earlier and
treat much earlier is actuallystarting to become a reality
because we can see it before theperson has all the symptoms of
the brain damage that occursfrom the protein accumulating.
Speaker 1 (07:13):
Thank you.
Yeah, that's big because we Ican't even tell you how many
people have come on the podcastand people who come into the
support groups.
Kari was a rare one.
He got a quicker diagnosis butthe wrong diagnosis, like Wendy
said, and sometimes up to fiveyears to get the proper
(07:34):
diagnosis, and that's a lot oftime that they could have been
living a better quality lifewith the right meds.
And one of the big things isbecause they're not diagnosed,
they get meds that make.
One of the big things isbecause they're not diagnosed,
they get meds that make the Lewybody worse.
So I'm very excited that thisis taking place and that you are
(07:55):
all working so hard towardsthis disease and I just pray
there's a cure someday in ourlifetime, but I guess this is a
start.
So, wendy, you want to jumpdown to your next question,
because he already answered mine.
Speaker 4 (08:13):
Yeah, yeah, and actually I just have.
When I was listening to thediscussion, a couple things
popped into my mind too was howimportant it is to understand
the pathology so that you areusing the right type of
medicines and you getting intothe right type of clinical
trials, and also a point thatwas made earlier about the
(08:36):
difference between pathologyversus a biomarker.
So my husband had the positiveDAT scan and at the time, um, I
thought that meant you know that, uh, synucleinopathy type of
thing like Parkinson's or MSA orLewy body.
But what I didn't realize atthe time is that it can also be
(08:59):
positive for cortical basalsyndrome, which is the disease
that, um, they suspected myhusband had.
And then ultimately, of course,the skin biopsy showed that he
has at least the alpha-synucleinpathology.
But I do think it's important tomention that probably a lot of
(09:19):
dementias are mixed and maybe,you know, at the time of the
autopsy or death, the mixeddementia has become pretty much
more likely than just a singledementia.
And I do wonder at times ifmaybe my husband has two type of
dementias.
We know that he doesn't havethe Alzheimer's because we can
(09:42):
tell by cerebral spinal fluidand scans, but we can't tell yet
other diseases that are causedby things like four-hour tau,
and so it's possible that maybemy husband has the four-hour tau
too.
But back to understanding thepathology and why it's so
important is that this Aricepreally works well for Lewy body
(10:06):
dementia patients.
It really helps with cognition.
But sometimes the doctors sayif you've got the wrong disease
and the person actually hascortical basal syndrome and you
give them something like Aricep,it can make psychiatric
conditions worse.
So that's why I think it'sreally important to know the
(10:27):
pathology and the disease so youcan treat it properly.
Speaker 1 (10:32):
Yeah.
Speaker 3 (10:35):
Sorry, I was just gonna sort of add to that.
I agree completely and I thinkin Lewy body it's unbelievably
important to think about themedications we choose, because
People with Lewy body dementiacan have behavioral problems.
They can be hospitalized orseen by psychiatrists and given
(10:55):
medications that will make theirdisease much worse.
If you don't know that it'sLewy body More so than the other
conditions Well, maybeParkinson's too, but usually
it's a little more clear.
But with behavioral problems,really understanding what
medicines are safe for a Lewybody patient to take and not is
critical, Because I mean, I'veseen, unfortunately,
(11:16):
circumstances where I think apatient's death was hastened
with Lewy body dementia becausethey were given the wrong
symptomatic medication.
So it is critical.
Speaker 4 (11:25):
Yeah, yeah, and that was definitely what happened to
my husband.
He was on lithium and he wasdoing okay, but it wasn't
impacting his cognition and madehim appear like he was having
tremors.
And then they put him on aurinary medicine that caused his
levels of lithium to go up andhe went into the full blown
(11:46):
delirium, and so it took a whileto get that all figured out and
sorted out, but he's able tohandle like the Aricep has
helped tremendously.
And so you got to experimentand you also have to know the
disease, what you're dealingwith.
So that's a really importantpoint.
(12:08):
I did notice and I think you'veaddressed this to some degree,
but I did hear that there's aSwiss biomarker or Swiss biotech
company that, during the March2022 International Conference on
Alzheimer's and Parkinson'sDisease, announced a potential
new pet tracer that candifferentiate MSA from
(12:32):
Parkinson's disease and Lewybody dementia in living patients
.
And initially I was going toask you if you guys were
evolving to be able to tell thedifferences between, like
Parkinson's and Lewy body andMSA.
But from what you explainedearlier, this NIH study might
(12:53):
help you actually get there.
You might actually come up witha conclusion that says, hey, we
can differentiate these four orfive different diseases.
So that's wonderful.
So the other thing is we talkabout clinical trials.
(13:15):
Um, one thing that's reallyimportant when you're looking at
the pathology or a biomarker isyou've got to be able to tell
if a certain intervention ordrug is actually working and
you've got to be able to have abiomarker to measure that and to
show improvement.
And right now, as you say, it'smore of kind of a yes, no, you
(13:39):
know whether they have the piecein or whether they don't.
This that maybe you can, but doyou think you'll be able to
evolve your test to be able totell disease progression or
severity so that it can beultimately used in clinical
(14:02):
trials?
Speaker 3 (14:04):
Yeah, so we're using it in clinical trials in just
that way now.
So we're working with threedifferent pharmaceutical
companies to do pre and postbiopsies and to see whether or
not the levels change.
Now what we know is that if youfollow at least Parkinson's
(14:24):
patients, you see about a 7%increase in the amount of
sunuclein per year, in theamount of synuclein per year.
So the hope would be then thatonce we have a drug that
decreases it, that we would beable to see that decrease or at
least that stabilization overtime.
So far those trials are stillongoing.
(14:45):
So far none of the drugs havebeen able to accomplish that yet
.
But the hope would be that oncethere's a drug that can reduce
the synuclein, that the SYN1test would be able to look that
yet.
But the hope would be that oncethere's a drug that can reduce
the synuclein that the SYN1 testwould be able to look at that.
Speaker 1 (15:00):
Yeah, this is.
I'm riveted.
That's why I'm just rivetedlistening to all this.
So, wendy, thank you forhelping us dig deeper into this,
but I, for time's sake, becausewe do a Zoom at 1030 on Mondays
central time, so it's 15minutes and I know I've got to
(15:22):
give my buddy Corey a rest.
Speaker 4 (15:27):
Do you?
Speaker 1 (15:27):
want me to ask my last question, if you go down to
page 10, because as a woman.
I'm asking this as a womanbecause the women in our groups
say how hard it is, that theyseem to have a harder time to
get diagnosed.
So has Sin 1 development testsbeen based on male symptoms?
(15:53):
I guess that's what I'm asking.
In your study, is it equalamount of male and female?
Because women with LBD seem tohave less REM sleep behavior
issues, could the test bemissing some differences in
(16:13):
females, like hormones or othervariables?
So I'm asking this for all thewomen out there who we have,
several that are struggling toget diagnosed and and it and
it's, it's bad.
It's bad where they say to themlike, oh, you're just going
through menopause or it's just awoman thing.
So I'm asking this for all thewomen out there trying to yeah.
Speaker 3 (16:39):
So it's a great, really, really complex question,
so I'll try to answer it a fewdifferent ways.
So first is, we don't see anysex difference in the pathology
and I have to get you the exactnumbers.
But if you look at the sex ofthe people that have gotten the
test done, there's not a hugedifference that we've seen so
far.
So if you look at the sex ofthe people that have gotten the
test done, there's not a hugedifference that we've seen so
far.
So I don't think the test wouldbe affected.
Now, could it be affected bythings like hormones and other
(17:02):
things?
I suppose it could, but so farwe haven't really seen that.
Then the second part of thequestion is why is it harder for
women to get diagnosed?
So that's really complicated,but I'll start by giving just
some facts.
We know, for example, thatwomen who have heart attacks are
much less likely to complain ofchest pain.
That's been well described for70, 100 years now.
(17:24):
We know that women are lesslikely to get seen for cognitive
complaints at the same time asmen.
Now one argument is that'sbecause if people have dementia,
it's usually the caregiver orthe spouse that brings that
person in.
It's very rare for a person tocome in and say I'm becoming
(17:47):
forgetful.
It's not impossible, but it'susually the spouse that says
they're becoming forgetful.
And one could argue that thefemale spouse is just more
observant than the male spouseand therefore men are brought in
much sooner than women.
My parents are both in their90s and I would say that applies
to them as well who both havesome cognitive issues.
(18:07):
So that is one issue.
It's sort of an observer bias,right?
So if the people closest tothem have to observe the
cognitive loss, that could be aproblem.
The second would be the patientbias, which is like the women
with the heart attack story.
Women just don't complain of itas often and that may be part
(18:30):
of the story of it as often, andthat may be part of the story
you were alluding to.
What I hope isn't the case, butwhich is a third possibility,
which is that women who presentcomplaining of cognitive
problems may be told more oftenthat it is something other than
cognitive problems, that it istheir depression, that it is the
divorce they're going through,the death of their whatever, and
(18:52):
that men don't seem to get thatresponse from doctors quite as
much.
I hope that's not the case.
But it's probably somecombination of all of those
things that lead to that.
Sometimes in our lab we talkabout the moonshot, right?
So what would happen with ourlab if we were JFK and we were
(19:16):
trying to get to the moon?
You know, kurt, your point.
My moon shot for what we'restarting to do here, and we'll
probably be long after I'm gone,would be kind of like the
colonoscopy.
So imagine, for example, we allat 50, we get colonoscopies, we
get mammograms because we'rescreening for cancer, right?
(19:36):
Imagine you could do one skinbiopsy at 50 and screen for
synuclein and tau and TDP43 andall of those proteins that are
going to build up in 20 or 30percent of the population as
they get older.
And then imagine that we've gotdrugs that now can block the
accumulation of those proteinsand you're starting them long
(19:57):
before you're symptomatic.
That's again my moonshot.
That's how you cure lewy bodyand alzheimer's.
You can't cure it once they'redemented.
It's just, it's just going tobe too hard.
Um, you've got to stop it fromever happening, and so to stop
it from happening.
You've got to stop it from everhappening, and so to stop it
from happening, you've got toidentify it, then get the drugs
(20:17):
and then treat the people.
So some of this may getresolved over time because we're
going to start screening forall of these neurodegenerative
diseases in a way that we havemedications for.
And that's sort of my you know,that'll be my dream.
Speaker 1 (20:35):
Keep dreaming.
Reach for the stars as teachersalways say Wendy has one.
Speaker 2 (20:39):
That was very good.
Go ahead.
Speaker 1 (20:41):
Yeah, wendy has one quick question and then we're
going to wrap up.
Speaker 4 (20:44):
That's an outstanding vision and that would be
awesome.
I think the question, one ofthe things they were trying to
figure out on that question is Ithink the question, one of the
things they were trying tofigure out on that question, is
is it possible that certainstrains of misfolded
alpha-synuclein are missing orthere's a missing pathology that
isn't being picked up in Lewybody dementia patients beyond
(21:06):
the PSIN, or maybe it's a dye orsomething like that.
Speaker 3 (21:18):
Could it be something that people are missing if
somebody thinks they have Lewybody dementia?
So there is a lot more herethat we don't know than we do
know, right?
So, for example, as best anyonehas been able to tell, it's the
same PSIN protein in all fiveof these diseases.
So why in Parkinson's diseasedoes that protein build up in
the substantia nigra and thelocus coeruleus?
Why in Lewy body patients doesit build up in the cortical
(21:39):
structures and affect theirmemory?
Why in multiple system diseasedoes it build up in many places?
And that's where people arereally getting to the concept
that you've introduced, which isare there different
conformations of the protein?
Does it fold differently andtherefore dictate which parts of
the nervous system it's goingto go to?
(21:59):
Are there additional proteinsthat fold with it that maybe
shuttle it to different parts ofthe nervous system?
Why do some people withParkinson's eventually develop a
terrible dementia, you know,and we call that Parkinson's
disease dementia, because theyhad Parkinson's for 10 years
first, and some people havedementia with Lewy bodies and
then eventually develop someParkinson's features later.
(22:22):
It all has to do with where theprotein is accumulating in the
brain, and I don't think anybodyhas any idea as to why that is.
Everyone's trying to study itand to figure that out.
Your theories are just as goodas anybody else's theories.
Which is?
Different shapes of theproteins, different other
proteins, sex differences?
(22:42):
Any of those things could betrue, but we just don't know.
Speaker 1 (22:47):
So I know I said that was the last question but, as
you're talking, I want to knowhow do neurologists out there
know that this test is available?
Because we're finding thatwe're telling our people in our
support groups and they're goingto the doctors and telling the
doctors about this test, and itshouldn't be that way Because
(23:08):
there's for the people thataren't attending our Zoom, like
it's.
It shouldn't be that way.
So how is this gettingdisseminated out to the medical?
Speaker 3 (23:17):
professionals.
We'll take some of the blamefor that, which is that we
launched two months before COVIDhit and so our first two years
really was spent just trying toemail some folks and you know,
patients weren't even cominginto doctor's offices for a year
and I mean, everybody remembersthe mask, right.
So we are a little behind,where we'd like to be for three
(23:40):
years, commercialized.
What I will say is I think weare now in 43 states, so
neurologists in 43 states haveused us.
I think we have over 500neurologists that are using us
across the country.
There are 13,000 neurologists.
So we have only really begun toreach out.
We advertise in journals, we doCME activities, we go to
(24:04):
national conferences, but we aredefinitely a little behind,
kind of where we'd like to be,and we do hear that patients
often go in and say, hey, couldyou do this test?
And the doctor's never heard ofus.
And we encourage, encouragethat.
So that's great, because thenthey call us and we get to talk
to them and we can usually getthem going.
Um, but we we do need to try toreach out a little more broadly
(24:26):
, um.
Speaker 1 (24:27):
So yeah, thank you for that.
Um, we're, trust me, we're.
We're kind of creating our ownlittle I don't know what.
What are we group of marchersthat are just shouting at the
rooftop to help one another?
But anyway, due to time, we'regoing to have to stop there.
But I really appreciate youanswering, especially that final
(24:49):
question regarding women versusmen getting a diagnosis,
because the person who sent thatquestion to us had valid
concerns in her struggles to getdiagnosed.
So thank you, wendy, for comingon and helping us with the more
(25:09):
technical questions and, drLevine, we can't thank you
enough for what you all aredoing to help get a diagnosis
for this disease.
Speaker 3 (25:20):
I appreciate it.
Thanks for having me on.
Speaker 1 (25:22):
Keep reaching for the stars, mister.
Please keep reaching, we willtry yeah.
Speaker 4 (25:28):
We appreciate what you're doing.
Definitely, yeah, we do,actually, both of you guys, all
three of you guys, thank you.
Speaker 2 (25:35):
Well, folks, that's all we have time for this week.
Thank you again to Dr Levineand to our guest helper, wendy
Kogan.
Remember you can email us withsuggestions on what you'd like
us to discuss on future episodes, or you can ask any questions
you have, and we'll sure do ourbest to help get you the best
answer possible.
Speaker 1 (26:02):
And remember that Curry sometimes remembers to put
to add the link to the to theweekly pod.
You're doing a good job, curry.
Yeah, you're slacking this weekbut most of the times, yeah, he
does remember to post the links.
Um, hey, I take blame too,because sometimes I forget to
push publish and I'm like afterit gets done and I'm like how
come you haven't posted?
But anyway, if you'reinterested in helping us as a
volunteer and advocate, pleasesend us an email at
louiebodyrollercoaster atgmailcom, because the more
(26:22):
people who reach out, the morepeople we can help.
Speaker 2 (26:26):
And if you'd like to learn how you can be a supporter
of the podcast, please see theepisode notes, as we post
information on that there.
Well, folks, thanks again forjoining us Until next week.
This is Linda and Curry signingoff.
Popular Podcasts
Cold Case Files: Miami
Joyce Sapp, 76; Bryan Herrera, 16; and Laurance Webb, 32—three Miami residents whose lives were stolen in brutal, unsolved homicides. Cold Case Files: Miami follows award‑winning radio host and City of Miami Police reserve officer Enrique Santos as he partners with the department’s Cold Case Homicide Unit, determined family members, and the advocates who spend their lives fighting for justice for the victims who can no longer fight for themselves.
24/7 News: The Latest
The latest news in 4 minutes updated every hour, every day.
Crime Junkie
Does hearing about a true crime case always leave you scouring the internet for the truth behind the story? Dive into your next mystery with Crime Junkie. Every Monday, join your host Ashley Flowers as she unravels all the details of infamous and underreported true crime cases with her best friend Brit Prawat. From cold cases to missing persons and heroes in our community who seek justice, Crime Junkie is your destination for theories and stories you won’t hear anywhere else. Whether you're a seasoned true crime enthusiast or new to the genre, you'll find yourself on the edge of your seat awaiting a new episode every Monday. If you can never get enough true crime... Congratulations, you’ve found your people. Follow to join a community of Crime Junkies! Crime Junkie is presented by audiochuck Media Company.