January 14, 2023 • 18 mins
Eisai Co., Ltd. and Biogen Inc. announced on January 6th that under the Accelerated Approval Pathway the U.S. Food and Drug Administration (FDA) has approved lecanemab-irmb, which has the brand name in the United States of LEQEMBITM, for the treatment of Alzheimer’s disease. The approval is based on Phase 2 data that demonstrated that LEQEMBI reduced the accumulation of Aβ plaque in the brain, a defining feature of Alzheimer’s disease. Newt’s guest is Dr. Marwan Sabbagh, MD. He is a behavioral neurologist in the Alzheimer’s and Memory Disorders Program and a professor in the Department of Neurology at Barrow Neurological Institute and was one of the leading doctors of the study.
See omnystudio.com/listener for privacy information.
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:04):
On this episode of This World Say. Company and Biogen
announced in January sixth that under the Accelerated Approval pathway,
the US Food and Drug Administration FDA has approved leacanamab IRMB,
which has the brand name in the US Laquembi, for
the treatment of Alzheimer's disease. The approval is based on
Phase two data that demonstrated that Laquembe reduced the accumulation
(00:28):
of plaque in the brain, a defining feature of Alzheimer's disease.
Using the recently published data from the large global confirmatory
Phase three clinical trial, Clarity, A d SA will work
quickly to file a supplemental Biologic's license application to the
FDA for approval under the traditional pathway. Here to talk
(00:48):
about this remarkable breakthrough for Alzheimer's disease treatment, I'm really
pleased to welcome my guest. Doctor Marwe Saba, who I
first worked with back in two thousand and eight, is
a behavioral neurologists and the Alzheimer's Memory Disorders Program and
a professor in the Department of Neurology at Barrow Neurological Institute,
and as one of the leading doctors on the study. Marlin,
(01:19):
thank you for joining me on news World. It's nice
to talk to you again, and I'm glad you're still
passionate about Alzheimer's. What let you have such a deep
passionate interest in Alzheimer's and in dementia. Yes, so it
doesn't run in my family. I had a fear of
getting old, and I thought that Alzheimer's was the embodiment
of everything sad and destructive about getting old. Fortunately, I've
(01:42):
been cured of that. I am very optimistic about the
future of aging, the future of Alzheimer's, and so that's
how I got in Alzheimer's. Could you just take a
minute talk to us about what is Alzheimer's. So people
understand Alzheimer's as the dementia phase. The dementia phase meaning
your cognitive memory disorders and memory issues get so bad
(02:02):
it starts to affect your daily life. That is dementias.
So dementia means you've lost your independence because of cognitive decline.
Dementia is a categorical definition, so there are many cause
of dementia. Alzheimer's is the most common type of dementia.
Two thirds of all dementia's Alzheimer's, but it is an
accumulation of proteins that should not be accumulating your brain.
The two main proteins are amaloid and and they accumulate
(02:26):
for twenty years before your first day ofgetfulness, So by
the time you walk into my clinic, your brain is
full of Alzheimer changes. What is the protein beta amyloid?
The protein beta amyloid is a protein that normally is
cleared out of the brain when it's a different form
of it. But when it starts to form the Alzheimer amoloid,
(02:47):
which is a forty two amino acid protein, it does
not clear out of the brain. It starts to accumulate
and stick together and clump together. And when it starts
to get to a certain stage of clumping together and
starts to damage that accumulation starts to damage the cells,
and then you get inflammatory changes and inflammatory reactions, and
(03:08):
the presence of amaloid triggers a whole cascade of other
things that lead to more problems down the road. So
amyloid is the earliest important seminal event that leads to
the downstream problems that ultimately lead to the dementia. And
then what are the crusted strands of the protein towel.
(03:28):
The best way to describe TAO is we have inside
our brain cells these long proteins called microtubules. Think of
microtubules as railroad tracks, and think of the cross hatches
as the cross hatches on the railroad tracks keep the
tracks together moving in the same direction. TAW is those
cross hatches, So the TAW keeps the microtubules assembled. When
(03:52):
TAO undergoes a biological change called phosphorylation, those cross hatches
of towel stop binding to microtubos, and microtubs literally get
jumbled up, and ultimately the cells die because they can't
traffic proteins and other things up and down cells. They
cannot move things inside the cells, and that's what causes
the cells to die. So the TOWE is these little
(04:13):
proteins that ultimately then get broken up when the cells die,
they're released and they're taken up by cells next door.
And the spread of tow correlates more reliably with cognitive
decline than the spread of amyloid. Is there any relationship
between the amyloid and the towel that because one perceived
the other are They're just parallel, independent developments at the
(04:36):
beginning that amoloid precedes the TOWE. There's some evidence that
amoloid is triggering the TOW, which TOWE is more of
a protein in response to injury. Amoloid is the injuring protein.
But after a while then they accumulate in parallel. Why
would somebody at a very early age suddenly have Alzheimer's.
(04:57):
Those are mostly people with genetic mutations that lead to Alzheimer's,
and there are a few of them. They're a handful
of the biggest group of people with young onset Alzheimer's
diseases down syndrome. They all get Alzheimer's more than eighty
ninety percent. We'll get Alzheimer's dimension their lifetime. That is
a good example of young onset Alzheimer's. Well this new
(05:18):
medicine have any impact on these early onset cases. For
the most part, we don't know the answer. That. I mean,
all the focus of the treatments have been around the
typical Alzheimer person right sixties, seventies, eighties onset. We have not,
as far as I know, done a lot of work
with this new treatment in the young onset Alzheimer's. There
(05:41):
is a study out of Washington University called the Diane Study,
and they were looking at drugs similar to this to
treat the young onset. But as far as I know,
that has not been successful. Alzheimer's for most people, you've
actually had it for years before it manifest itself in
any kind of avil modification. Is that accurate? That is
(06:02):
an accurate statement. So we know that by the time
you walk into the clinic you may have been accuminting
you know, amyloid and town in your brain for fifteen
twenty years or so. So the dementia phase is a
late manifestation of the ethology. If we can find a
way to cure Alzheimer's, we have an enormous impact both
on the quality of life and productivity, and also on
(06:25):
the physical costs of just the entire of the health system.
Great summary, exactly right. The last fifteen years have been
very productive and breakthroughs, and when I was speaker, we
doubled the size of the NIH budget. This is an
example of the kind of breakthroughs that are now beginning
to really pay off in terms of the quality of
(06:46):
life for Americans. And you led huge initiatives that have
paid off huge dividends that all the work you led
led to big funding initiatives that have advanced the fields greatly.
So thank you. If you think you're at risk for Alzheimers,
(07:20):
what are the things you can do to slow or
prevent the progressional disease? In prevention, you know, people are
looking at the fact that you should be engaging in
ways to reduce your risk. That would include aggressive blood
pressure management, cognitive stimulation, brain games or things like that,
and physical exercise are the three things that have been
(07:43):
shown that the National Academy of Sciences, Medicine and Engineering
have sufficient evidence to recommend. The World Health Organization would
add more to that, and the Lancet Commission would add
more to that. But we are now looking at the
concept of brain health in a way to engage people
to do preventive strategies that they can start today and
(08:03):
not just wait till they're having problems. Wasn't there a
study one so I think it was of nuns who
played bridge versus nuns who didn't, and the just the
act of playing bridge stimulated their brain and chromatically changed
the trajectory of brain diseases. That was the Snowdon study
from University of Kentucky and their nun study from the
(08:24):
nineteen eighties, and that's exactly right, and that was the
first evidence of cognitive stimulation. Brain stimulation on a continuous
basis that has shown to be protective. And we've seen
multiple studies since then confirming that observation. For our listeners,
any need to realize this is the sixth leading cause
of death in nined States. This is a major part
(08:46):
of our health trajectory. Then the work you're doing is
a big part of that. And now, for the very
first time, the Food and Drug Administration is beginning to
approve drugs in this area, which is tricky because their
standard acquired a turnaround time that was reasonable. Now, when
you're dealing with long term brain diseases, the studies take
so long. You do a lot more damage to people
(09:08):
by not approving and taking the risks than you do
by waiting for the ultimately multi year outcome. But they
have approved six drugs and LAKEMBE is going to be
number seven. Have you found the FDA to be more
knowledgeable and more reasonable in this area? I have to
say that the FDA, because I know a lot of
those officers at the FDA are paying a lot of attention.
(09:30):
They're very very well informed, they're very motivated to stay informed,
and they're listening very carefully to everything. They're very very
close to the science. When they make decisions. I assure
you they have really gone through this very carefully, very thoroughly,
and I know them well enough to know that they're
(09:51):
very careful people speaker. I think they have a very
hard job, very difficult job, but they make no mistake
about it. They're very thorough and very careful. They have
two challenges. One is to make sure the drug actually
works and the other is to make sure it doesn't
do more harm than good. The initial wave of the
first five drugs that they approved, we're really sort of
symptom oriented rather than taking Alzheimer's on head on. And
(10:14):
in terms of changing the course of disease, that's correct.
It would be like tilenol for a fever. These are
drugs that improve the symptoms but don't stop the progression
or substantly change the disease. And so this new drug,
look CAMBI, being the second one to what we call DMT,
or disease modifying treatment, is a real game changer. Look
(10:35):
CAMBI as an additional break in that direction. You are
a researcher on a study for the new drug, how
does it differ from prior drugs? So what the drug
does is it's called a biologic or a monoclonal antibody.
And understand that monoclon antibodies are manufactured proteins that you
inject or infuse, and they're basically there to find whatever
(10:59):
their design to find. Right. So Lakembi is a manufactured
protein and it's designed to find amyloid and grab it
and take it out of the body. That's all it does.
They understand that, you know, biologics or monoclone lanibodies are
used in all kinds of diseases. Right you watch TV
and you talk about sooriasis and arthritis. Those are all
(11:19):
monoclone lanibodies, much like la Kembi is for Alzheimers. So
this is a manufactured protein binds amoid, finds it and
clears it out of the body and out of the brain,
and it does it spectacularly well. That clarity study that
you mentioned your opening remark removes ninety percent of the
amoloid out of your brain in less than twelve months,
So we know it does what it's supposed to do.
(11:41):
After you've achieved that in the first twelve months, do
you need to keep taking it to continue draining out
the harmful transitions or can you sort of back off
for a while because you've relieved ninety percent of them.
It's a speculative thing. In the labels say that you
will continue to intravenous infusions every two weeks in definite lead,
and that's the state of the science right now. You know,
(12:04):
a year from now that might change. What I think's
going to happen, though, is you'll take it for a
year or two IV. This is speculative. I'm not speaking
on anybuddy's authority. Right then you'll either go to a
shot like an injection every once in a while, or
you'll just get it less often. So I think the
IV every two weeks will just be on the short term,
(12:25):
but we don't have a definitive position on that yet.
And then how long does the intravendis treatment take. It
takes about an hour to take the treatment, so you
go to a clinic, yes, okay, but for an hour
every two weeks. If we're clearing up nine, what could
lead you to have real cognitive problems. That's a pretty
good trade. Absolutely. And if you were at the beginning
(12:46):
of the Alzheimer process what we call mild cogning repairment
or pre dementia, and you're still independent but you're having
some memory issues, wouldn't it be awesome that you don't
go on to get dementia. You're still independent, you still
enjoy your call of life, and this drug slows the
progression to dementia. People can continue independent living, probably continue
(13:06):
to work if they want to. It's really a game changer.
But as I understand it, you have to be in
fairly early stages for this to work. Yes, this is
a drug that unfortunately not everybody's going to get. The
data is very clearly suggest that only the people at
the beginning stages, so mild cognment, impairment, or mild dementia,
(13:28):
will be appropriate for this. If you're more advanced in
your dementia, if you don't have amyloid, if you have
a pacemaker and you can't get an MRI, A lot
of people will not get the drug. Speaker, I have
to tell you that our estimates only suggested maybe twenty
percent of people walking in the door will get the drug.
And most people will not if you have any sense
(13:52):
that you're beginning to have cognitive impairment. The earlier you
are diagnosed, the greater the likelihood that you could get
a drug this to dramatically postpone the onset of serious
cognitive problems. That is exactly right, and we expect to
see that. And the other thing that we're seeing that's
coming to the market now is a possibility of a
(14:15):
screening blood test like a PSA. Like you and I
as men, we always go get our pay check. We
might have a screening blood test that's actually coming to
the clinic as we speak. So I'm not sure it'd
be a diagnostic, you know, like you just go get
your infusion after the blood test, But if it's normal,
then you know you don't have Alzheimers, and if it's admirable,
(14:36):
you could get more testing. So that is also a
big development in the field. And we could be using
the screening blood test later this year. So a lot
of big changes in twenty twenty three, which offers enormous
hope in the long run. It's the point at which
the onset begins, not your age. So if you're sixty
an early onset. You should get checked immediately. If you're
(14:59):
eighty or ninety and you suddenly have on said, you
still are treatable if they caught early enough. So it
really does create sort of a wave effect that as
people get better at this, we begin to cut off
by countering it. In the first year or two or
three people becoming seriously impaired. Yes, that's correct, which is
(15:19):
an enormous revolution. Yes, absolutely. Let me ask you a
closing question, which is what would you say to people
who are worried about Alzheimer's and the possibility of the
great breakthroughs that are coming. Speaker, you have had a
major impact on American society over the last thirty years,
and I'm telling you that because you saw under your
(15:44):
watch the transformation of other diseases. Right, So, in your time,
you saw HIV turn from a terminal disease to now
a chronic, manageable disease. You saw multiple sclerosis turned from
a disease where you were going to be in a
wheelchair for sure in ten years to now people live
(16:04):
a normal quality of life. I start with that because
we are now going to see that happen with Alzheimers.
It will go from a terminal disease as you and
I know it. We've invested much of our careers in this,
to a chronic disease. One day in the very near future,
you will have a little bit of forgetfulness. You'll go
get your blood tests, you'll go get your confirmation, pet
scans and things like that. Start on a cocktail regiment,
(16:26):
you know, one, two, three, four or five drug approach,
and then you won't get worse and you'll have a
normal life. And that day is coming soon. And so
I am very excited about leken because it is the
beginning the transformation of Alzheimer's from a criminal disease as
you and I know it, to a chronic disease. I
want to thank you for joining me, and I think
the work you're doing to find a treatment for Alzheimer's
(16:48):
disease is so important for all Americans. And I'm looking
forward clearing about the next great breakthrough, and I look
forward to you coming back and joining to talk again
about what's happening. Thank you. Thank you to my guest
doctor Marjuan Saba. You can find out more about the
new Alzheimer's disease treatment Lacuimbie on our show page at
(17:12):
newsworld dot com. News World is produced by Gangwish three
sixty and iHeartMedia. Our executive producer is Garnsey Slope, our
producer is Rebecca Hell, and our researcher is Rachel Peterson.
The artwork for the show was created by Steve Pendley.
Special thanks to the team at Dinguish three sixty. If
you've been enjoying Newsworld, I hope you'll go to Apple
(17:33):
Podcasts and both rate us with five stars and give
us a review so others can learn what it's all about.
Right now, listeners of Newtsworld can sign up for my
three free weekly columns at Gangwish three sixty dot com
slash newsletter. I'm new Gangwish. This is Newsworld.
On this episode of This World Say. Company and Biogen
announced in January sixth that under the Accelerated Approval pathway,
the US Food and Drug Administration FDA has approved leacanamab IRMB,
which has the brand name in the US Laquembi, for
the treatment of Alzheimer's disease. The approval is based on
Phase two data that demonstrated that Laquembe reduced the accumulation
(00:28):
of plaque in the brain, a defining feature of Alzheimer's disease.
Using the recently published data from the large global confirmatory
Phase three clinical trial, Clarity, A d SA will work
quickly to file a supplemental Biologic's license application to the
FDA for approval under the traditional pathway. Here to talk
(00:48):
about this remarkable breakthrough for Alzheimer's disease treatment, I'm really
pleased to welcome my guest. Doctor Marwe Saba, who I
first worked with back in two thousand and eight, is
a behavioral neurologists and the Alzheimer's Memory Disorders Program and
a professor in the Department of Neurology at Barrow Neurological Institute,
and as one of the leading doctors on the study. Marlin,
(01:19):
thank you for joining me on news World. It's nice
to talk to you again, and I'm glad you're still
passionate about Alzheimer's. What let you have such a deep
passionate interest in Alzheimer's and in dementia. Yes, so it
doesn't run in my family. I had a fear of
getting old, and I thought that Alzheimer's was the embodiment
of everything sad and destructive about getting old. Fortunately, I've
(01:42):
been cured of that. I am very optimistic about the
future of aging, the future of Alzheimer's, and so that's
how I got in Alzheimer's. Could you just take a
minute talk to us about what is Alzheimer's. So people
understand Alzheimer's as the dementia phase. The dementia phase meaning
your cognitive memory disorders and memory issues get so bad
(02:02):
it starts to affect your daily life. That is dementias.
So dementia means you've lost your independence because of cognitive decline.
Dementia is a categorical definition, so there are many cause
of dementia. Alzheimer's is the most common type of dementia.
Two thirds of all dementia's Alzheimer's, but it is an
accumulation of proteins that should not be accumulating your brain.
The two main proteins are amaloid and and they accumulate
(02:26):
for twenty years before your first day ofgetfulness, So by
the time you walk into my clinic, your brain is
full of Alzheimer changes. What is the protein beta amyloid?
The protein beta amyloid is a protein that normally is
cleared out of the brain when it's a different form
of it. But when it starts to form the Alzheimer amoloid,
(02:47):
which is a forty two amino acid protein, it does
not clear out of the brain. It starts to accumulate
and stick together and clump together. And when it starts
to get to a certain stage of clumping together and
starts to damage that accumulation starts to damage the cells,
and then you get inflammatory changes and inflammatory reactions, and
(03:08):
the presence of amaloid triggers a whole cascade of other
things that lead to more problems down the road. So
amyloid is the earliest important seminal event that leads to
the downstream problems that ultimately lead to the dementia. And
then what are the crusted strands of the protein towel.
(03:28):
The best way to describe TAO is we have inside
our brain cells these long proteins called microtubules. Think of
microtubules as railroad tracks, and think of the cross hatches
as the cross hatches on the railroad tracks keep the
tracks together moving in the same direction. TAW is those
cross hatches, So the TAW keeps the microtubules assembled. When
(03:52):
TAO undergoes a biological change called phosphorylation, those cross hatches
of towel stop binding to microtubos, and microtubs literally get
jumbled up, and ultimately the cells die because they can't
traffic proteins and other things up and down cells. They
cannot move things inside the cells, and that's what causes
the cells to die. So the TOWE is these little
(04:13):
proteins that ultimately then get broken up when the cells die,
they're released and they're taken up by cells next door.
And the spread of tow correlates more reliably with cognitive
decline than the spread of amyloid. Is there any relationship
between the amyloid and the towel that because one perceived
the other are They're just parallel, independent developments at the
(04:36):
beginning that amoloid precedes the TOWE. There's some evidence that
amoloid is triggering the TOW, which TOWE is more of
a protein in response to injury. Amoloid is the injuring protein.
But after a while then they accumulate in parallel. Why
would somebody at a very early age suddenly have Alzheimer's.
(04:57):
Those are mostly people with genetic mutations that lead to Alzheimer's,
and there are a few of them. They're a handful
of the biggest group of people with young onset Alzheimer's
diseases down syndrome. They all get Alzheimer's more than eighty
ninety percent. We'll get Alzheimer's dimension their lifetime. That is
a good example of young onset Alzheimer's. Well this new
(05:18):
medicine have any impact on these early onset cases. For
the most part, we don't know the answer. That. I mean,
all the focus of the treatments have been around the
typical Alzheimer person right sixties, seventies, eighties onset. We have not,
as far as I know, done a lot of work
with this new treatment in the young onset Alzheimer's. There
(05:41):
is a study out of Washington University called the Diane Study,
and they were looking at drugs similar to this to
treat the young onset. But as far as I know,
that has not been successful. Alzheimer's for most people, you've
actually had it for years before it manifest itself in
any kind of avil modification. Is that accurate? That is
(06:02):
an accurate statement. So we know that by the time
you walk into the clinic you may have been accuminting
you know, amyloid and town in your brain for fifteen
twenty years or so. So the dementia phase is a
late manifestation of the ethology. If we can find a
way to cure Alzheimer's, we have an enormous impact both
on the quality of life and productivity, and also on
(06:25):
the physical costs of just the entire of the health system.
Great summary, exactly right. The last fifteen years have been
very productive and breakthroughs, and when I was speaker, we
doubled the size of the NIH budget. This is an
example of the kind of breakthroughs that are now beginning
to really pay off in terms of the quality of
(06:46):
life for Americans. And you led huge initiatives that have
paid off huge dividends that all the work you led
led to big funding initiatives that have advanced the fields greatly.
So thank you. If you think you're at risk for Alzheimers,
(07:20):
what are the things you can do to slow or
prevent the progressional disease? In prevention, you know, people are
looking at the fact that you should be engaging in
ways to reduce your risk. That would include aggressive blood
pressure management, cognitive stimulation, brain games or things like that,
and physical exercise are the three things that have been
(07:43):
shown that the National Academy of Sciences, Medicine and Engineering
have sufficient evidence to recommend. The World Health Organization would
add more to that, and the Lancet Commission would add
more to that. But we are now looking at the
concept of brain health in a way to engage people
to do preventive strategies that they can start today and
(08:03):
not just wait till they're having problems. Wasn't there a
study one so I think it was of nuns who
played bridge versus nuns who didn't, and the just the
act of playing bridge stimulated their brain and chromatically changed
the trajectory of brain diseases. That was the Snowdon study
from University of Kentucky and their nun study from the
(08:24):
nineteen eighties, and that's exactly right, and that was the
first evidence of cognitive stimulation. Brain stimulation on a continuous
basis that has shown to be protective. And we've seen
multiple studies since then confirming that observation. For our listeners,
any need to realize this is the sixth leading cause
of death in nined States. This is a major part
(08:46):
of our health trajectory. Then the work you're doing is
a big part of that. And now, for the very
first time, the Food and Drug Administration is beginning to
approve drugs in this area, which is tricky because their
standard acquired a turnaround time that was reasonable. Now, when
you're dealing with long term brain diseases, the studies take
so long. You do a lot more damage to people
(09:08):
by not approving and taking the risks than you do
by waiting for the ultimately multi year outcome. But they
have approved six drugs and LAKEMBE is going to be
number seven. Have you found the FDA to be more
knowledgeable and more reasonable in this area? I have to
say that the FDA, because I know a lot of
those officers at the FDA are paying a lot of attention.
(09:30):
They're very very well informed, they're very motivated to stay informed,
and they're listening very carefully to everything. They're very very
close to the science. When they make decisions. I assure
you they have really gone through this very carefully, very thoroughly,
and I know them well enough to know that they're
(09:51):
very careful people speaker. I think they have a very
hard job, very difficult job, but they make no mistake
about it. They're very thorough and very careful. They have
two challenges. One is to make sure the drug actually
works and the other is to make sure it doesn't
do more harm than good. The initial wave of the
first five drugs that they approved, we're really sort of
symptom oriented rather than taking Alzheimer's on head on. And
(10:14):
in terms of changing the course of disease, that's correct.
It would be like tilenol for a fever. These are
drugs that improve the symptoms but don't stop the progression
or substantly change the disease. And so this new drug,
look CAMBI, being the second one to what we call DMT,
or disease modifying treatment, is a real game changer. Look
(10:35):
CAMBI as an additional break in that direction. You are
a researcher on a study for the new drug, how
does it differ from prior drugs? So what the drug
does is it's called a biologic or a monoclonal antibody.
And understand that monoclon antibodies are manufactured proteins that you
inject or infuse, and they're basically there to find whatever
(10:59):
their design to find. Right. So Lakembi is a manufactured
protein and it's designed to find amyloid and grab it
and take it out of the body. That's all it does.
They understand that, you know, biologics or monoclone lanibodies are
used in all kinds of diseases. Right you watch TV
and you talk about sooriasis and arthritis. Those are all
(11:19):
monoclone lanibodies, much like la Kembi is for Alzheimers. So
this is a manufactured protein binds amoid, finds it and
clears it out of the body and out of the brain,
and it does it spectacularly well. That clarity study that
you mentioned your opening remark removes ninety percent of the
amoloid out of your brain in less than twelve months,
So we know it does what it's supposed to do.
(11:41):
After you've achieved that in the first twelve months, do
you need to keep taking it to continue draining out
the harmful transitions or can you sort of back off
for a while because you've relieved ninety percent of them.
It's a speculative thing. In the labels say that you
will continue to intravenous infusions every two weeks in definite lead,
and that's the state of the science right now. You know,
(12:04):
a year from now that might change. What I think's
going to happen, though, is you'll take it for a
year or two IV. This is speculative. I'm not speaking
on anybuddy's authority. Right then you'll either go to a
shot like an injection every once in a while, or
you'll just get it less often. So I think the
IV every two weeks will just be on the short term,
(12:25):
but we don't have a definitive position on that yet.
And then how long does the intravendis treatment take. It
takes about an hour to take the treatment, so you
go to a clinic, yes, okay, but for an hour
every two weeks. If we're clearing up nine, what could
lead you to have real cognitive problems. That's a pretty
good trade. Absolutely. And if you were at the beginning
(12:46):
of the Alzheimer process what we call mild cogning repairment
or pre dementia, and you're still independent but you're having
some memory issues, wouldn't it be awesome that you don't
go on to get dementia. You're still independent, you still
enjoy your call of life, and this drug slows the
progression to dementia. People can continue independent living, probably continue
(13:06):
to work if they want to. It's really a game changer.
But as I understand it, you have to be in
fairly early stages for this to work. Yes, this is
a drug that unfortunately not everybody's going to get. The
data is very clearly suggest that only the people at
the beginning stages, so mild cognment, impairment, or mild dementia,
(13:28):
will be appropriate for this. If you're more advanced in
your dementia, if you don't have amyloid, if you have
a pacemaker and you can't get an MRI, A lot
of people will not get the drug. Speaker, I have
to tell you that our estimates only suggested maybe twenty
percent of people walking in the door will get the drug.
And most people will not if you have any sense
(13:52):
that you're beginning to have cognitive impairment. The earlier you
are diagnosed, the greater the likelihood that you could get
a drug this to dramatically postpone the onset of serious
cognitive problems. That is exactly right, and we expect to
see that. And the other thing that we're seeing that's
coming to the market now is a possibility of a
(14:15):
screening blood test like a PSA. Like you and I
as men, we always go get our pay check. We
might have a screening blood test that's actually coming to
the clinic as we speak. So I'm not sure it'd
be a diagnostic, you know, like you just go get
your infusion after the blood test, But if it's normal,
then you know you don't have Alzheimers, and if it's admirable,
(14:36):
you could get more testing. So that is also a
big development in the field. And we could be using
the screening blood test later this year. So a lot
of big changes in twenty twenty three, which offers enormous
hope in the long run. It's the point at which
the onset begins, not your age. So if you're sixty
an early onset. You should get checked immediately. If you're
(14:59):
eighty or ninety and you suddenly have on said, you
still are treatable if they caught early enough. So it
really does create sort of a wave effect that as
people get better at this, we begin to cut off
by countering it. In the first year or two or
three people becoming seriously impaired. Yes, that's correct, which is
(15:19):
an enormous revolution. Yes, absolutely. Let me ask you a
closing question, which is what would you say to people
who are worried about Alzheimer's and the possibility of the
great breakthroughs that are coming. Speaker, you have had a
major impact on American society over the last thirty years,
and I'm telling you that because you saw under your
(15:44):
watch the transformation of other diseases. Right, So, in your time,
you saw HIV turn from a terminal disease to now
a chronic, manageable disease. You saw multiple sclerosis turned from
a disease where you were going to be in a
wheelchair for sure in ten years to now people live
(16:04):
a normal quality of life. I start with that because
we are now going to see that happen with Alzheimers.
It will go from a terminal disease as you and
I know it. We've invested much of our careers in this,
to a chronic disease. One day in the very near future,
you will have a little bit of forgetfulness. You'll go
get your blood tests, you'll go get your confirmation, pet
scans and things like that. Start on a cocktail regiment,
(16:26):
you know, one, two, three, four or five drug approach,
and then you won't get worse and you'll have a
normal life. And that day is coming soon. And so
I am very excited about leken because it is the
beginning the transformation of Alzheimer's from a criminal disease as
you and I know it, to a chronic disease. I
want to thank you for joining me, and I think
the work you're doing to find a treatment for Alzheimer's
(16:48):
disease is so important for all Americans. And I'm looking
forward clearing about the next great breakthrough, and I look
forward to you coming back and joining to talk again
about what's happening. Thank you. Thank you to my guest
doctor Marjuan Saba. You can find out more about the
new Alzheimer's disease treatment Lacuimbie on our show page at
(17:12):
newsworld dot com. News World is produced by Gangwish three
sixty and iHeartMedia. Our executive producer is Garnsey Slope, our
producer is Rebecca Hell, and our researcher is Rachel Peterson.
The artwork for the show was created by Steve Pendley.
Special thanks to the team at Dinguish three sixty. If
you've been enjoying Newsworld, I hope you'll go to Apple
(17:33):
Podcasts and both rate us with five stars and give
us a review so others can learn what it's all about.
Right now, listeners of Newtsworld can sign up for my
three free weekly columns at Gangwish three sixty dot com
slash newsletter. I'm new Gangwish. This is Newsworld.
Popular Podcasts
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.
24/7 News: The Latest
The latest news in 4 minutes updated every hour, every day.
Stuff You Should Know
If you've ever wanted to know about champagne, satanism, the Stonewall Uprising, chaos theory, LSD, El Nino, true crime and Rosa Parks, then look no further. Josh and Chuck have you covered.