Episode Transcript
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Speaker 1 (00:00):
Guess what, Mango? What's that? Well, you remember a few
years ago when the social media sites and apps, and
I'm thinking Facebook especially, they started using this facial recognition
programming and that was used to recognize all of us
and these photos that we were posting. And I remember
when it first started happening. I think this is honestly
just a little bit creepy, Like, how did you know
(00:21):
that was my friend Steve? I mean, the guy was
wearing a hat, he had on glasses, then he had
longer hair than he might have weighed five or six
more pounds, Like, how did you know that was Steve?
I know, it was so impressive, but also so creepy.
I felt the same way. I kind of had mixed
emotions about it. But you know, as much as the
world of artificial intelligence can sometimes weird us out and
(00:44):
leave us feeling a little bit violated, even you know,
the more I've read about its potential applications in the
world of medicine, the more I'm actually fascinated, you know,
by what it might be capable of in the decades ahead.
So how do you mean exactly, Well, I've been reading
some about how so many conditions and genetic ones in particular,
have what some in the medical field would call a
(01:05):
certain face, and that is a set of similar features
that might indicate whether someone might have a certain genetic syndrome. Now,
the advantage of technology is obviously that these machines can
process so many millions of pieces of data at one time,
and they'd be looking for these common features, even very
subtle ones. So some of those same programmers who were
(01:25):
helping places like Facebook, they're getting involved to help with
the diagnosis of Alzheimer's, something that's often incredibly difficult to
diagnose before significant damage has been done in the brain,
and they're often looking for these subtle speech delays or
slight hiccups as you might describe them, that a doctor
might not be able to see it first. And it's
still very early, but of course we all hope this
(01:47):
leads to better diagnosis and better treatment, and the progress
to date does give us some real hope. I feel
like most of us have been affected by Alzheimer's in
some way, knowing a loved one who's suffered from it.
I know both of us have. So you know, today
we wanted to talk a little bit about that, Like
what we know about Alzheimer's, what kind of progress we're
making and fighting it, and who seems to be doing
(02:09):
the best job of caring for those with Alzheimer's. So
let's get started, right hey, their podcast listeners, Welcome to
(02:36):
Part Time Genius. I'm Will Pearson and as always I'm
joined by my good friend man guest shot Ticketer and
on the other side of the soundproof glass, hunched over
his brand new copy of Mandarin for Dummies. It's been
a while since I've seen a dummies book, but anyway,
that that's our friend and producer Tristan McNeil, and of
course he's on theme as usual. You know, I was
reading just this week about how learning a new language
(02:57):
can help stave off Alzheimer's in some cases. And this
was from a study out of York University in Toronto
where they actually examined over a hundred long time bilingual
Alzheimer's patients along with over a hundred monolingual patients, and
it turned out that on average, the bilingual patients have
been diagnosed with Alzheimer's about four years later than the
monolingual patients. So the idea is that because learning a
(03:19):
second language gives the brains such a strong workout, it
can actually help keep the full effects of the disease
at bay longer, which is really interesting. But you know,
it's honestly sometimes tough to say for certain, because they're
all kinds of genetic and environmental factors that can increase
or decrease a person's chances of contracting Alzheimer's, and we'll
(03:40):
be talking about a few of those later on. But ultimately,
no one is immune to the disease, and the greatest
risk factor associated with it, of course, is is just
age itself. In fact, studies have clearly shown that the
number of people with Alzheimer's disease increases with age, so
much so that roughly one in five people now suffer
from it by the age of eight five. And I
(04:02):
know all of this is upsetting to think about, and
people who have Alzheimer's disease and their family are already
dealing with it on a daily basis, and those of
us who have been lucky enough not to have to
face it in some big way would probably rather focus
on just about anything else. But the truth is this
is something everybody needs to stay informed about, particularly if
you plan to live past the age of sixty. Another
(04:23):
good news is that scientists are already hard at work
on new research and new treatments, and that's what we'll
be focused on today. You know, all those promising approaches
to Alzheimer's disease that could hopefully lead to earlier detection
and improve symptom management and hopefully one day of course
secure that's right, But before we get to the more
hopeful side of the topic, we should probably do a
(04:44):
quick crash course on what the disease is exactly. So
for starters, Alzheimer's disease is a chronic, progressive neurodegenerative disease,
which means it's a form of dementia that leads to
severe cognitive loss and eventual death. And while there are
several different kinds of dementia, Alzheimer's is the most common,
accounting for somewhere between sixty eight percent of all dementia cases.
(05:06):
So really, dementia is something of an epidemic at this point,
I would think, because you know, some of the stats
I found all researching, we're pretty jaw dropping. Apparently, Alzheimer's
is now the sixth leading cause of death in the
US and the seventh worldwide. And that really wasn't the
case even fifty years ago. Yeah, So Alzheimer's was formally
recognized as an epidemic back in the seventies, and sadly
(05:29):
that designation still stands today. In fact, that the world
has a larger aging population than ever before, which inevitably
means that the number of people who developed the disease
is only set to grow. For example, this organization called
Alzheimer's Disease International, they estimated that about five million people
in the US and nearly fifty million people worldwide currently
suffer from dimension one form or another, but by twenty
(05:52):
fifty the number is projected actually to reach one hundred
thirty one million. Wow. So it's obvious in light of
that why they such a big push to find a
cure as soon as possible. But you know, I'm curious
how long have we known about the problem, Like, is
Alzheimer's something we've been trying to get a grip on
for centuries or this a relatively new threat. Well, dementia
(06:14):
as a broad concept is popped up in medical text
going all the way back to ancient Greece, but the
first case study for Alzheimer's in particular was in nineteen
o one, and that's when this German neuropathologist named A.
Louis Alzheimer, you know who the disease is named after,
began treating a woman at an asylum in Frankfurt, and
the fifty one year old patients seemed to suffer from
(06:35):
some kind of psychosis. In addition to rapid memory loss,
she reported I guess uh, strange feelings of jealousy towards
her husband. She also had these odd behaviors, like she'd
dragged furniture to and fro She'd hied uh. Sometimes she'd
think people were out to kill her, so then she
would scream out loudly. It was pretty sad, and so
was Dr Alzheimer able to help her in anyway? No,
(06:57):
not really. But when the patient died five years later,
Alzheimer was able to dissect or brain, and his findings
formed the basis for the first formal description of pre
senile dementia. So what did he find when he looked? So?
Today we know that the main effects of Alzheimer's, like
memory laws, decreased thinking ability, Personality changes like these are
(07:18):
all the result of dyeing brain cells and the atrophy
of certain key regions of the brain. And the reason
these brain cells start to die off is because something
has disrupted the communication between the neurons and the brain.
So Alzheimer's biggest contribution was really identifying what that something was,
or at least most likely what it is, because when
(07:39):
he dissected that patient's brain and examined it under a microscope,
he identified these tiny tangles and plaques dotting the gray tissues.
And and these are the masses that that are some
kind of protein build up, right, yeah, there are. There
are these two types of proteins at work. It's the
amyloid and the tao. And while we don't know what
prompts the accumulation of these proteins are how exactly they interact,
(08:01):
their presence is usually a telltale sign of Alzheimer's. So
the amaloid is recognizable because it bunches together into sticky
clumps through these beta amaloid plaques. And the tow is
easy to spot because it accumulates as tangles of these
watered up protein strands. You know, even before we started
doing our research for today's episode, I'd always heard that
one of the biggest obstacles for treating Alzheimer's is that it's,
(08:24):
you know, notoriously difficult to diagnose. By the time the
symptoms manifest enough to be caught, much of that damage
has already been done. But why is that, like, if
these plaques and tangles are so noticeable. Yeah, it's a
good question, and the answer is that we actually haven't
found a reliable or accurate way to measure these protein
build ups, especially in living patients. So more than a
(08:46):
hundred years after that initial case in Germany, there's still
no definitive way to diagnose Alzheimer's without dissecting the brain
post mortem to look for these hallmark plaques and tangles.
And in recent years, some postmortems have given a reason
to question whether the presence of these build ups is
really telling the whole story anyway. Oh, so what do
you mean by that? Well, there have actually been some
(09:07):
cases where patients who were said to have Alzheimer's were
revealed to not have plaques and tangles in their brains.
And maybe even weirder, there are also cases where post
mortem exams show massive build ups in the brains of
people who had excellent memories. So while these plaques and
these tangles appear to have some part in the onset
of Alzheimer's, it isn't true in all cases, and as
(09:27):
a result, a growing number of researchers are starting to
think that chronic inflammation might actually play the larger role
in the disease than they initially thought. So here's how
Scientific American broke down the new hypothesis and article from
last November. In the brain tissue damaging long term inflammation
can also be caused by a build up of cells
known as microglia. In a healthy brain, these cells engulf
(09:49):
and destroy waste and toxins, but in Alzheimer's patients, the
microglia failed to clear away this debris, which can include
toxic tow tangles or amyloid plaques. The body then activates
more microglia to try to clear the waste, but this
in turn causes inflammation. Long term or chronic inflammation is
particularly damaging to brain cells and ultimately leads to brain
(10:10):
cell death. Okay, so in this case, the inflammation, which
could be worsened by the plaques and the tangles would
would actually be the real culprit behind the dying brain cell.
So how would just been thinking about this? How would
that impact the search for for treatments, though, I mean,
from everything I've read, it seems like most researchers have
been focusing on the other ways to prevent or destroy
(10:33):
these protein build ups. So I mean, I hate to
ask this, but have we been heading in the wrong
direction this whole time? Well it's too early to say
for sure, but I really hope not. It would be
devastating to see such a colossal amount of effort and
money lead to a dead end. I mean, we hear
about new promising treatments all the time, but all too
many of them disappear from headlines a few months later
(10:54):
because they were later proven ineffective during trials. And in fact,
at this point, none of the hot twenty three experimental
Alzheimer's drugs developed between two thousand and fourteen have made
it past the later stages of clinical testing. And that's
obviously a concern for all sorts of reasons, you know,
not the least of which is just how much it
(11:14):
costs to develop even one new form of treatment. For example,
that there was this two thousand sixteen study from the
Journal of Health Economics, and it found the average research
and development cost for a new medicine are about two
point six billion dollars. Good lord, it's hard to even
wrap your head around that kind of money for something
like that. But you know the truth is that, you know,
(11:35):
we as a country still aren't spending as much on
Alzheimer's researches we likely should be. I mean, stimulate spending
for Alzheimer's research was increased to around I think it
was around one point eight billion dollars this year, and
that does get it pretty close to that two billion
dollar mark that the Alzheimer's Association has has long been
saying that researchers needed in order to treat the disease effectively.
(11:58):
But this funding has to be every year, so there's
no guarantee that that upper trend will continue long term.
And not to mention that's just funding for new research,
I mean that the actual cost of health care for
dementia already exceeds two hundred billion dollars each year in
the US. Yeah. But despite the uncertainties that still surround Alzheimer's,
like all that plaques and tangles, research we've been spending
(12:21):
so much money on will still be super useful no
matter what. And that's partly because many researchers are now
pushing for a more personalized approach to Alzheimer's treatment. It's
similar to the way we're dealing with cancer, like there's
no one treatment that's effective for every kind of cancer,
or even for every case of the same kind, and
it's the same way with Alzheimer's. So the idea you
had the new approach is to use multiple drugs to
(12:43):
target the many different changes in the brain that can
occur with Alzheimer's. Okay, I see. So for instance, you
might start a patient off with one drug if you're
trying to reduce that build up of amyloid plaques or
something like that, and then you might switch to another
if inflammation is the bigger issue, or or change it
up if it's different for another patient exactly. So, Alzheimer's
(13:04):
is obviously this complex disease and it doesn't manifest the
same across the board, so it's helpful to have as
many tools at our disposal as possible to treat it,
and that way we can mix and match medications to
create treatment plants tailor made for each patient's pelecular profile.
Al Right, well, that does sound like a more promising
approaches as well. As a nice reminder that it's worth
(13:24):
tackling this problem from as many different angles as we can.
I mean, you never know which one might lead to
that game changing solution that we're always looking for. Absolutely,
And in the meantime, there's still some effective ways to
reduce your chances of contracting Alzheimer's, and even a few
new ideas for how to detect and diagnose Alzheimer's without
having to wait for a postmortem. Yeah, well, I definitely
(13:46):
want to talk about those, but before we do, let's
take a quick break. You're listening to Part Time Genius
(14:09):
and we're talking about the most promising efforts to treat
Alzheimer's disease. All right, mango, So we talked about how,
for decades now, the prevailing theory has been that Alzheimer's
is caused by these cell killing protein build ups in
the brain. And you noted how chronic inflammation is also
thought to have some role in that degeneration. And what
strikes me about all this is it it seems like
we know where the accumulations and inflammation may come from,
(14:32):
but we don't really know why they occur. Yeah, that's true,
but but a person's genetics do provided least some clues
as to what's going on. For for example, we know
that the trigger for most cases of Alzheimer's is a
single mutated gene and it's on one of our chromosomes.
Then remember that we all have two copies of every gene,
one from each of our parents, so potentially someone could
(14:53):
have two copies of this mutated gene. Al right, So
how big a factor is this mutation on whether a
person develops Alzheimer's or not? I mean, it really depends
on how many copies of the muta genes someone has.
So if a person has one copy, then there's up
to chance of them developing the disease, And if they
have two copies, then the likelihood jumps to as high
(15:13):
as eight seven m alright, And so how common is
it to have one or two of these genes? So
apparently about of the population has one copy, but it's
only two percent that have two copies. And testing for
the genes is actually something you can do through something
like twenty three and ME or one of those other
personal genetics tests. You know, though, you know, whether you
(15:36):
want to stress yourself out with something like that is
another question entirely. Yeah, I can see. I'm you know,
a lot of people might feel like that level of
self knowledge is is something they're not quite prepared to handle,
and especially considering that many researchers say there's more to
the disease than just genetics. For example, I was reading
how some scientists think that the true causes of Alzheimer's
can be traced back to more environmental factors. That includes
(15:59):
everything from your diet to how many times you've been
you know, hitting the head in your lifetime too. Of course, yes,
you know how many languages you speak? Yeah, definitely, so
that language one is actually rooted in the fact that
people who stay mentally active experienced less cognitive decline as
they age, and amazingly, that remains the case even for
people whose brains were later found to be riddled with
(16:19):
familiar signs of Alzheimer's, like those plaques or tangles we've
been talking about. So even when the disease is already
set in, elderly patients who make it a habit to
read or write or play thinking games like chess can
sometimes stave off its symptoms for a lot longer. In fact,
one two thirteen study found that people who didn't routinely exercise,
their brains experienced cognitive decline full forty eight percent faster
(16:42):
than those dident Yeah, that's pretty pretty good endorsement for reading.
But you know, you know, for those times when your
brain just needs a break or you know, it does
look like there's some other ways, and and one of
these that many people might find of interest is by
knocking back a couple of of drinks. Or at least
that's the word from a study that came out earlier
(17:03):
this year in Scientific Reports. Honestly, that kind of sounds
like a made up name for a dun over like this.
This was in Scientific Reports, So I should have a
drink a lot, that's right. But the researchers found that
drinking just two glasses of wine daily is enough to
net you a positive effect, which it works due to
the way the alcohol interacts with the brain. So apparently
(17:25):
the wine enhances the brain's ability to remove those damaging
toxins that build up in the brain, which of course
includes those TAO and beta amyloid proteins that we've been
talking about. The brain typically does this by pumping in
some cerebral fluid to flush away those troublesome plaques and tangles.
But there's something about alcohol that gets the old cerebral
(17:45):
fluid flowing more efficiently. And in case you're not a
wine drinker, there is some evidence that other forms of
alcohol work too. For instance, there was another study from
a couple of years ago that found that beer drinkers
tend to have fewer ammoloid build ups than non beer drinkers. Now,
as always, I do need to pause here and say
the key part here is moderation. Excessive alcohol consumption is
(18:07):
obviously not a good thing for anybody. Yeah, I mean,
it's really wild to lay out all the environmental factors
potentially connected with Alzheimer's, Like I saw this one report
in the Journal of Neuroscience about how even something like
sleeping on your side can help delay the development of
both Alzheimer's and Parkinson's. And apparently it goes back to
the fluid flush routine our brains used to clear out waste. Like,
(18:30):
it turns out the fluid flows most effectively when we're
asleep and on our sides. All right, so it sounds
like we've got the solution here. We just need to
do some Sudoku puzzles all day long. Line on our
side and then drink ourselves into a wine comas that
that's the solution here, Yeah, and pick up cantonese. I
think it's not the part of right, right, Okay, that's right.
I forgot, But I mean, you know it's it's there's
(18:52):
no surefire way to hold back Alzheimer's either, you know that.
That's the thing about all these environmental risks we're talking about,
like they can only suggest probable connections between things that
have already happened. Like I've even seen studies that link
drinking soda, both regular and diet, to the onset of Alzheimer's.
And and while there might be a correlation between getting
Alzheimer's and drinking soda, that doesn't mean that one necessarily
(19:14):
caused the other to happen. Well, that's a good point,
And I mean these kinds of lifestyle considerations can be
kind of reassuring for us to think about. But the
research I do find most exciting is this stuff aimed
at finding new detection methods for Alzheimer's. After all, it's
two thousand and eighteen, and it feels like we need
a better system than having to dissect these brains post mortem. Yeah,
(19:37):
I agree, and that's why I was excited when I
first found out that we actually do have tests that
can identify those gene mutations I mentioned earlier, the ones
that make a person more likely to develop Alzheimer's. But
as it turns out, many people who develop Alzheimer's don't
actually carry that genetic marker. Well, many who do never
end up exhibiting Alzhemer's symptoms. Well, so this is kind
of like the plaques and tangles then, right, like that,
(19:59):
they're reliable markers that maybe point the way to Alzheimer's,
except for all of these cases where for some reason
they don't, yeah, exactly, And and that means that even
genetic testing can't provide any real degree of certainty one
way or another. And that's what makes it all so confusing, Like,
even if you don't have the genetic markers, you could
still develop the disease. Well, thankfully, some researchers have begun
(20:22):
branching out from genetic and environmental factors and they're concentrating
on these so called biomarkers instead. Now, the idea here
is that the body exhibits tell tale biological signs of
Alzheimer's that we don't necessarily have to look at the
brain to find so that we can look for these
clues in all kinds of places that might be in
the blood or in the cerebro spinal fluid we mentioned earlier,
(20:45):
or even in the eyes of all places, And honestly,
that last one is probably my favorite because all it
involves is administering these fancy eye drops, and that's just
so much less obtrusive than digging around in somebody's brain. Yeah,
I mean that that obviously sounds way better there to me,
But walk me through what makes these eye drops so fancy. Well,
even though we have things like pets cans to help
(21:06):
us take a closer look at living brains, it can
still be incredibly tough to identify those beta em aloid
build ups that often point to Alzheimer's. And that's largely
because the betas are just one of many kinds of ammolloids,
and they're all kinds of hard to tell apart. Plus,
there are many different neurological disorders that are linked to
specific ammolloids, So if you can't tell which protein you're
(21:28):
looking at, then you really can't determine which disorder it's
pointing to. I see, So how did the eye drops
help with that? All right? Well, this is where things
get really cool. So you know how the eyes are
closely connected to the brain, right, Well, the connection is
so close that amyloids actually accumulate in our eyes too,
not just the brains. So the researchers are hoping that
(21:49):
by adding these fluorescent markers to eye drops, they'll be
able to light up the ammoloids in the eyes and
different colors, and of course each color would correspond to
a different ammoloid and bike stay chin from that to
the disorder it's associated with. So in theory, you could
have a doctor diagnosing a patient's condition just by looking
them in the eye. Isn't that incredible? Yeah, it really is.
(22:11):
And it actually reminds me of this other new Alzheimer's
tests I've read about. It's called the Opposite or the
University of Pennsylvania Smell Identification Test, and it's basically one
of those scratch and sniff cards with like forty different
odors on it, which is really clever because you know,
we've known for a while now that people with neurological diseases,
including Alzheimer's, often lose some or all of their sense
(22:33):
of smell. So if a patient nails the opposite, you
pretty much know that they're not going to have Alzheimer's,
at least for the next few years. And I know
there are plenty of other reasons why people lose their
ability to smell, So you know, it's not like it's
just this comprehensive test for Alzheimer's or anything. But as
Kate Horowitz from Mental Fauce puts it, the results are
instantaneous and at it's a far cheaper starting point than
(22:56):
other brain scans. Huh, well, that's that's true. But all well,
we've talked about ways to potentially delay the onset of Alzheimer's,
as well as some new ideas for how to detect
and even diagnose it earlier. So now why don't we
take a look at a few of them may maybe
more out of the box approaches to Alzheimer's treatment and
how they hope to make a difference in the lives
(23:17):
of those with Alzheimer's. That sounds great, but first let's
take another quick break. Okay, well, so what kinds of
(23:39):
unorthodox approaches to Alzheimer's treatments are you excited about? All right,
so I came across two rest examples that really stood
out to me, and they're pretty different because one highlights
the power of the individual in this ongoing fight, and
one showcases what a motivated community can give back to
those who are suffering from Alzheimer's. So I'll start with
the first one, which is this may a new app
(24:00):
and it's called Timeless and it's being developed by a
fourteen year old girl named Emma Yang. And yes, you
heard that right. Emma is indeed a teenage program prodigy.
According to an article in Fast Company, Emma code of
the app herself and the hope that it will one
day help her grandmother, who has Alzheimer's, to remember her
loved ones. I mean, first off, that is so inspiring
(24:23):
and also heartbreaking, but it also sounds like a really
great concept. So how does it work well. The idea
is to use facial recognition as a way to remind
the user who a certain person is and also what
their relationship is to them. So once the Timeless app
is loaded up with all of this information and Alzheimer's
patient can refer to it anytime they have trouble recognizing
(24:46):
someone's face, and all they have to do is take
a quick photo of the person, and the app will
pull up all of their information. So the hope is
that once a patient refers to the same entries enough times,
they'll start to better retain that information. And that's not
the only thing it does either, So Emma has also
programmed the app to provide appointment reminders and even help
(25:06):
users recognize when they might be repeating a task that
they've already completed. So, for instance, if a patient calls
a friend for a second time because they, you know,
forgot about the first call they made, the app will
notify them that this is the second call to that
number in that short period of time. So while this
isn't something that would be useful in the later stages
of Alzheimer's, it could be a way to help prolong
(25:28):
those family interactions in the meantime. I mean that that
is really clever. I'm guessing the app hasn't hit the
market though yet. Right now, m is still working on
securing all the funding that she needs to get it
out the door, but it sounds like the plan is
to release it within the next couple of years. Well,
I mean, I'm obviously rooting for her, but I'm curious, like,
what's the more community driven program that caught your eye.
(25:49):
So this one's part of a cultural program that was
started a couple of years ago by a handful of
museums that are in Wisconsin and Minnesota, and it's called
Spark and it works in partnership with Alzheimer's Association. Is
a way to help stimulate patients memories. So according to Smithsonian,
the program's main goal is to quote use artwork and
other sensory input to help stimulate long term memory retention
(26:13):
among patrons. And so some of these tours even have
the patients interact with sensory items along the way you
think about like scented candles or a piece of textured cloth,
and the ideas that all of this can help spark
their memories. So, for example, if a group of patients
was looking at a sculpture while a scented candle was burning,
and then you lit that same candle a few hours
(26:33):
later and ask the patients about the sculpture, the scent
might help them recall more about that piece and their
perceptions of it, and you know, they would have a
better memory of it than without that sensory input. I mean,
that's really awesome. So do you have any sense of
like how many museums offer programs like this, Well, so far,
I think there are fourteen of them that are part
(26:55):
of the Spark program and they hold art tours and
painting classes, as even dances, and these are all for
Alzheimer's patients and their caregivers. But these programs are actually
modeled after a similar initiative that was at MoMA and
that started a little over a decade ago. And because
of the success of these kinds of programs, you've got
museums all over the US that have started investing in
(27:17):
their own ways, and all of these are efforts to
help them, you know, those with memory laws re engage
with art. That is such a great idea. And and
since we're talking about ingenious, community driven Alzheimer's programs, I
do want to talk just a little bit about this
government funded nursing care company outside of Amsterdam that runs
what it refers to as a dementia village. So I'm
sure you've heard about this, but it's an entire model
(27:39):
town known as hoke Awake, and there are more than
a hundred fifty resident patients living together in groups there.
It opened in two thousand nine as a way to
combat the social isolation and lack of activity that people
with dementia often deal with, and instead of feeling cooped
up with nothing to do, patients are encouraged to carry
out everyday activities in this controlled environment. And it's built
(28:00):
like a functioning tiny town, so they can go grocery shopping,
they can visit the hair salon, catch a movie at
the theater, or even grab a cup of coffee at
the cafe. All of these storefronts are staffed by caretakers,
and they also populated the town and help look out
for patients safety. It's really incredible. Yeah, and I love
this concept and you're thinking about it. It gives these
(28:21):
Alzheimer's patients a chance to socialize more and and even
regain some of that independence that they had before. And
imagine it must have such a big impact on their
quality of life overall. It actually reminds me a lot
of that town in Belgium where there's like this seven
hundred year old tradition of residents taking in patients with
neurological disease or mental illnesses. So the towns people just
(28:44):
kind of adopt these patients. Into their families and look
after them like their own And it's that same kind
of all for one mentality that I get from that,
you know, that hoc Awake approach. Yeah. Plus this prop
town set up in general is just kind of awesome, right,
Like it's like Truman Show, but without any of that
exploitation aspect to it. What's the fun and that no,
(29:05):
but you're you're right well, And it's also cool to
see this immersive approach to dementia care catching on in
other places, like I read there's a similar facility in Ontario.
Now there's actually a daytime care center in San Diego
and it's set to open I think later this year,
and that one was partly inspired by hok Awake. So
at a daytime center, and I guessink the patients don't
(29:26):
actually live there full time. Yeah. So the project is
largely the brainchild of Scott Tardey, who's the CEO of
a nonprofit called Glenner Alzheimer's Family Care Centers, and his
idea was to use set design to craft this immersive
environment for Alzheimer's patients to visit and reminisce during the day.
And reminiscence is really the key word here, because the
(29:48):
unique aspect of this project is that it's patterned after
a clinical practice called reminiscence therapy. Now, this is when
facilitators use prompts like photographs and music to help patients
recall events and fee feelings from earlier in their life,
and it works really well. There's all kinds of studies
to show that this form of treatment actually helps boost
both cognitive function and quality of life. So the idea
(30:12):
here was that if you can build an entire town
designed to seem familiar, the effects of this kind of
therapy might be even greater. So I'm curious, how do
you make a place feel familiar to a whole bunch
of different people. Well, the nonprofit did something really smart here.
They designed the whole town, which is called Glenner Town
Square by the way, to look like it's from the
period between nineteen fifty three and nineteen sixty one. And
(30:35):
they did this because that's the period when most of
today's dementia patients were young adults. So, for example, if
a patient is in their early eighties and two thousand eighteen,
that means they were born in the mid nineteen thirties
and would have been you know, eighteen nineteen twenties, somewhere
around that in the mid fifties, right, So that's interesting,
But like why focus on when they were young adults
(30:56):
over when they were kids or adults or some other
period of their lives. Well, apparently the memories from the
person's twenties and thirties are the ones that stick around
the longest. It Scott tart To explained, quote graduation from
high school, college, first jobs, marriage, perhaps children, These are
the milestones typically in somebody's life. So that twenty year
(31:17):
period seems to be where memories are the strongest. M
I mean, it's really interesting, and I think it's curious
that like this example is more pleasant filled than Truman Show,
but it's it really is stunning to see how people
are thinking outside the box and coming up with new
approaches to deal with Alzheimer's. But you know that there's
one group of people affected by Alzheimer's that we haven't
(31:39):
talked much about today, and and that's the tens of
millions of people who watched their loved ones struggle with Alzheimer's.
And what I find so inspiring about the ordeal is
that despite all the pain, they go through while caring
for friends and family members, they remain eager to find
the disease in any way they can. Yeah, that's very true.
And actually I found this Wired article from last September
that talks about a new way everyday people are helping
(32:01):
researchers just get a little bit closer to that cure
for Alzheimer's. And this program is called Stall Catchers, and
it's actually a video game where players examine images of
mouse brains and they try to spot any clogged blood vessels,
which they call stalls in this case, and and those
could be obstructing blood flow in the brain. This kind
(32:21):
of reduced cerebral blood flow has been linked to Alzheimer's,
So if you can treat this, there's a chance that
memory loss could actually be reversed. And the method has
already proven effective and lab mice. But there's one important caveat,
and that's that all the drugs tested so far to
improve blood flow have also destroyed the mice's ability to
ward off infections, which is obviously a deal breaker for humans.
(32:46):
And so as a result of this, researchers continue to
test new drugs in search of one that will leave
patients immune systems intact. But here's the problem. You know,
every time they test the new drug, they then have
to check images of the mice brains for stall halls
in order to see if that medicine is or isn't working.
And since each new drug brings about thirty thousand images,
(33:07):
to sort through the results of each trial can take
up to a year just a process. Wow. So so
I'm guessing that's where the game comes in. Yeah, that's
exactly where it comes in. So the researchers have teamed
up with this nonprofit innovator called the Human Computation Institute,
and so together they've developed this online game to help
crowdsource the data that they need. Players will sift through
(33:29):
thousands of grainy, black and white slides of these mice brains,
and they're hunting for any sign of stalls, which show
up as these small black spots in the images. So far,
more than six thousand people have logged onto play Stall Catchers,
and that's helped speed up the researchers work tremendously. In fact,
when game activity is at its peak, the players effectively
(33:50):
complete a week's worth of research in a single hour.
So process that you know would otherwise take decades, might
just take a few years instead, which could really mean
all all the difference for patients currently dealing with Alzheimer's.
I mean that that really is incredible. So do we
have any info on who the user basis for Stallcatchers, like?
Is it mostly people whose friends and family have been
(34:11):
affected by Alzheimer's? Yeah, I mean that's really the heart
of the game's community, and and that, to me is
such a powerful reminder of why it's important to not
be discouraged when the latest promising treatment for Alzheimer's falls through.
And this is something Miranda Cats actually touches on in
her piece for Wired. She's describing how the friends and
family members of Alzheimer's patients have responded to stall Catchers,
(34:34):
and this is how she puts it, Frustrated by high
nonprofit overheads and the glacial pace of research, they've left
at an opportunity to take things into their own hands.
And though a true cure for Alzheimer's is still distant,
Stallcatchers has already proven an effective treatment for one of
the diseases most insidious symptoms, helplessness. Yeah, I mean that
(34:56):
that really is so important to keep in mind. You know,
according to the All Cemer's Association, more than of what
we know about the disease was only discovered in the
last twenty years. So while progress might seem slow when
you consider what we've known about Alzheimer's for over a century, now,
at least we're now at a point where researchers are
covering a massive amount of ground fairly quickly. And I
(35:17):
know it sounds cliche, but we really are closer to
a cure than ever before, even if that happy outcomes
still has many years left to go. Yeah, that's true.
And you know, in the meantime, you've got these ridiculously
smart people that will continue coming up with new and
clever ways to manage symptoms in Alzheimer's patients and to
keep hope alive in their loved ones. Yeah. So with
(35:37):
that in mind, what do you say we dive into
the fact off and check out a few more promising approaches.
All right, let's do it, h Okay, So I want
to talk about a couple of very different groups that
have made for very interesting studies. And the first is
(35:58):
in a village in the mountains of northwestern Colombia, and
it's called Antioquia, which happens to be home to the
world's largest concentration of Alzheimer's suffers, And to make matters
more difficult, they're primarily people dealing with early onset Alzheimer's. Now,
this is because of a gene that's been passed down
through the generations and has unfortunately stayed in the population
(36:19):
because of inbreeding, and sadly, what it often means is
that rather than children eventually taking care of their parents
as those parents age, the reverse often happens, where the
elderly population is having to care for their children in
their forties and fifties. Oh man, that's tragic. So in
our research for today's episode, I was reading about how
scientists have been able to study the gradual impact of
(36:42):
Alzheimer's on writers as they battled the disease. And one
of these was Iris Murdoch, who is this philosopher and
writer who is eventually unable to write because her demension
has just got so bad. But because she wrote twenty
six novels, researchers were able to look at her writing
over time and found that while the structure of her
novels pretty much stayed the same, in her later works,
the vocabulary was far more limited, and there was actually
(37:04):
a similar study downe on Agatha Christie's work and they
found a twenty decrease in her vocabulary later in her
writing career. In fact, you know, it's kind of strange,
but one of her last novels, Elephants Can Remember, actually
involves the writer dealing with memory issues. But you know,
the whole thing really is fascinating that if you have
this legacy of written work, you know, it's not just
(37:25):
literature departments but scientists who can actually analyze it for humanity. Yeah,
it's definitely interesting. They're they're taking a look at that.
So I mentioned earlier there was another group that also
made for very interesting studies. And the other one I
wanted to talk about is this multi decade study. It's
called the nun Study, and it's actually one of the
largest Alzheimer's studies ever conducted. There was a researcher from
(37:47):
the University of Minnesota named David Snowden that got the
study going in the mid nineteen eighties, and it was
with a group called the school Sisters of Notre Dame
who agreed not only to have these certain evaluations done
during their lives. It also to have their brain studied
after they passed away. Now, what makes this group so
helpful to study is that it's a relatively homogeneous group
(38:08):
that lives pretty similar lifestyles. So it's a good bit
more control than what you could do with with most
other groups. The study is actually still going, but they've
had some very interesting findings over the years, and including
the fact that researchers have been able to look at
autobiographical essays that these sisters wrote when they joined the sisterhood,
not on average that would have been in their early twenties,
(38:31):
and even from those essays, they are able to predict
those who are more likely to develop Alzheimer's. So those
who wrote the more complex essays were found to be
less likely to develop the disease. It's just it's just
wild to me that they could find predictors like that
so early in these women's lives. Oh man, that is fascinating.
So here's something I think about a lot, right there.
All these studies out there that tell us one week
(38:53):
that something is bad for us, and then the next
week it's good for us. And here's another one of
those studies, and it's about cell phone use. Well, I mean,
I understand that that it might not be as harmful
as we once feared, but how in the world could
this be a good thing. Yeah, so I'm not suggesting
anyone start increasing their cell phone use, but a study
out of South Florida did find the exposing mice to
(39:14):
microwave radiation from cell phones both seemed to protect them
from Alzheimer's and in some case even seemed to reverse
the effects. So, as one of the study leads, this
guy wants Sanchez Ramo said, quote, it's such dramatic and
counterintuitive effect. I joked that the animals must have been
mislabeled or that the power wasn't switched on. And you
know that this effect was there for both the mice
(39:35):
who were exposed to the radiation before they showed signs
of Alzheimer's and for those who were exposed after they
started showing signs. And again, you know, we're not recommending
anyone start using their phones more because of this interesting study.
It's just that it's fascinating to think that there's studies
that you don't expect the results to come out the
way they do. You know, I've actually got another one
(39:56):
like that where you never know if the effect of
something is going to be positive or negative. And this
one involves caffeine, and of course we bring the mice
in again for a study, and it's a study led
by researcher Gary Aaron Dash and his team found that
a group of mice who were bred to end up
with Alzheimer's, if one group was given regular water to
drink and the other was given water with caffeine infused
(40:18):
in it, those who had receive the caffeine actually had
a fifty percent decrease in their beta amyloid levels. No,
those were, of course those tangled proteins that we talked
about earlier, And the amount of caffeine was roughly the
equivalent of giving a person five cups of coffee and
a day. And while this was a promising finding that
perhaps caffeine could be introduced in some way to help
those who have already developed Alzheimer's, it's of course still early,
(40:42):
And as with the study you last mentioned, there's definitely
not a recommendation here that people go out and start
consuming lots of caffeine. So, you know, I do think
it's good to end on a couple of hopeful facts,
even if there's still a long way to go with
all these studies. And I actually say we should dedicate
today's trophy to the many brilliant researchers, Kara loved Ones
and millions of brave patients who remained determined to fight
(41:03):
this disease. I second that. So here's the continued progress
and the fight against Alzheimer's. Thanks so much for listening,
(41:25):
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