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