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Why this could be a 'turnaround decade' in the fight against Alzheimer's

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Researchers have identified a new blood test that could reveal signs of Alzheimer’s disease decades earlier than ever before.

The potential breakthrough is just the latest piece of positive news when it comes to identifying and treating dementia patients — including the recent approval of a long-awaited drug that slows the progression of early-stage Alzheimer’s disease.

On a recent episode of Village Media’s Closer Look podcast, we sat down with one of Canada’s leading experts on dementia: Dr. Howard Chertkow, a senior scientist at the Baycrest Academy for Research and Education.

He talked about why he thinks this could be a “turnaround decade” in the treatment, prevention and early diagnosis of Alzheimer’s disease.

Reach out to Frisco and Scott

SPEAKER_01

This is the first drug that is what we call disease modifying therapy. That means it's not just improving the symptoms. What we haven't had is a drug that actually can change the course of the disease.

SPEAKER_03

It's Sunday, August the 2nd, 2026. Welcome back to Closer Look. I'm Scott Sexmith. Frisco is away on assignment this week. You may have noticed some recent headlines about another potential breakthrough in the fight against Alzheimer's disease. Researchers have developed a new method through blood tests that could help identify early signs of the disease. The research paper is just the latest piece of positive news when it comes to identifying and treating patients suffering from dementia, including the recent approval of a long-awaited drug that slows the progression of early stage Alzheimer's disease. On a recent episode of our podcast, we sat down with one of Canada's leading experts on dementia, Dr. Howard Chertko, a senior scientist at the Baycrest Academy for Research and Education. He talked about why he strongly believes this could be a turnaround decade in the treatment, prevention, and early diagnosis of Alzheimer's disease and other types of dementia. Here now is that conversation. We're very pleased to be joined tonight by Dr. Howard Chertko, senior scientist at the Baycrest Academy for Research and Education, and one of Canada's top dementia experts. We've got a lot of timely things to talk about, Dr. Chertko. So welcome to the show. We appreciate your time tonight.

SPEAKER_01

Delighted to be here. Thanks for having me.

SPEAKER_03

All right, let's uh start with the uh big news of the week. Health Canada has approved a drug that is shown to slow the progression of Alzheimer's disease. Uh, known by its brand name, Lakembi, the drug targets the buildup of a certain type of plaque in the brain that is believed to be an underlying cause of Alzheimer's. Uh Doctor, can you tell us about this drug and what the new Health Canada approval will mean for patients across the country?

SPEAKER_01

Well, there's a lot to be said, and this is an important milestone. This is the the first drug, Lakembi, or the drug generic name is Lacanema. This is the first drug that is what we call disease-modifying therapy. That means it's not just improving the symptoms. We do have drugs that we've used for years that can calm a patient with Alzheimer's, uh, that can improve the memory to some extent for a few months and can make a person less agitated. So we're treating the symptoms. What we haven't had is a drug that actually can change the course of the disease. And this is really what we need because, as you know, Alzheimer's is a progressive, untreatable, hitherto untreatable, fatal condition. And Alzheimer's in its full expression with dementia or in this very mild uh prudromal phase is going to be affecting more than a million Canadians. So it's having a drug is hugely important. Having two drugs or 10 drugs would be even better. So what is the situation here? Well, for the past 10, 15 years, a good deal of effort has been directed at this bad protein amyloid, which we've known was in the brain of people with Alzheimer's disease since Dr. Alzheimer's first looked through a microscope in 1906. We've seen this amyloid. You don't see it in young people, you don't see it in normal people in their 20s, you see it in older people, and you almost you usually see it in people who have the diagnosis of Alzheimer's disease. Now, there are a few caveats here. And now, since we've been getting autopsies on people and big studies where we check people's memory, and when they die, they donate their brains. Big studies around the world have looked at this. We know you can get to be in your 90s and have a normal memory. And if you you die, they look in your brain, they do see some amyloid protein. So having the amyloid does not equal having Alzheimer's dementia. But most people who we see in the memory clinic, I work in a memory clinic, I'm a neurologist at Baygrass. When we see we make a diagnosis of Alzheimer's, usually their brains contain amyloid. Maybe in a quarter or a third of cases, they don't have amyloid, but usually there's amyloid. And so the effort has been to what happens if we get rid of the amyloid in the brain? And there have been tremendous billions of dollars put into developing methods to use antibodies to get into the blood, get into the brain, and remove either the precursors to amyloid, the amyloid precursor protein. And now finally, we have a number of drugs that are very effective in getting rid of amyloid. So what does that mean? Well, the hope was, and this is the hope 20, 30 years ago, that if we could get rid of the amyloid, the Alzheimer's would go away. People would go back to being normal, their memory would return to normal, they wouldn't get any worse. That does not appear to be the case. Nobody has been cured with these drugs. And uh the struggle has been many of the initial anti-amyloid drugs didn't make any difference clinically. They were they were a bus. If you would have looked at the literature 10 years ago, people were saying, well, maybe getting rid of amyloid doesn't do anything for for our patients with dementia. But now we have better medications, something called donanomab, and the the current one, Lacanimab, trade name Lakembi. They're the best we've had in clearing out almost all the amyloid from the brain. And what happens? What appears to happen is that overall it slows the progression of Alzheimer's disease by about 27% or 30% or 35%. Not in everybody. And there may be some people in there who are doing better than that, some people who are doing worse, but overall it's slowing the disease. And you know, that's giving people maybe an extra six months or 12 months of of mild dementia where they're having a good quality of life. So it's not negligible. Um, look, we've just finished the World Series, so I would say it's not a home run. It's more like uh hitting a single, it's getting on base. And we know, you know, if you get on base and then you have another single and another single, before you know it, you've got a uh a uh real treatment or a cure. So this is hopefully the first step and an important first step, but it alone is not going to be a cure for Alzheimer's disease.

SPEAKER_02

That's a great analogy. Thank you for that, Doctor. It obviously makes us help helps us all understand a little bit better. Is it critical for this drug to be effective to find to be in the early stages of Alzheimer's in order for this particular drug to be effective?

SPEAKER_01

We don't actually know that. It was tested on people in the early stages. Why? Because the odds are, you know, what's the goal here? We don't want to take someone who has severe dementia who's already in a long-term care institution and slow their progression, whatever we really achieved. The hope is to take people who are just in the very early stages and give them meaningful extension of their thinking and their active life. So if the goal was to test, and they tested people with either mild dementia or or what we call mild cognitive impairment. No, dementia is a clinical term. It means you've got memory loss and problems with judgment and planning sufficient to interfere with your day-to-day activities, whether that's handling your finances or working or driving or planning your life. So that's the definition of dementia. There are people we see who have memory loss, who are still doing everything. Uh, they don't have functional impairment, and we call that mild cognitive impairment. So these are the people who are targeted, people with mild dementia, mild cognitive impairment. Now, would the drug have worked in more severe patients? Um, we don't really know. But uh clearly the goal was to go after the disease in its mildest form. Um, there are actually a lot of things we do know about the drug, uh, and other things we don't know. What we do know is that overall it slows progression. There are uh there are things you have to do before you use a drug. For example, you have to make sure there is amyloid in the brain, because as I've said, not everyone with dementia has amyloid in their brain. So, how do we determine that? We don't take out a piece of brain, but we look with imaging of the brain, with PET scanning that can show the amyloid. We routinely take out spinal fluid and look for the amyloid level in the spinal fluid. And now there are ways to look in blood plasma and look at the levels of either the amyloid or other associated proteins that tell us in someone where we have a high clinical suspicion they have Alzheimer's, say almost 99% sure this person has amyloid in their brain. So that's the first step. Then we have to make sure that they're not at risk of having side effects. So it has been shown that in these studies, that some people, maybe one out of five, develops what are called amyloid-reated amyloid-related imaging abnormalities. That's things that swelling in the brain or very tiny bleeding hemorrhages in the brain. As you pull out the amyloid, it has this effect on the brain. It causes almost like a little bit of inflammation in the brain area. Now, usually those are without side effects and people aren't even aware of them. But it's only by doing MRI scans frequently we see this person's having some swelling in the brain. And what do we do in the trials? What we do, we hold off giving the medication for a month or two months until the swelling goes away. So you have to check with MRI scans. So you have to make sure before you start the medication that they don't have already have little tiny bleeds. You have to track the as you're giving the medication with MRI scans. And you have to check on the person's genes because there are certain genes that put you at higher risk of having swelling or bleeding when you start the medication. So there's a whole set of tests that have to be done by your doctor, usually by a specialist, before you're told in the States or around the world that we're going to offer you to go on this medication.

SPEAKER_03

Doctor, you've said uh the next 10 years could be a turnaround decade uh for dementia research in terms of the way we deliver treatment, uh prevention, and the ability to diagnose earlier. What makes you so confident that we're at that turning point now?

SPEAKER_01

Aaron Powell When, you know, I don't have a crystal ball and uh I but I there's a lot of room for optimism. First of all, as I've talked about the diagnostic tests, uh these these have just exploded over the past 20 years. The our ability to diagnose has far outstripped our ability to treat. So now that we have actual blood tests, this will make the diagnosis, precision diagnosis accessible in a way it's never been possible before. Now, it's not easy to get a PET scan in downtown Toronto. Try going to Northern Ontario and getting a PET scanner of rural areas, is almost impossible. Blood tests will make diagnosis and accurate diagnosis much easier. And we're going to need this sort of precision in the diagnosis if we're going to get these drugs to people who will benefit the most. So the explosion of diagnostic tests, not only for amyloid, but for the other protein, tau protein, which is the other major thing we see in the brains of people with Alzheimer's. In addition to the diagnostic test, we have the new disease-modifying medications. So Lakembi, Lacanimab is the first, but there's going to be other anti-amyloid drugs, and a lot of work going on, drugs to block the tau protein, which may prove to be as important or even more important than amyloid, drugs to block certain aspects of inflammation we see in the brain, and totally different mechanisms. There are small studies which have been successful, showing that drugs that we have stimulate the sigma 1 uh enzyme totally unrelated to amyloid and tau, that may have as much benefit as blocking these other proteins. So it may be that there are subgroups of Alzheimer's where one patient, the disease is due to the Tau protein, another patient is due to the amyloid. We may need to personalize our treatment. We may need to use combinations of treatment, but all of this is going to become going to be worked out in the next decade. So I my prediction is that 10 years from now we'll have sort of an armamentarium of drugs and be able to target the people who are going to benefit from drug A or drug B or drug A plus B. And this is so I think we're going to see real advances and we're going to see advances in prevention. We now understand risk factors for dementia in a way we simply didn't 20 years ago. We're learning more, and there's some shocking and somewhat scary things becoming evident in the past few years. But we know that lifestyle interventions do make a difference at any age. And we believe that there are probably medications you can add to the lifestyle interventions that will lower your risk, mitigate your risk as an individual of getting dementia. So for better prevention, we're going to see within 10 years, better treatment and really precision diagnosis. So together, I think this is going to be the transformational decade that we're going to have.

SPEAKER_02

It is fascinating, Doctor, because obviously the numbers are climbing, right? According to the Alzheimer's Society of Canada, I believe there are close to 800,000 people in the country right now living with dementia, and that number is expected to climb, I believe, to close to 1 million by 2030. Obviously, all these advances we're making are hugely important. But why are the numbers climbing, I guess, Doctor? And is the is the health care system and the society in general ready for that kind of growth?

SPEAKER_01

Well, uh uh absolutely not. And um the numbers you have are quite correct. There are going to be lots of people with dementia. And if you include the people with prodromal Alzheimer's who don't yet meet criteria for dementia, it's going to be over a million very shortly. Um look, our healthcare system uh could do with a lot better planning. You would think that the governments are planning carefully on how to deal with the chronic diseases of old people, but they're really not. And the more the fact that people don't have family doctors, we've been relying so much on emergencies for what the family doctors should be doing. And you don't the last thing you want is for older patients with chronic diseases to be ending up in emergency. Um, it's been calculated that with respect to dementia, we have fewer specialists looking after patients with dementia in Canada per capita than any other G7 country. We have fewer MRI scans, and they're used much more than in other countries. We're short of MRIs, we're short of diagnostic equipment, we're short of personnel, we're short of people, and the system is not geared to look after older people and uh uh uh pay a fee for service system. You know, a family doctor doesn't like having an older patient with multiple chronic illnesses because they take a lot of time. And so we haven't developed the the nurse practitioners and the clinics, the family practice clinics. There is a network in Canada, but in some areas of Canada, like Quebec, they're really pushing development of family practice memory specialists. In other parts of the country, they haven't even started thinking about it. So we're not in good shape for dealing with this tsunami of dementia, which is really coming. And of course, Canada is province by province. So uh what's being planned in one province may be totally different if you go to a different province. And this uh this does reflect another shortcoming of our medical system, that we haven't done the proper planning to plan how to care for people. And maybe now that there are treatments, that's going to kick start pressure on the government to really look at the big picture and get organized.

SPEAKER_03

Uh Doctor, uh, you mentioned uh lifestyle changes a moment ago, and I want to follow up on that. You've noted that up to half of dementia cases uh could be prevented through lifestyle choices. Which ones have the strongest evidence behind them and uh which one uh might surprise people?

SPEAKER_01

Okay. So the the strongest evidence are for obvious ones. We know that Alzheimer's disease, we talk about the proteins being laid down in the brain, but a lot of the dementia is related to vascular, to blood flow. And the the things that people do that are good for their heart is also good are also good for their brain. So that means treating high blood pressure, treating diabetes, cholesterol, no smoking, those things that you can do for your vascular health. Now, you'd think this is old hat. You've heard about this for years, but you know, if you go and look at patients with high blood pressure over age 65, only about one out of four have proper control of their blood pressure. That means three out of four, they either don't have a doctor or they're not taking their medications or they're not being followed properly. So we could do a lot better with the areas where we have lots of medications. In addition to treating those known illnesses, exercise over and over again, exercise is the most robust thing that people can do. The recommendations, 150 minutes a week of robust exercise. Those are really good recommendations, but many people aren't following them.

SPEAKER_02

And uh so uh I see you looking at us, Doctor, with that look. I can tell you're looking at us when you say that. You might as well just point fingers, Doc.

SPEAKER_01

Not pointing any fingers. You know, we have uh at the Baycrest, we've started the Kimmel Family Center for Brain Health, a dementia prevention center where we do assessments and then we get people into programs and we look at when people's risk factors when they come in the door. And these are people at high risk, they have a family history or they have very mild memory changes. And we look, for example, at their diet, because we now know what is a good diet for the brain. And about 0% of our people are on the real good diet for their brain. Um, and more and more, part of that's education, uh, and part of that's cultural. You know, the Mediterranean diet with less red meat, more green vegetables, olive oil, fish, uh, lower fats, no desserts. Okay, we know about those, but it's hard for people to move towards these healthier diets, although that is happening. So, diet, exercise, we know that that being overweight is a big driver of what we know called inflammation, sort of very low-grade inflammation in the blood, largely being driven by obesity. So um obesity is a factor, not just because it causes diabetes, but it causes inflammation. So these are are robust things in people's lifestyle they can do. But there are other things that would be surprised some people. For example, flossing your teeth. People who floss their teeth at least once a day have a lower rate of getting Alzheimer's and other dementias.

SPEAKER_03

And what's what's the science behind that, Doctor?

SPEAKER_01

Well, uh, you know, it's not only that your grandmother was right when she told you. The science is that uh in our gums, there's what we call a biofilm. And it takes about 24 hours to accumulate, and it contains certain bacteria, something called P. gingivalis, which is which is uh uh um P. gingivalis is uh bacteria, the toxins or the bacterium itself gets into the brain and it's toxic. By flossing once a day, you get rid of the biofilm, you cut down the P. gingivalis, you get rid of the toxins. So it's a there's actual science behind flossing, which we didn't really know about this 10 years ago. Um, there are social factors, and don't ask me to explain the why, but the associations between people who are lonely, who don't have friends, who don't have a social network, who people who say they don't really have a purpose in life have a much higher rate of going on and getting dementia. Um is so, you know, how do you give people a purpose in life? Well, we're very big on volunteerism in getting older people out of their homes and volunteering to help other people. And uh we see dramatic changes in how people view their lives and their sense of meaning, and this impacts on the brain. Depression is and stress are bad for the brain. For men, being married in midlife is very good for preserving your brain health. For women, it doesn't seem to help them at all. That makes sense, and maybe that's because men. Who are married live a better lifestyle, or maybe it's the social factors, it's rather complicated. So there's social factors, cognitive stimulation. I'm sure you've heard about uh uh brain plasticity, learning another language, taking classes, stimulating your brain, doing the sudoku or crossword puzzles, all these things have been shown to be beneficial uh as opposed to people who retire, sit on the couch, and watch uh bad movies for the rest of their life. So it's quite a list of lifestyle interventions and things that people can do at any age. The one thing I should add before I forget is head injuries. Head injuries are bad. Um, we're very much in favor of teenagers wearing helmets when they're biking, and we're very much against contact sports like boxing, which are causing brain damage every time you knock someone out. So protecting your brain from trauma and head injuries is also in the long term an important thing to do.

SPEAKER_03

Uh, Doctor, we did a uh recent show on uh warning labels on alcohol as it relates to the uh possibility and linked to cancer. Uh what do we know about that uh where Alzheimer's is concerned? What do we know?

SPEAKER_01

Well, you know, the the this has gone up and down. Certainly, alcohol is a toxin to the brain. If you drink enough, you get brain shrinkage. This was shown by Peter Carlin at University of Toronto many years ago. You get brain shrinkage, you stop drinking a lot of alcohol, your brain gets back to its normal size. And we know that alcohol as a brain toxin, alcoholic dementia has been known for many years. There was a period over the past two decades when the argument was made that antioxidants are very good for preventing dementia. And one of the strongest antioxidants is actually in grapeskin. It's called resveratrol. And there was one study that showed that people who had at least half a glass of wine a day, uh, which gives you antioxidants, that would actually lower the risk of dementia. Uh, that study was funded by the Bordeaux manufacturers of France. So that's a little suspect. But but we were thinking that that red wine a little bit as a source of antioxidants. But now it seems to be that the the bulk of evidence has moved more and more to saying there's no safe level of alcohol for other conditions. So I'm no longer encouraging people to drink that half glass of wine. Get your antioxidants in orange juice or with other things in your diet. Um, and uh look, the sadly, the the days when we could say there was a level at which alcohol was safe, I think those days are are going away.

SPEAKER_02

I don't want to say this is a depressing conversation, Doctor, because it's not. It's very informative. Um, but that's a little depressing. Not even a little bit of wine with dinner. That's tough. Um we know you're super busy, so just a couple more questions, Doctor. I have read lately or have seen news reports about this uh dementia simulation that someone has created, research has created where it's actually like an outfit or a virtual reality if you can see what it's like to be someone with dementia. Have you have you seen that? Or uh well, what's the purpose of that?

SPEAKER_01

Well, I know this has been developed at CABI, a Center for Aging Brain Health and Innovation, which is based here at Baycrest, has looked into certain certain suits that can simulate dementia. I know uh uh uh uh Dr. Suzuki on the nature of things was wearing one in one program we did together. Um I think this is just a device to help people understand what it's like if you can't see well and if you can't hear well. And by the way, hearing loss is another factor in dementia. We know that people who have hearing loss who do not get hearing aids have a higher risk of getting dementia. And so uh loss of hearing in these sous loss of vision, and uh, but other than that, I'm not sure that there is a little bit of helping people to understand what it's like to have dementia, which is which is useful, but I'm not, you know, I'm not sure how that helps our patients really.

SPEAKER_03

Uh Doctor, I know you're tight for time. Uh anything that we didn't uh cover tonight uh that we should have, maybe biggest advice for people in preventing dementia?

SPEAKER_01

Well, I think that um people are excited on the advent of disease modifying medications. I think we're the fact that Health Canada has approved Lacanimab is important, but it will still be at least a year, I would think, until the committees involved uh hammer out a price, hammer out national approval, and things get onto provincial formularies. And then the the question is going to be uh, is this uh uh the the best investment of public dollars? Because it's expensive therapy. Um and I would argue that if we can get these medications to people who really benefit, it's going to be worth it. The problem is that at this point, we don't have all the facts that we need as physicians. For example, there is some evidence that men respond more effectively than women, um, that people from different backgrounds, born grown up in the United States and Canada, do better than people from Europe. We don't know anything about non-white uh people. And the trouble with disease modifying therapies, you have to understand if I'm treating someone with a migraine, I say, write a prescription, I say, here's your migraine medication, come back in a month and tell me if it worked. And they come back and say, My migraine's gone, or they say my migraine's not gone, and you can adjust the medication. With these therapies, disease modifying therapies, I won't know if it's working and the patient won't know if it's working. We're only going on trust of the literature and trust of the studies that have been done. So we have to put a higher bar, we have to put pressure on the pharmaceutical industry to give us all the information so we as physicians can help our patients the best. We want these expensive medications available for the people who are going to benefit, and we have to figure out how to assess their benefit and who to target for these medications in the future. That has to be where the, and this is where government pressure and working with the academic uh experts is going to be very important. Um, and I'm excited about the what is going to come. But this is going to be an era where it can't be a black box as it usually is in Health Canada. There has to be dialogue between the the researchers, the physicians, and government to do what's best for our patients.

SPEAKER_03

All right, good stuff. There's Dr. Howard Chertko, senior scientist at the Baycrest Academy for Research and Education. Uh, Doctor, very informative. We appreciate your time tonight.

SPEAKER_01

Thank you very for having me.

SPEAKER_03

Our thanks again to Dr. Chertko for joining us today. That's our show for this week. As always, we appreciate your time each and every week. Be sure to follow us on our social channels. Subscribe and watch back episodes at closerlookpodcast.ca and reach out anytime at closerlook at villagemedia.ca. Today's show is always produced by Zach Trenzo, and for everyone who makes Closer Look possible each and every week. Thanks for watching. I'm Scott Sexmith. Enjoy the rest of your weekend. We'll see you next time, right here on Closer Look.

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