Transcript
Elan Eisen: Today on the Health Insider, we’re joined by Doctor Howard Chertkow who is one of Canada’s leading neurologists, Scientific Director at Baycrest’s Kimel Family Centre for Brain Health & Wellness. Welcome, Doctor Chertkow, thank you very much for being here. This topic today is near and dear to my heart.
My mother suffers from Alzheimer’s and is in assisted living facility. And of course, this subject is of great interest because of my mother also because I know that genetically at risk and we’ll get to that, but let’s start with the basics. What do we now understand to be the main causes of Alzheimer’s and other forms of dementia?
Dr. Howard Chertkow: Well, that sounds like a simple question but it’s actually a very complicated question because dementia – well, what is dementia? Dementia is changes in thinking and memory and your higher brain processes of handling your life and judging and planning your life that usually occur as people get older, but we now understand are not normal in the brain.
Now these changes, it’s like a family of illnesses, It’s not one disease. Alzheimer’s disease is the leading cause of dementia, which is a clinical umbrella term. And there are other different diseases, diseases defined by looking in the brain, looking at the chemistry, looking under the microscope. So it’s a family of illnesses.
EE: So what causes dementia?
Dr. Howard Chertkow: Well, the simple answer is there’s a set of risk factors and the, the greatest risk factor is aging. 10,000 years ago people lived to be 38 and now they’re living to be 78 on average, and our bodies were not really well designed to get this old. That’s the basic genetic fact.
And so things start to break down. Your eyes get cataracts or hearing gets lost, your bones start to degenerate, and the brain starts to lose its cells. But more than that, we see abnormal proteins in the brain that don’t occur in young people. And these proteins are associated with loss of memory.
Are the proteins the cause? Are they a side effect? Is it loss of the brain cells? Is it a combination of things and problems with blood flow? There may be more one mechanism resulting in dementia and even something which is sort of coherent like Alzheimer’s disease, which is a diagnosis based on seeing certain brain changes. It’s more to do with oxidative stress, one group where it has to do with amyloid being laid down and another protein, Tau.
So it may not be that it may look like one thing, but actually multiple causes or multiple subgroups. The basic answer is that in Alzheimer’s disease, it’s about half genetic and half environmental. So, we are born with genes we inherit from our parents. There are some genes that have no effect on the brain. There are other genes that make your brain more resistant to sort of the trials and tribulations of lifelong aging. And there are other genes that make you more susceptible to these bad effects on aging. And these are called risk genes.
Very rarely can we say “this gene causes Alzheimer’s disease”. You know, everyone who’s got this gene will get Alzheimer’s disease. This is maybe one out of 20 cases have we call this familial Alzheimer’s disease. Families where half for or even more of the children develop Alzheimer’s disease. But in most cases, the genes, the things you’re given by your parents are just one part of the picture. This makes it very complicated because we see people in our memory clinic who develop Alzheimer’s disease and their family members say no one’s ever had this in the family. No one’s ever had this and we have to think it’s something in the environment and we can come back to what those things are in a minute.
And there are other families where they say, well, everyone seems or most people in the family get Alzheimer’s or dementia when they get over 80. And this is just expected. So there’s genes, some families are bad genes. Some cases it seems to be much more environmental.
EE: And yet I think it’s you that has been quoted as saying that the the risk for Alzheimer’s can actually be reduced by 50%.
Dr. Howard Chertkow: Explain that amidst this myriad of possibilities, when you look at the population, you can do statistics and say what percentage of Alzheimer’s disease or dementia cases – actually usually dementia – what percentage are attributable to things like smoking or things like high blood pressure or things like obesity.
This is a field called epidemiology. They look at risk factors in a population and it turns out there are many things which have to do with bad blood flow. Things that are bad for your heart are also bad for your brain. So, a chunk of the risk is related to high blood pressure. High blood pressure, smoking, high cholesterol, diabetes, obesity, all these things that are bad for your heart are also bad for your brain.
And that underlies a real truth. We’ve learned with Alzheimer’s diseases that blood flow and things that impair blood flow cause hardening of the arteries; things that cause strokes and heart attacks also cause dementia. And so, and these are all things that we know how to treat. We know how to treat blood pressure, although only about one out of four people with high blood pressure over age 65 are being adequately treated. The easiest chunk of the problem to deal with is related to what we already know, high blood pressure, diabetes and so on.
But it also appears that inactivity, lack of exercise, poor diet, things in your lifestyle or mine can be mitigated. And those also contribute to the risk of getting dementia. So if you add up all these things that could be lifestyle changes, turns out you could probably reduce in theory, and I emphasize in theory – if you corrected all – you could probably reduce about half the cases of dementia.
It’s important to stress that this is theoretical because look, we’ve known how to treat high blood pressure for 50 years so there shouldn’t be anyone wandering around with high blood pressure. But you may have noticed in Canada, not everyone has a doctor, not everyone is prescribed the right medications. Not everyone takes their medication.
We all know that exercise is good. What percentage of people in the population are doing exercise? So, there’s a gap between what we could be doing to mitigate or prevent dementia and dementia and bad aging of the brain. It’s a gap between what we know could be done and what is being done.
Part of our role as physicians and as a population and in public health is to try to close that gap, as we’ve done in smoking. The number of Canadians smoking now is far less than 50 years ago. So, it’s a public health intervention.
And then there are other things that people aren’t aware of. For example, good sleep. Sleeping less than six hours a night increases your risk of getting dementia and Alzheimer’s disease. Because we now know that there are toxins in everybody’s brain which are cleared out during sleep. My grandmother always sleep is important, sleep is magical. Turns out she’s right and by sleeping you’re cleaning the toxins in your brain. I’ve added an hour to my sleep and seven or eight hours gives you the time to clear out the toxins.
People who floss their teeth once a day clear out certain toxic bacteria in the gums. Again, everything your grandmother told you to do. Floss your teeth, brush your teeth, look after your mouth. Turns out you’re getting rid of toxic bacteria that somehow are increasing the risk of Alzheimer’s disease. And we’ve shown this in Canada; we’ve shown this in other countries.
There are risk factors in the environment. The leading one, of course, is always exercise; you should be getting 150 minutes a week of vigorous exercise. Not everyone is doing that, and everyone should be because clearly this is a very robust way to protect your brain.
People are hearing about the Mediterranean diet, the modern diet, eating less red meat, eating more green vegetables, and it looks like people who follow these diets lower their risk of getting dementia and Alzheimer’s disease.
So, there’s a lot that people can do – you can’t affect your genes, but you can affect your environmental risk factors. I suppose the problem is that the list, the list is incomplete. This is why we have meetings every year, researchers finding new risk factors that we didn’t know about.
For example, this year there was research in New Mexico that found that people dying with Alzheimer’s disease had 10 times the level of microplastics in their body and their brain as other people. Is that causing their Alzheimer’s or contributing to it? We don’t even know.
But it’s sort of a shocking discovery, and we’re finding it now because they didn’t have the techniques to find these nanoplastics 20 years ago. So, it’s becoming more evident that pollutants and plastics, and every time you heat something up in the microwave in a plastic dish, microplastics get released into your food. So we’re going to have to rethink our exposure to plastic.
In Mexico City, where it’s quite a polluted city, they’re finding the changes of Alzheimer’s disease and the brains of people in their 30s and 40s who die in traffic accidents. Their brains are looked at and it looks like they look like the brains of 80-year-olds with Tau protein and amyloid protein. So there’s lots of evidence accumulating that if you live close to a major highway, your risk is increased.
If you live in an area in England which has more trees and more parks, your risk of Alzheimer’s goes down South. Pollution, diet, exercise, all these things that that you can do in your life or or can try to change. There are many things people can do to lower their risk.
EE: So interesting. And then there’s the familial, as you said, the Alzheimer’s gene. And I can’t tell you how many people have told me. Are you going to get tested for that Appo 4 gene? And then I hear from somebody that, well, what are you going to do with that knowledge once you have it? So what are your thoughts about that? Can you explain what this gene is exactly?
Dr. Chertkow: So, genes you inherit as I’ve said, and one of the genes which is maybe the strongest risk factor is called apolipoprotein E type 4. You get one contributor from your mother, one from your father, so people have an E4 or an E3 or an E2. If you have an E2 from each parent, you’re actually protected to some degree from getting Alzheimer’s. If you get an E4 from each parent, it increases your risk. It has something to do with what this protein does is carry fats in the bloodstream and probably plays a role in the synapses and communication in the grain. But somehow this E 4 gene, if you have it, it increases your risk.
Now, what’s important to say is that It’s not the only gene. We need a sort of app where you people put in their genes and then they put in how much they exercise and what their diet is and how many microplastics they have in their body and how much pollution they’re exposed to. And then you’d have sort of an algorithm. We, we don’t know enough to do that yet, but we now know it’s not just one gene for Alzheimer’s. There are 84 risk genes, and each can contribute a little bit of risk.
In the research lab, we can take a small sample of blood, and we can run all of these genes and print out what we call a polygenic hazard score for each individual to tell them if they are at high risk genetically or medium risk.
We have a dementia prevention center at Baycrest called the Kimmel Family Center for Brain Health. I mean you have to realize that most of the people entering the center have some reason to worry about having Alzheimer’s or dementia in their family or the someone early signs or yeah. Only about 10% of the people who come in our door scores high genetic risk because you might have the APOE4, but you might have other genes that that protect you.
There’s a balance in all of these, these 84 genes.
EE: So what does the APOE4 gene do?
Dr. Chertkow: Well, it probably makes your brain more susceptible to damage from brain trauma or other sorts of brain insults have to do with what’s called oxidative stress. You probably heard about free radicals and how people take vitamin C and drink orange juice to protect from free radicals in the body. Vitamin C protects the body from oxidative stress, which we’re getting from the environment.
EE: So APOE4 makes you less able to tolerate oxidative stress.
Dr. Chertkow: If you want a piece of advice, if you have 2 copies of an APOE4 gene, you probably shouldn’t play football because people who play football are getting knocked on the head and getting trauma to their brain. Their brain is probably less able to withstand injuries than someone else and they probably shouldn’t play contact sports. We do, however, know that there are people who have APOE4 gene – even one or two copies – who live up to age 95 and they don’t have Alzheimer’s disease. And we know that there are people without the E4 gene who do get Alzheimer’s.
EE: There’s something I’ve often wondered: What is the difference between correlation and, you know, when something exists in an Alzheimer’s patient, how do you know that it isn’t just a correlation? Those who have Alzheimer’s or a lot of them also have this as opposed to causal where, where does one end and then the next begin?
Dr. Chertkow: Yeah, that’s a billion-dollar question, because when you see two things that go together, you don’t know if one is causing the other or they’re both being caused by something else. They’re an item. And that’s why the only way to the only, the main way to prove causality is you do what’s called a randomized trial where you control, for example, you give a drug or you, and we see a lot of associations. For example, we see association, people with Alzheimer’s disease have amyloid plaque, this amyloid protein in their brain when we look in the brain. So, is that the cause of Alzheimer’s disease or is that a product of the brain trying to fight against Alzheimer’s disease?
Scientists have been arguing about this for 30 or 40 years and the question still isn’t answered. It was hoped that, and certainly it is a billion-dollar question because the pharmaceutical industry has spent billions of dollars developing anti amyloid drugs better and better in the past 20 years. Antibodies and immune, immune factors that you inject in someone’s vein, they hook onto the amyloid and get rid of it from the brain. The hope was that this would stop Alzheimer’s disease or reverse it or return people to normal if amyloid was indeed the cause. Well, even with the best anti amyloid drugs – two have been released in the United States and are available to people with Alzheimer’s – they don’t reverse the disease or even stop it however, they slow the progression by about 25 to 30%.
So, what does that prove? Well, it’s not nothing. And for some patients that is meaningful slowing of the disease. But it, it’s not the home run that we’d hoped for, to get rid of the bad protein and people will be cured.
EE: OK, interesting, very interesting. One of the things that you haven’t made mention of. And I’m wondering what your opinion is. You know, a while back there was a movie on Netflix, I think was called Alive Inside. It talked about the impact of music on, on patients with dementia and how these patients came alive. And sure enough, I saw this movie and I recorded all this music from my mother’s childhood. I played it for her. And I found that when I first saw her, she’s almost in a catatonic state and playing the music, it slowly brought her to a much more conscious, interactive state where she was laughing and singing along and I was able to engage with her whereas I couldn’t otherwise. It wasn’t sustaining, but for those moments that I was with her, it really made a difference for me anyway, and seemingly for her. What, do we know about music and dementia?
Dr. Chertkow: Well, you know, music is a fascinating area because music engages different circuits than just talking and just asking questions. And it connects with emotions. There are Parkinson’s patients with severe Parkinson’s who, who can barely move, and you put on a song they like, they’ll get up and dance. And somehow music can bypass, maybe because of the emotional impact or maybe because it’s old memories, but sometimes you see remarkable, you know, we have people who can’t talk, and you put on a song and they’ll sing to the song. So, it’s certainly always worth using art and music to try and connect with people with any form of dementia. And that’s a great story from your mother.
We do see that it doesn’t, as you say, cure the disease, but people have a lot of reserves. You’re tapping into their cognitive reserve and, and residual memories and residual brain function in a unique way. This is why, for example, if you have a relative with severe Alzheimer’s disease, the thing to do is not try and talk about the weather or current politics. You go with books of pictures from long ago because the old memories are much more likely to remain and people will get excited and talk about things from their childhood and years ago when they can’t tell you anything they did earlier in the day. So, you’ve always got to tap into residual abilities.
EE: OK, so where’s the hope? What, what excites you the most these days in terms of research?
Dr. Chertkow: Well, I think that this is the decade we’re really going to make advances in prevention for a number of reasons. We now know how to find people in the very earliest stages who have changes in their brain on imaging and blood biomarkers even when they have very mild memory loss or even no memory loss. And we know who’s at risk. We can find these people, and we now know, lifestyle changes, education, but also, there are about two dozen medications which can probably slow the progression.
I believe we can figure out a combination of medications, which are feasible, not expensive enough to break the bank and non-toxic, find people at risk, get them the medications, get them to do the lifestyle interventions. I believe we could probably prevent more than half of the cases of dementia there.
There are so many possible intriguing drugs. Some are currently in clinical trials, some I’m sure you’ve heard about. They’re even looking at the key trials on Ozempic and things like Viagra and Cialis and other PD5 inhibitors. These are medications that are available for other reasons, and it appears that people who use these medications have about 50% lower risk of getting Alzheimer’s disease.
There are medications already available that probably make a difference. Thing is toxicity in price and how they work together, so the trials have to be done properly. But there are things out there, some are being tried, and some are just coming down the pipe that I think are really going to make a difference for prevention.
As far as treating people who have early Alzheimer’s, I think that’s coming. But the problem is we’re up till now we’ve been treating it as a one size fits all, an anti-amyloid drug for everybody. Well, you know, it worked, probably worked in some people and not others. So we have to move to what’s called precision medicine where we figure out for each individual what is the mechanism causing their brain injury. And then that’s what we target.
We have to start viewing Alzheimer’s disease and dementia as multiple subgroups and then target the therapy for the individual person. Those are the 2 advances and approaches that excite me. I think we’re going to see some serious prevention and treatment developments over the next few years. And I think it’s AI. Tell the young neurologists and young geriatricians you’re lucky because I’ve had in my career for you know how many years, waiting for the effective treatments for dementia.
Alzheimer’s remains the only one out of the top 10 diseases of aging, the only one for which we don’t really have an effective treatment to stop it, so I think the next generation of doctors are going to be the ones who are able to give those medications and the people developing memory loss now may be the ones that benefit. I think it’s very hopeful – medicine has a lot to offer in the coming years for dementia. I think we’re going to have much greater impact in the future than we’ve had up till now.
EE: It’s very encouraging. And on that note, I think we’ll, we’ll wrap. So, thank you very much. It was fascinating. I learned a lot and really appreciate it, and I wish you and your colleagues the best of luck and success in discovering a cure for Alzheimer’s. Thank you so much, Doctor Chertkow, for joining us.
Dr. Chertkow: You’re very welcome, happy to be here. Thanks for having me.
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