Full Show Transcript
Ben Fuchs (00:00):
All right. I’m looking forward to speaking to our guest today. We’ve been speaking about Parkinson’s disease now for about a week or so, and talking about dopamine and talking about tyrosine. My guest is a brain disease researcher, Dr. Russell Lebovitz, and he specializes in various brain illnesses, including Lewy Body Dementia and Alzheimer’s disease, as well as Parkinson’s disease. We’re going to talk about the seven early warning signs for Parkinson’s disease. Please welcome to The Bright Side, Dr. Russell Lebovitz. Hey, doc.
Dr. Russell Lebovitz (00:28):
Hey, how are you today?
Ben Fuchs (00:29):
Good morning. And I’ve been checking out your blog and you got some great stuff on there. Tell us a little bit about Parkinson’s disease and what you’re doing for early detection.
Dr. Russell Lebovitz (00:39):
Sure, thanks for asking. Parkinson’s disease, first of all, can affect anyone. It cuts across the spectrum and it turns up mainly people in their sixties, although it can come earlier and it can come later, but most are, it appears first for people in their sixties. And what Parkinson’s is is irreversible damage to certain regions of the brain that help us control our movements. And so when we get Parkinson’s, we find that movements that our whole lives have come easily and without thinking suddenly become very difficult. We can become stiff. We lose that fast, the facility of easy control. Maybe sports aren’t so easy to do anymore. And then, Parkinson’s is a progressive disease. Because over time, these regions of the brain that control movements are destroyed more and more until we reach a point where it’s very difficult to move the way we used to.
Ben Fuchs (01:43):
When you say destroyed, that seems really dramatic. What is it that would cause a part of the body or part of the brain that’s so significant as the area that’s affected in Parkinson’s disease, the substantia nigra? What would be a cause of destruction of this very vital area?
Dr. Russell Lebovitz (02:00):
Yeah. It’s a very recently recognized mechanism of disease that underlies not only Parkinson’s, but most of the other neurodegenerative diseases, including Alzheimer’s, a number of other dementias, ALS or Lou Gehrig’s disease. And it’s, what happens is, that something damage occurs in the brain over time and it leads to something which we would call Proteins Gone Rogue. And what happens is there are a few normal proteins in the brain that are absolutely required for normal activity, but a small subset of these proteins have a very unusual property. They can behave like transformers in the movie or on the television show. And literally without changing much about their primary structure, these proteins can basically flip into alternative shapes, they can transform. And proteins that can flip into at least two alternative forms, one of which is harmful, are called prions. And in the case of Parkinson’s, the protein that’s gone rogue, the protein that’s the transformer is called alpha-synuclein.
Dr. Russell Lebovitz (03:10):
And again, alpha-synuclein is a good guy normally, but when it flips into this new form, this Darth Vader form, it has two properties that are damaging. One is an accumulation of the prion form of alpha-synuclein kills nerve cells. But even more importantly, what this form, this transformed form is it can convert the normal good form into the bad form. So, really just one or two cells that suddenly have alpha-synuclein gone rogue can then spread from cell to cell. And the regions that are most susceptible to synuclein damage in people happen to be what you mentioned, the substantia nigra of the midbrain, which helps us control movements.
Ben Fuchs (03:58):
So, are you saying that Parkinson’s is now thought to be a prion disease?
Dr. Russell Lebovitz (04:02):
Well, yes, it is a prion disease. The only difference that we can tell between the prions involved in Parkinson’s and those involved in the original disease called the CJD or mad cow disease is there’s really no evidence, while the prions in Parkinson’s and probably in Alzheimer’s can spread within a person from cell to cell. There’s no evidence that it can spread between people, which is the case for CJD and for mad cow disease.
Ben Fuchs (04:36):
So, can you eat… And with mad cow disease, obviously the name mad cow came about because people were afraid that they would eat the cows that had this prion contamination or prion effect. Can that happen with Parkinson’s also? Can you eat prions?
Dr. Russell Lebovitz (04:50):
Yeah. So, that’s the difference here. When I talk about transmissibility within the brain, it seems to spread. It doesn’t seem to spread into other tissues in a concentration that’s so high or has the ability to transmit between people. There’s no evidence for transmission of Parkinson’s between people. But within the brain, it’s a similar mechanism.
Ben Fuchs (05:14):
Or by eating, or by food. When you say transmissibility, it’s not transmissible through food.
That’s right, it’s not transmissible through food or really any mechanism that we can see. Whereas mad cow disease, as you have mentioned is clearly was recognized because it can be transmitted between individuals or between animals and people. No evidence for that kind of transmissibility for Parkinson’s, Alzheimer’s, so we might refer to these as prion-like diseases because within the brain, the mechanism is the same.
Ben Fuchs (05:47):
Can you detect these prions?
Dr. Russell Lebovitz (05:49):
Well, that’s what Amprion does. We developed technology. Actually, we developed the technology originally to detect the classic prions you’re talking about in mad cow disease. And the test that was developed in the early 2000s is still the most sensitive test for detecting mad cow disease, but that’s a very rare disease. And what we’ve done is adapt that technology to detect other prion-like particles, including those for alpha-synuclein. And we now have enough data published all in peer-reviewed journals on the link between misfolded alpha-synuclein in the brain that we can detect to be able to offer a clinical test that can detect this disease at almost all stages. As far as we can tell from research studies, we can detect it in people who have symptoms. We can detect it in people who have early symptoms and people who don’t even have symptoms yet.
Ben Fuchs (06:52):
All right. Hang on that thought. I want to talk about of the prions and Alzheimer’s disease. And I want to know what we can do about prions. And are you saying prions? I’ve always said, prions.
Dr. Russell Lebovitz (07:01):
It’s either one have people use. Yeah. [inaudible 00:07:03].
Ben Fuchs (07:03):
Yeah. I wonder if we could do anything about those. All right. We got to take a break. We got Dr. Russell Lebovitz with us. We’re talking about brain health and Parkinson’s disease. His website is amprionme.com. We’ll be back with Russell Lebovitz right after this break. Don’t go away.
Ben Fuchs (07:16):
Okay. We are back on The Bright Side. I’m Pharmacist Ben. We’re talking to Dr. Russell Lebovitz about Parkinson’s disease. His website by the way is amprionme.com. You got a really cool blog up there. Let me see if I understand this, Dr. Lebovitz. The prion is a triggering factor that triggers this alpha-synuclein protein to fold in this abnormal way. Is that correct?
Dr. Russell Lebovitz (07:39):
Well, it is. A prion is actually a misfolded protein that can actually replicate by recruiting the normal form of the protein when they contact one another. So it is, the misfolded structure of alpha-synuclein is the definition of a prion.
Ben Fuchs (07:55):
Gotcha. So, the misfolded protein itself is the prion. So, what triggers this misfolding? Does anybody know? And how can you get rid of it, or can you?
Dr. Russell Lebovitz (08:04):
Well, these are all great questions. We don’t know exactly how it’s triggered, but if we follow people who get the disease and see what clusters there are, there are certainly several links that we can talk about. One is about 10% of people with Parkinson’s disease appear to have a familial or a genetic link. And when we follow the genes, there are a handful of genes that seem to be involved in increasing the probability greatly of getting Parkinson’s. But that’s only about 10%. The other 90% are what we call sporadic disease. We don’t know the exact cause, but we can find links.
Dr. Russell Lebovitz (08:44):
So you tend to see Parkinson’s more than expected in certain athletes, people who get repeated head injuries. So, boxers are the classic. Muhammad Ali [crosstalk 00:08:56] for example. But there are others as well. People who hit their head even subtly, but many times. People who had certain virus infections that affect the brain seem to have an increased probability. So, it maybe related to inflammation in the brain that on rare occasions triggers this. And because, as we’ve talked about the prion diseases self-replicate, a very rare event can then over 20 or 30 years lead to wiping out of whole regions of the brain.
Ben Fuchs (09:29):
I’ve been reading a lot about lipopolysaccharides and intestinal permeability issues. Do you know anything about that associated with Parkinson’s?
Dr. Russell Lebovitz (09:37):
Well, it’s interesting. What we do know is that at least with respect to Parkinson’s, there is a subset of patients where the disease may actually start in the gut and travel along the vagus nerve to the brain. It’s not clear that this happens in everyone, but there is data that one can find misfolded synuclein in the gut caused by certain bacteria. And it may be their lipopolysaccharides, I’m not sure that’s completely established. But once you get these misfolded synuclein prion-like particles in the gut and they travel through the vagus nerve to the brain, that seems to be sufficient to start the disease in the brain. So, I agree with you that the gut may play a role here for some people.
Ben Fuchs (10:24):
What do you mean by travel along the vagus nerve? I don’t quite understand that.
Dr. Russell Lebovitz (10:30):
Well, so what happens is these are particles. They’re maybe the size of viruses approximately. So if you have these particles in the gut in some place and they contact the nerve ending, so the vagus nerve starts in the brain and has very long processes that extend into the gut and other tissues. And those very long processes part of the nerves, so some of our nerve cells are literally inches, almost a foot long. And so along those nerves, the long processes can transport a number of things in both directions. So, if one-
In the nerve cells itself?
Dr. Russell Lebovitz (11:13):
In the nerve cell itself.
Ben Fuchs (11:14):
Dr. Russell Lebovitz (11:14):
Ben Fuchs (11:14):
Wow. That’s very interesting. So what can people do if they have this kind of, if they have a prion-related brain deterioration issue? Is there anything they can do?
Dr. Russell Lebovitz (11:25):
Well, so what we know now is that these diseases, as you have mentioned and I have certainly validated for you, kill brain cells. And what we know is that unlike almost every other tissue in the body, the brain does not regenerate. And there are a lot of reasons for that. So the key here is that once the regions are destroyed, you never go back. You never reconstitute. So what one can do, sorry, is to learn as early as possible about the presence of the disease. And then, the strategy becomes until there are drugs that can stop this in its tracks, which there are not now, but there are a number of clinical trials, slowing down the disease is a very useful strategy. But slowing it down works better the earlier you detect it. So, one of the things we talk about is that early detection empowers early prevention. So the things that one could do are one, it looks like there’s data that changing one’s lifestyle, eating a more healthy diet, exercising more, the same things that are heart-healthy tend to be brain-healthy.
Dr. Russell Lebovitz (12:38):
And so, the earlier one is able to put in an aggressive program of changing lifestyle that seems to be able to work. And if you slow this disease just a little bit at the early stage, you might be able to get 10 years or more of productive life before symptoms. The second thing that one can do is to enroll in clinical trials. This is how we learn about these diseases. There are over 500 clinical trials available to patients in the United States right now, and they cover everything from lifestyle changes to supplements, to drugs. And so, one can enroll in studies that fit their preferences. And then, the third thing that one can do is that if you are 45 years old and you learn or 50 years old that you’re likely to have a disease, that you have a disease incubating, that in 20 years may make it difficult to get around, it may make it impossible to travel, then you can just rearrange your life priorities so that you get to do those things earlier rather than later.
Ben Fuchs (13:46):
Are there… I know you list seven on your blog. You’ve got seven early warning signs for Parkinson’s disease. But a lot of these seem kind of generic, like trouble sleeping, and posture changes, loss of smell. What’s a really clear red flag that people should be concerned about?
Dr. Russell Lebovitz (14:05):
Sure. Well, one of the things you’ve mentioned that we have seven signs that are early for Parkinson’s and they sound very generic, but the actual form for each of these is specific enough that one could be able to at least have a guess. And so I will tell you that until a year ago, the best sign that was very clear, that was unusual in anyone other than a patient with early Parkinson’s was sudden loss for no reason of sense of smell and taste. So, that was our best sign. However, with the onset of COVID turns out that’s a sign of COVID as well. So, that is much less specific. I’d say other ones that are important here, you said, trouble sleeping, but trouble sleeping here isn’t just that one is anxious and can’t get to sleep.
Dr. Russell Lebovitz (14:57):
What happens in early Parkinson’s with trouble sleeping is a very specific sleep disorder where a person suddenly starts thrashing around and moving in concert with their dreams. And the way we notice this the most is if it’s someone who has a partner, that partner starts reporting being hit in the face or being kicked much more. And it’s just sudden onset and it doesn’t go away. So, there’s one that’s pretty specific. And if you want to go through any of the others, every one of these has something that’s unique to… A little bit different in a patient that has early onset Parkinson’s. And that’s what a movement disorder specialist, a neurologist who really focuses on Parkinson’s and related diseases will be able to look into.
Ben Fuchs (15:45):
Okay. So if somebody is suspecting that they or a loved one has or is developing Parkinson’s disease, how can Amprion help them what should they do?
Dr. Russell Lebovitz (15:54):
Well, everything we do, we have a regulated clinical test to detect misfolded alpha-synuclein. So, it would need to be done through a doctor. And so seeing either first the primary care physician who may refer them to a neurologist, it is then possible to get a sample to run the test. It takes about a week. And the test is very clear, the answer of yes or no. And if the answer is yes, that means that these prion-like particles are present in the brain and the disease is progressing. We don’t always know how long it will take. It takes 10 years in some people, 20 in others, but we can definitely say that there’s a disease incubating. And if there are early signs, then the correlation is very high.
Ben Fuchs (16:44):
What’s the relationship between COVID and Parkinson’s?
Dr. Russell Lebovitz (16:47):
That’s an amazing question that we don’t know the answer yet. But it’s because, I mentioned earlier that one of the things where there’s a correlation even before COVID was inflammation in the brain or viral infection of the brain. And it looks like almost everyone who has COVID gets massive inflammation of the brain. So there is a giant concern that we may have an epidemic of Parkinson’s in the next 15 to 20 years, but we don’t know that yet. But ultimately one way to tell that, and we’re looking into this, would be to do a research study on people who have had COVID and where we can look to see the presence of misfolded synuclein in COVID survivors compared to the general population.
Ben Fuchs (17:37):
Doc, we’re out of time. Thank you so much, Dr. Russell Lebovitz, amprionme.com. And that’s all the time we have for today. Thanks for listening to The Bright Side, friends. I’m Pharmacist Ben. Have a wonderful, beautiful, awesome, spectacular day. We’ll talk to you later, folks. Bye for now.