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Syn-One Test®: A Diagnostic Tool for Parkinson’s

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  • Discover the groundbreaking Syn-One Test to aid in the diagnosis of Parkinson’s
  • Learn about the earliest signs of Parkinson’s, even before visible symptoms
  • Understand the importance of early detection
  • This video is part of The Parkinson’s Solutions Summit
Kenneth Sharlin, MD

Well, welcome again to the Parkinson’s Solutions Summit. I am your host, Dr. Ken Sharlin. I am very excited today to interview a special guest, Dr. Todd Levine, one of the co-founders of CND Life Sciences. He is also acting as their Chief Medical Officer. This is a very important interview. Listeners and viewers are going to get some key information that really may change the way that they think about Parkinson’s disease from the diagnostic perspective and how the diagnosis is made, but also potentially from the therapeutic perspective, which I think is at least equally, if not more exciting. So without further ado, welcome, Dr. Todd Levine.


Todd Levine, MD

Thank you for having me today.


Kenneth Sharlin, MD

Dr. Levine, before we dive into our discussion, tell the viewers a little bit about your background and your company.


Todd Levine, MD

Great. Well, I am a neurologist, and I did my medical schooling at Duke University. I then did an internship in medicine and a residency in Neurology at Washington University in Saint Louis. I then specialize, actually, not in movement disorders but in diseases of the nerves and muscles. We call those neuromuscular diseases. I spent two years after my residency doing that fellowship. That was a time when a new technique was kind of brought to the world, and that technique involved taking skin biopsies and looking in the skin to look at the nerves. As opposed to studying the nerves through sort of indirect tests or physical exam tests, it allowed us to visualize the nerves for the first time and in a very convenient way for patients. I started a lab to do that, which then began to receive specimens from all over the country, from doctors and neurologists, primarily to study these nerves. 

Now, about ten years ago, while that lab was developing, my two other co-founders, Roy Freeman and Chris Gibbons, who are professors at Harvard Medical School, were doing similar work as I was with the skin, but they began to ask the question, Could we look inside of the nerves? Could we see what is happening? Not just with the nerves and looking at overall nerve health, but could we look inside the nerves to see what changes were happening? They began to study this protein called alpha-synuclein. They began to publish on the fact that, yes, using that same very simple skin biopsy technique, they could look inside the nerves in the skin and they could detect alpha-synuclein in patients that had a group of diseases that we call synuclein opposites, and that includes Parkinson’s disease, multiple system atrophy, dementia with Lewy bodies, and pure autonomic failure, as well as a prodromal disease called REM behavior disorder. 

About seven years ago, the three of us got together over a beer in Boston and said, Hey, let us see if we can now start to bring this technology, which was being developed by many labs across the world, we could bring it to patients and neurologists in the U.S. We founded CND Life Sciences. CND Life Sciences spent about three years perfecting the technique. For the last 3 to 4 years, we have now been offering commercial testing so that patients and doctors outside of research trials could now have the ability to visualize this abnormal protein in patients that might have these diseases.


Kenneth Sharlin, MD

Wow. Yes, it is very interesting because, while this is a relatively new test, the idea of alpha-synuclein goes back to the earliest pathological observations of Parkinson’s disease. Can you talk just a little bit about the Lewy body? 


Todd Levine, MD

Absolutely. You are correct. It is about 100 years old. A pathologist began to study the brains of people who had passed away from Parkinson’s disease. He found a very characteristic finding and that finding was inside the nerves of the brain. There were these basic blobs; I would like to call them blobs because, just think about a collection of stuff that is built up, and that was called the Lewy Body after him. His name was Lewy. That has been the sort of pathological definition of the disease for a century now. No one knew what the Lewy Body was until really about the 1990s. At that point, because of the development of several different techniques, it became clear that that blob was, in fact, the accumulation of a lot of proteins. 

The way I like to explain this because it is unbelievably important in what we call neurodegenerative diseases is that in our bodies, the thing that does what we need it to do, so whatever function you need to do inside your cell, that is all done by proteins. We make proteins; the protein goes and does the thing it needs to do, and then you have to degrade that protein, so it is a continuous cycle. You can imagine that there can be some diseases where you are not making the right protein, and therefore it cannot do the thing that you need it to do, we call that a loss of function, or you make that protein and it does not degrade. Then that protein is just going to build up inside the cell. At some point, there is so much of that garbage in the cell that the cell will not be able to survive. The term that we use for that now is called protein apathy. 

The most common neurodegenerative diseases—Alzheimer’s disease, Parkinson’s disease, multiple system atrophy, dementia with Lewy bodies, Lou Gehrig’s disease—are all related to this concept of some poor regulation of protein synthesis, the creation of that protein, and then protein degradation. There can be different proteins in each disease. The protein that causes Alzheimer’s disease, we do not think, is the same as the protein that causes Parkinson’s disease. But when you look inside the brain, there are still these accumulations of proteins that should not be there. 

In the 1990s, they discovered a genetic mutation that caused Parkinson’s disease. That genetic mutation was in the gene that coded for the synuclein protein. At about the same time, using newer techniques, we determined that the synuclein protein is the main protein inside the Lewy bodies. Since the 1990s, the belief has been that Parkinson’s disease is what we call synuclein apathy. Protein apathy is all the different protein diseases, and then synuclein apathy says there is something wrong with the regulation of the synuclein protein. It is building up and is becoming toxic to these nerves.


Kenneth Sharlin, MD

Yes, it is fascinating. Especially now with the FDA approval of Lecanemab, the pending approval probably of Donanemab with Eli Lilly just releasing its Phase three trial data, which was stunning, to say the least, particularly for the early stages of Alzheimer’s, which would be mild cognitive impairment without impairment of activities of daily living. There is not as much destruction of neurons and therefore less removal of this amyloid protein. The protein that we associate with Alzheimer’s disease appears to have a huge impact on disease progression. I hope we see the same with ALS, with multiple sclerosis, with ALS, where the TDP 43 protein, and with MS is a relatively new one for me, as I am very interested in this overall subject. 

However, the bassoon protein that is at least associated with the neurodegenerative phase of multiple sclerosis appears to play a major role. It is a little bit of a digression, but it is an interesting observation. It makes you ask very big questions about, who is in control here. There is an old theory called the selfish gene theory. But maybe this is all about the selfish protein, and it is the way that cells protect themselves against, if you will, mistakes or malfunctions. 

I am a big Star Trek fan, and I always say that the Enterprise and all those starships have various levels of defense, the phasers and the photon torpedoes and all that stuff. In the end, they are their shield. But in the end, if all else fails, the ship is capable of self-destructing. Maybe these diseases are the end point of multiple attempts by the cell to manage various incoming signals that have either resulted in these misfolded or excessive levels of protein or, in some other way, the reasons that these proteins are produced, maybe partly from genetic influences plus environment, what we might call epigenetic influences. 

But at any rate, this is so important, and I call this 21st-century medicine with my patients and myself. The reason that we call this 21st-century medicine is that we are now in the age of biomarkers, or biological markers, and alpha-synuclein is one biological marker. If we go back and look at the diagnosis of or how Parkinson’s and other related movement disorders are diagnosed, it is largely been clinical. Isn’t that correct, Dr. Levine?


Todd Levine, MD

Yeah, and in fact, that is still the gold standard. We are trying to change that a little bit. But one of the reasons it is important, and I think you alluded to this, is that you may get Parkinson’s disease in multiple different ways. Some patients will have a genetic predisposition. Some patients could have a toxic exposure that causes Parkinson’s disease, like the camel dune stuff that we see on TV all the time. Some patients may have reasons that we cannot understand. The result seems to be the same, which is the formation of the Lewy body. But each person could get there in a very, very different way. I think until we’re able to put people into smaller and smaller buckets and say this is what the problem is, we will never really get the true homerun breakthrough. I agree with you completely. It is unbelievably exciting to finally have drugs that will affect amyloid and slow the progression of Alzheimer’s disease. 

But on the other hand, there are many other reasons to have dementia. We know, for example, that in the dementia space, if you take the best clinicians, the best neurologist that you can find, and the neurologist says, okay, that is Alzheimer’s disease, and then the person passes away and you do an autopsy, you find out that about 25% of the time it was not Alzheimer’s disease, and then you find out that about 15% of the time it is Alzheimer’s disease plus something else. You can imagine now that if you are trying to use one medicine, the big hammer hits all these little teeny nails. You are never going to do a good job. We need much more targeted therapies. To do that, we need the biomarkers and the analogy that I use. I think most people sort of get here if we think about horrible diseases like Alzheimer’s disease and Parkinson’s disease, another disease that you would say you and I think are old enough, is HIV. 

When HIV came into the world, everybody died of HIV. But two things happened, so now nobody should die of HIV. People can live with HIV and live a completely normal life. Those two things were a bunch of drugs that we could cycle people through and see what was working for them. Then the second was a very fast way of measuring the level of the virus, because, again, if people get Parkinson’s disease in multiple ways, not everyone may respond to the same type of therapy. We now have 37, I think, different molecules that are in development to treat alpha-synuclein in patients with Parkinson’s disease. 

Imagine a world where you’ve got 20 of those drugs and you can rapidly put somebody on those drugs within, let us say, a month or two. You could say, Are you affecting synuclein in the way that you want to? If not, go to the next drug. That is what the HIV world did. They just got a bunch of drugs. They cycled people through very quickly, and they could measure the viral load. And as soon as the viral load was zero, they said, Oh, that is the right combination for that person. But everybody has different drugs. I kind of think of these as being the same thing, which is that it’s highly unlikely that we are going to find one drug that cures everybody with Parkinson’s. But if we had 20 drugs and we had a way of measuring quickly whether those drugs were effective, we could probably stop Parkinson’s disease.


Kenneth Sharlin, MD

Yes. I am going to steal a phrase from another podcaster I heard recently, and said, If you have seen one patient with Parkinson’s disease, you have seen one patient with Parkinson’s.


Todd Levine, MD

So it is perfect, you know.


Kenneth Sharlin, MD

But that being said, it is interesting that we come full circle on these big, chronic neurodegenerative disorders where we have the descriptions of the original cases of Alzheimer’s or the original cases of Parkinson’s. Then we go through all of these years of relying solely on clinical observation, which still has huge value. For folks who are listening, to be clear, as you know, it has been stated that it remains sort of a gold standard. We certainly will discuss the preclinical disease, that is, the disease before it is fully manifested as the rigid kinetics shuffling gait, which may be unilateral tremors, changes in facial expressions, etc. That is when I see that in my office, I always say, I make the diagnosis as I am walking into the exam room. I do not even have to really, go through a detailed history and examine the patient. I do, of course, but it is a very visual diagnosis. The response to dopa therapy becomes what clinches the diagnosis in general. 

But that being said, we have now moved from knowing about Lewy bodies to finding out that Lewy bodies are primarily composed of this alpha-synuclein protein. Now some data suggests that alpha-synuclein is not just in the brain; it is found in the digestive tract. Some people think that Parkinson’s, at least in some cases, may start in the gut and then migrate perhaps to the brain by way of the vagus nerve. That is one theory. It is also found in the skin. I guess what you are saying is that our skin has nerve endings, and this is a systemic disease.


Todd Levine, MD

Correct? Yes. The gut connection is fascinating to me. We are doing some studies now, and, there was just an article published, I think in the last 30 days, that shows that you can see these synuclein accumulations in the gut in people with Parkinson’s disease. We also know, for example, that if you are over the age of 50 and you have idiopathic constipation, your risk of developing Parkinson’s disease is four times that of the normal population. Another great example of that is if you take a mouse and you create a transgenic mouse that is going to develop Parkinson’s disease, the first place that you see synuclein accumulate is not the brain of the mouse; it is the gut of the mouse. That is why a lot of this gut-brain-axis story in Parkinson’s disease is probably not too far afield. I think that is interesting. Then we have known for a long time that Parkinson’s is more of a systemic disease, not just the gut. We know that there is trouble regulating blood pressure and heart rate. We know that bladder symptoms can occur, and everyone has looked for a convenient, accessible biomarker to say that this is the synuclein that is building up. Therefore, we believe this person does have Parkinson’s disease in the right setting. 

Then, as we work with pharma companies and our lab is now working on about ten different research trials, if you are that pharma company, you want to take someone who has synuclein, treat them with your drug, and then prove that there is less synuclein. One of the big pluses of that, again, to go back to the HIV analogy, is that if I want to see that I can change the clinical course of Parkinson’s disease, I might have to treat a patient for a year or two because 

Parkinson’s disease does not change in a month. But if there was a test or I could rapidly see if I was affecting that protein again, I could run my clinical trials faster. I could make sure the patients are responding faster because we probably had some drugs that have been tested for Parkinson’s disease that have failed for two main reasons. One is the clinical diagnosis of Parkinson’s disease, as I referred to before, and Alzheimer’s disease is often wrong. 

Chuck Adler and Tom Beach are both here at the Mayo Clinic in Phenix. They published it ten years ago, but 230 patients came to autopsy who had been diagnosed by expert neurologists, and the expert neurologists were only right 68% of the time. I tell people all the time that if I tried to get through medical school with a 68% average, I would not be talking to you right now. That is the best clinician that we have. So we are certainly enrolling some people into Parkinson’s disease trials who do not have the disease, that is number one. 

Then, number two, we may not have treated them long enough because Parkinson’s disease does not change that rapidly. If you have a six-month trial, maybe you will not see the effect, but maybe you will in three or five years. That test, again, think about another analogy I use: think about trying to treat glucose in a patient with diabetes. The nice thing about managing diabetes is that you can check the glucose conveniently and easily 20 times a day, and the patient can adjust their medicine and food intake to try to compensate for that. That allows us to very rapidly treat diabetes. But we do not have that in Parkinson’s or Alzheimer’s. We are hopeful that this cinnamon test will give us the ability to visualize that protein. We can hopefully, over a few months, is the protein going up or is the protein going down.


Kenneth Sharlin, MD

What we are saying, folks, is that these biological markers can not only facilitate the diagnosis, but they can help to determine if there has been a treatment response, which is profound because there are scales and clinical scales to evaluate Parkinson’s that are widely used in clinical research. But this is one other measure that is very important and is being used. If we look at some of these other major diseases, such as Alzheimer’s and multiple sclerosis, we do a lot of trials in both of those areas. At Charlotte Health Neuroscience Research Center, we are doing MRIs, and as we are doing PET scans, we’re doing lumbar punctures. Here we have a test that is simple for any clinician. 

You do not have to be a neurologist. I do not know if you guys are necessary, what you are, and perhaps you could talk about that, what positions you are sort of accepting samples from that you are engaging in contracting with so that, can any physician do this? But I would say and I would like to know that, but I would say in general, this is a very simple test, and when I explain the test to my patients before we even have them in the room for the procedure, I say, Look, here is a pen and the actual piece of skin that we remove is about the size of the tip of this pen. That is why I said, you have had a cut in your life, way worse than this biopsy. We do three of them. We take three skin samples and after the numbing experience, which most people know is a little bit uncomfortable in general, whether you are having, a dental procedure or otherwise, really this is an entirely painful test that the actual, harvesting of the skin probably takes 5 minutes.


Todd Levine, MD

Yes, any clinician can do them. We are mainly talking to neurologists because we’re talking about dementia and Parkinson’s disease, but we do have geriatricians who do it. We have primary care doctors that do it, and we have some neurologists, unlike you, who just say, I do not want to learn a new technique, and then we could even send it to a dermatologist or anybody. It is very simple. We say it takes about 15 minutes. That is on the long end of doing all three. 

Your comparison is exactly right. I tell patients that when I put it in the light, like a cane, it is going to burn like crazy for 5 seconds. All they have to do is breathe through it for 5 seconds, and then they are pretty much numb for the rest of the procedure, and they do not feel anything. It does not hurt. The next day, it heals up like a little scab. There are no stitches, and it can be done anywhere in the country. It is shipped to our lab in Arizona.


Kenneth Sharlin, MD

We have also touched on some of the preclinical features of Parkinson’s disease. It is important to remind folks that when we are looking at alpha-synuclein, which can be seen in diseases that are in the same family as Parkinson’s, multiple system atrophy, prognostic failure, and Lewy body dementia. I would like you to talk about some of the recent presentations that you have been making. Your company has made public your research and even distinguished it using this test to distinguish between these different hyperkinetic movement disorders. But that being said, you have touched on REM sleep behavioral disorder. We have talked about constipation often for decades, although that is not to say that everybody who is constipated should have a skin biopsy and even mood or personality changes that may precede the actual movement disorder. 

I probably borrowed the take-home message from a colleague of mine who said that everybody who has turned age 65 and goes to their doctor for their preventative exam should have a cognitive AP. Doctors should be sort of going through that review of systems and seeing, how your sleep, how is your digestion rate, and mood have been. If we start to see a pattern, the possibility of thinking about preclinical Parkinson’s becomes very valid. Especially we, once we get into the and fingers crossed because I believe it is coming soon. The age of disease-modifying therapies for Parkinson’s, can we prevent this? 

Data released by Eli Lilly and Company on their new Alzheimer’s drug and Donanemab showed that individuals who had just mild cognitive impairment but had the pathology of Alzheimer’s, meaning if we image the brain because they primarily used PET scans to look at amyloid into our proteins, but those individuals are highly functional, we would not look at them and say that they had dementia when they received inanimate, they had a 60% slowing in the expected progression of disease. That is amazing. Early identification and intervention, I think, is going to be the mantra across the board, including Parkinson’s disease.


Todd Levine, MD

Yes. That is what you just mentioned, which is probably the thing that I get the most excited about when I think about our test. The reason is, and I think you probably would agree with me, if you wait until somebody has dementia for 20 years and then you think we are going to have a drug that is going to reverse that, I think, highly unlikely to happen any time soon. But what the biomarkers allow us to do is detect people before they have lost a lot of neurons. If we know that we are at risk of developing Parkinson’s disease, what can we do to slow that progression and prevent these diseases from ever occurring? I think that is really where I get excited. We talk about sort of two levels of early detection if you will. 

One is what you were sort of alluding to, which we will call prodromal. The prodromal symptoms of Parkinson’s disease could be REM behavior disorder, constipation, dizziness, depression, or even bladder symptoms. Those types of symptoms could prompt us to say, Should we look and see if synuclein is starting to build up now? That then leads to what I call when I talk to neurologists: So what question? Okay, if I found out today that I was building up synuclein, what would I do with that information? We do not yet have an anti-synuclein drug the way that we have an anti-amyloid drug, but we also know that diet, exercise, and sleep—all of these things slow the progression of Parkinson’s disease. I talk about that as wellness. Just like if I found out today that I was pre-diabetic, what would I do? I sit around and do nothing and let myself become diabetic, or hopefully, I will exercise and diet and focus on wellness in the hope that I can prevent ever becoming diabetic. 

We are really in an era now, at least with these diseases, where we can detect these people in that prodromal stage and, at least in the short run, focus on that wellness. Those things that do have, I think, were just a paper that said 75 minutes a week of exercise slows the rate of progression of Parkinson’s disease. That is not 10 minutes a day. That is not a lot. If that were you or your brother, would you be able to say, Okay, now we have to do that? That is the prodromal stage, and that is what I am excited about. Then again, once we get an anti-synuclein drug from one of these 37 molecules that farmers and companies are developing now, what questions will be answered? Well, if you are developing synuclein and there is an anti-synuclein drug, do not wait until you have Parkinson’s. Take it five years before your Parkinson’s and hope you never get Parkinson’s. 

Then there is a further stage, which we call presymptomatic. This is more complicated, so this would say the analogy here would be, for example, we know certain genes are related to developing Alzheimer’s. Let us say,  I am 56 and think, I am still an okay neurologist. I am still thinking, Okay, but I got my genetic test and it turns out I have two APOE4 genes. I do not have any symptoms, but I now know I am at a much higher risk of developing Alzheimer’s disease somewhere down the road. Now you have the same; So what question? What do you do with that? Some people do not want to know that, but if you just go out and biopsy, let us say, a thousand people that had no symptoms of Parkinson’s disease, we believe somewhere between two and 5% would already be accumulating alpha-synuclein. 

One of my dreams, and actually it is a study that we are doing right now, is that most people in the U.S. at 50 go get a colonoscopy. Because if you get your colonoscopy every ten years and they remove the polyps, then you never get colon cancer to completely change that disease. If they are in, they are already doing a colonoscopy and biopsies on all the lesions that they biopsy. What if you could biopsy the colon in every human being at 50 and see who is accumulating synuclein, who is accumulating amyloid, and who is accumulating Tau? 

Now you have sort of a neurodegenerative screening test, and then again with the hope that there are drugs so that, as we say, you are developing TDP 43. We are going to put you on an anti-TDP 43 drug so that you do not get frontotemporal dementia. That is where I would get now; that is the Holy Grail, and you probably never actually get to hold the Holy Grail, but you can imagine a world where that happens, say, in the next 10 to 20 years. Now we know that the incidence of neurodegenerative diseases has decreased by half.


Kenneth Sharlin, MD

Well, I mean, now you can take a little swab out of the inside of your mouth, send it in, and get a digital record of your entire genome. Perhaps it’s not that far-fetched. There will be these screening panels for these major diseases that we have early interventions for. Yes, I am not farfetched at all. Now, the same person, but part pardon me, sir.


Todd Levine, MD

Not too Star Trek.


Kenneth Sharlin, MD

But the skin punch biopsy is not the only test out there that we might use in a setting where we do need to distinguish Parkinson’s from other disorders like essential tremor or drug-induced Parkinson’s. Now we know that, with your particular test, we can even distinguish the different subtypes of movement disorders that fall in the Parkinsonism family from each other, the degenerative Parkinsonism family from each other. We have had that scan, for example, which I have used for several years, but I must admit it is a lot less common for me to order, and that is a SPECT scan these days because I can do a scan punch biopsy right in my office. They are different tests. They are not testing the same thing.


Todd Levine, MD

Yes. They are complementary in a lot of ways. If you think about the Syn-One Test, is looking for the accumulation of abnormal protein. The data that we just presented at the American Academy of Neurology shows that we have about a 95% sensitivity and a 96% specificity. a very specific and sensitive test. However, many other diseases cause those same parts of the brain to deteriorate over time. Not all of them are associated with synuclein deposition. Two of the more common are associated with the accumulation of a protein called Tau, which we also see in diseases like Alzheimer’s disease. If you do a DaTscan, the DaTscan gives you a broader look. It says, Is there evidence that these nerves involved in movement are dying? And then the Syn One test says, Is there evidence that the synuclein protein is accumulating abnormally in this person? 

You can imagine if you have an abnormal DaTscan, but a normal Syn-One test, then what that tells you is, yes, those movement disorders and structures in the brain are dying, but it is not due to synuclein, and therefore it is very likely it’s due to Tau. Now, again, that is one of the reasons we would love to have that Tau test, which we are working on, because then we could specifically answer all but so you can end up, as you said, with Parkinsonian diseases, diseases that look like Parkinson’s disease but are not related to synuclein. The reason, again, that is so important these days is because we are developing these targeted therapies. You can take a symptomatic medication like cinnamon, like levodopa, and give it to anybody whose basal ganglia is deteriorating and hope that you see some response. But when you start to think about targeted therapies targeting synuclein, targeting Tau, and targeting amyloid, you’ve got to start with, well, I am not going to give an anti-synuclein drug to a patient that, as a Tau disease, does not make sense.


Kenneth Sharlin, MD

But it was the wrong antibiotic. Right?


Todd Levine, MD

Yes, exactly. The two do work together nicely to provide a lot of information, even in advance of just what the one test tells us.


Kenneth Sharlin, MD

Excellent. As we start to wrap up our interview, I want to bring up the Syn-One Clinician Network which may be very helpful to folks who are affected by these movement disorders because they want to find a provider or someone who can perform this test.


Todd Levine, MD

Yes, we have on our website a network of doctors across the country who have agreed to let us put their information up because they are comfortable with this in one test; they are comfortable doing the biopsies. That is one way to kind of reach out. We have a very good patient services team at the lab. If there is nobody locally, they are available for you. I would call here. We probably know somebody close, even if they are not on the network right now. Then we have done a lot of work. Even again, if you are, you would talk to your primary care physician, who would say, Oh, that makes a lot of sense to look for this, but I don’t want to do it. I don’t want to think about bringing something new into my practice right now. 

We have done work even with in-home nurse practitioner groups, which is a great way to get someone to come to your house. They could do the biopsy in your living room. It is incredibly simple. Then they shift the biopsy to us, just like your doctor would, and then your doctor can get the results. We have a lot of ways to help patients get access to this, but we have right now over a thousand. So there are about 15,000 neurologists in the country right now. About a thousand of those have used our lab over the past four years. We are growing. We should have pretty good coverage across most of the country.


Kenneth Sharlin, MD

I talked a little bit about your research, and I know you have been a presenter at some major meetings recently, presenting on the sensitivity and specificity of your tests. Are there some major upcoming events we can look forward to for CND Life Sciences?


Todd Levine, MD

Most of the major meetings for this year are over, except for the Movement Disorders Society meeting, which is going to be in Copenhagen in August. We are going to be presenting our data there as well. We are working with a lot of investigators across the country on what we call investigator-initiated trials. Now that this test is available, I will give you just one pitch for what I think, again, is how smart people are. There is an amazing movement disorder. A neurologist at the University of Michigan, he believes, as many people do, that Parkinson’s may be a spectrum. If you think about, what you mentioned earlier, which is that as a neurologist, we could often be across the parking lot and see a person walking, and we will say, Oh, that is Parkinson’s disease. But then you see older people, and this is my dad, who is 92, who is hunched over, that they walk slowly, and they are not Parkinsonian, but they are just developing one of these gait disorders of the elderly, and how many people in 90s walk the way they did when they were 50. 

Dr. Bonine in Michigan believes that there may be a different form of Parkinsonism related to synuclein. We are biopsying a large number of folks, kind of those over 80-year-olds that have developed kind of slow gait or hunched gait, but not the clear features of Parkinson’s disease. We have also uncovered, we say, five synuclein apathy, which we labeled already. Just this year, there was a publication of a disease called Lubag, which is a disease that includes Parkinsonism, but many other features like dystonia and other movement and dementia, and it is confined to the Filipino population. It turns out that’s synuclein apathy. In five cases, all five had synuclein and even though it is not Parkinson’s disease, I think as we start to measure this protein, I think we are going to find that, yes, PD is the biggest, and dementia with Lewy bodies and multiple system atrophy, but there may be many other diseases where the accumulation of this protein has just never really been thought about. That would be fascinating.


Kenneth Sharlin, MD

I think it is so important. Dr. Todd Levine, what do you share the website for your company so that people can look that up and read more?


Todd Levine, MD

Yeah. The company is called CND, that is Charlie, Nancy, and David, Life Sciences, and the website is just cndlifesciences.com. I think the website is pretty good. It can give you a good background. As I said,  what patients think about when they think about the past talks a little bit about insurance coverage. Again, one of the nice things is that this test has been very well paid for by Medicare and most of the patients that we are talking about because of these diseases are of Medicare age. Commercial insurance is always a little more hit-and-miss just because there are so many rules, out-of-pocket deductibles, and so forth. But we can work with patients on that as well. All that information is on the website.


Kenneth Sharlin, MD

On a personal note, we have had very little trouble getting coverage for our patients, and the turnaround time is also important to a lot of folks. How quickly I will get my results is very good. We usually schedule their follow-up visit 3 to 4 weeks after the biopsy is complete. They have their answers, and we move forward with a diagnostic or therapeutic plan. It is excellent, etc. 

The contact information for your company is right on the website as well. I might add that there is a fascinating one-minute video or so. If you want to see what alpha-synuclein looks like in almost three dimensions in the video, it was nicely done. I would encourage folks to get a visual by going to the website as well.


Todd Levine, MD



Kenneth Sharlin, MD

Well, thank you so much for spending time with us today at the Parkinson’s Solution Summit. I know that viewers have learned a tremendous amount from you. Again, please keep up the excellent work. I know we are very committed to your company and the type of work that you are doing. It has changed my neurology practice when it comes to movement disorders. I am excited about how all the puzzle pieces are coming together. We are just a hair behind the Alzheimer’s folks, but there is a lot of work still to be done in that area, of course. But I see us converging on disease and modifying therapy, hopefully in the next few years as the research and clinical trials evolve. This will be central to the diagnosis, and treatment of patients.


Todd Levine, MD

Well, I appreciate it. Thanks for your support.


Kenneth Sharlin, MD

Thank you. Have a wonderful day.


Todd Levine, MD

Thanks. Bye.

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