Episode Transcript
[00:00:00] Speaker A: I've always dreamed about this moment, Brandon. When I actually was being trained as a neurologist, I always dreamt about us having more opportunity to peek into the brain.
[00:00:15] Speaker B: Spyros, thank you so much for taking the time to have this conversation. I've been so looking forward to it.
[00:00:19] Speaker A: Thank you very much, Brandon. It's a pleasure to join your podcast and provide an overview of Nuphoria.
[00:00:26] Speaker B: Yeah, of course. So I'll. I'll give you a chance to introduce yourself in just a minute, but for the audience, Spyros has had a incredible career across R and D and development in neurology and psychiatry across large pharma and also biotech. But Spyros, maybe give me an overview quickly of your career and how you came to to lead Neuphoria.
[00:00:42] Speaker A: I'm a neurologist and a neuroscientist by training. I trained in primarily neurodegenerative diseases. Very early in my career. I found psychiatric symptoms fascinating and I was attracted to the neuropsychiatric symptoms of neurodegenerative diseases. I was a practicing neurologist and an academic neurologist at the University of Miami. Right around 2007, I realized that my personal purpose was better served developing medications for a lot of people rather than caring for patients one by one, it's the same purpose treating patients, providing treatment solutions and improving patient lives, but at a different scale.
So I joined Biogen back then, and after Biogen, I spent about a decade in large organizations like Pfizer and Allergan working on CNS disorders. Altogether, I've worked both equally in psychiatry and neurology, in rare conditions and in more prevalent conditions. Over the years.
And right about 2017 I realized that I also have an entrepreneurial spirit in me and I decided to jump into company creation, early company growth and company transformation. Fast forward. About two years ago, I crossed paths with what was then Bionomics Therapeutics and the transformation for this company and the opportunity was tremendous. So I was tasked to bring this company over to the States. Bionomics has been a biotech company that was formed in Australia.
A very good pipeline, robust plans to bring medications to patients, but it was missing the investors that support the US biotech ecosystem. So the effort just finished. We launched Euphoria back in December after two years of very hard work while advancing, of course, the Nomexis pipeline. And now we are a US Based company with very much the same focus and same passion about neuropsychiatric diseases, particularly stress and anxiety disorders. We also work in the area of Alzheimer's disease. We have a program in partnership with Merck. Merck is responsible for developing the Alzheimer's disease program. They're currently in phase two. So that's how I came about. I was fascinated by the opportunities this company's transformation could provide to patients and the potential for BNC210, which is a lead program for Nephoria.
[00:03:12] Speaker B: Yeah, absolutely. And you've, you've seen the insides of a few different development organizations at this point. What really captured you about bionomics?
[00:03:21] Speaker A: Nimbleness, an opportunity for scale, opportunity to do things fast and efficient, the right amount of governance and of course, the most important for me, very robust science.
I was attracted by, I'm attracted by programs, I'm attracted by science.
So when I did my own diligence on the BNC210 program, past data sets and the potential, I immediately thought that this is something that could reach the market. This is something that could impact in a meaningful way millions of patients lives. So that was my driver to join the company and that's the potential that I saw.
We're a very small company. Again, we have an opportunity to move fast, execute with excellence and bypass the unnecessary bureaucracy that comes with large organizations.
[00:04:17] Speaker B: Tell me a little bit more about BNC210. What was it about it that really sparked your interest here?
[00:04:21] Speaker A: So, yeah, BNC210 is a small molecule. It is what we call an Alpha 7 nicotinic acetylcholine receptor negative allosteric modulator. I know it's a mouthful, but I just want to start very high level. Basically it's an allosteric modulator of a channel of a receptor that is intimately implicated in processing of anxiety disorders, mood and, or anxiety levels, mood and cognition.
So it's expressed in areas of the brain that actually control emotional processing, like the amygdala, which is the most important emotional processing center in, in our brain. And it's conserved, it exists in, you know, all mammals, but also is expressed in areas like the prefrontal cortex and areas that control cognition. So it's not, it's. And it's a, it's a novel mechanism of action. It's not one of the established mechanism of actions that target, that are targeted with current therapeutics.
[00:05:28] Speaker B: And how do you think about it in terms of the, the broader landscape of assets that are, that are being kind of pursued in this category?
[00:05:35] Speaker A: Yeah, so, you know, this is a very important question. In the space of social anxiety disorder and ptsd, that's the space that we're focused. There is Very limited competition. And I just want to take a moment just to talk about numbers here, because numbers are very important when we talk about competition just yet. The numbers are vast. At any time point, there are about 18 million based on valid epidemiological data that have been published and are cited by NIH websites, etc. These are not numbers that euphoria came up with. These are established, valid numbers. 18 million patients. 18 million patients suffer from social anxiety disorder at any time point for PTSD. The numbers are also staggering. There are about 10 million patients at any time point for both anxiety, social anxiety disorder, and PTSD.
The last category of drugs approved was approved 25 years ago.
And this, this is a category that is well established. SSRIs, they're antidepressants. They were approved for and developed for depression. And they were also positioned for other disorders such as stress, anxiety disorders and their use. But they do not provide, you know, the ultimate coverage for this patient. So there's a lot of unmet need just in. In. In, you know, in the instance of ptsd. About. It's. And that's very well, as these are very well established.
There are only 20 to 30% of patients with PTSD that reach remission in their symptoms using SSRIs. Now, the situation in social anxiety disorder is even more intriguing considering the demographic. It's a condition that affects young individuals, adolescents and young adults. The only thing that Is approved is SSRIs. Again, the remission rates are very low.
So there's very little about, you know, for these patients in terms of treatment modalities, patients that are in their prime, adolescents and young adults. And we're not talking about the regular jitters, okay? We're not talking the jitters that you get when you go on a date or when you go and deliver a speech in front of an audience or you play tennis in front of a competitive. In front of an audience. We're talking about a very profound fear of judgment that causes paralyzing anxiety and affects your quality of life. So these patients want to engage in anything they'd rather isolate. And this is what they do. They isolate. They miss school, they miss work, they miss the warmth of their family.
They miss the social interactions. These people want to have social interactions, but they're so profoundly affected by this fear of being judged that they're paralyzed. So this describes social anxiety disorder. And what do these patients do?
They actually isolate. They avoid. Okay. Social anxiety disorder is the number one cause of social isolation in young individuals.
And it's creating all Sorts of all sorts of issues. If left untreated, it causes a variety of additional psychiatric symptoms down the road. Depression, addiction, etc. If left untreated, suicidality increase. So it's, it's imperative that these patients have treatment options available to them. So what is available to them? Okay, let's say we have a patient with social anxiety disorder. They isolate, but they want to do something more. What do they do? Unfortunately, there is a lot of self treatment.
You know, they resort to alcohol. Okay, they resort cannabis use. So that's the first line. So first line is isolation. Second line is what can I do? I can seek psychotherapy, that's one.
Or I can self medicate. And you know, typically there is a little bit of both.
The next is seek medical attention. So people do not seek medical attention typically until there's a real impact on their lives. So they reach the doctor's office and they're put on, you know, most probably they're going to be put on an ssri and only about a fourth of these patients are going to respond to an SSRI. So there's a need for further coverage. SSRIs actually are chronic treatments. You know, they don't act to reduce your anxiety levels imminently. You have to wait for three, four weeks. And in this patient demographic there's a box warning for SSRIs for your audience that is very important.
They actually increase suicidality, suicidal ideation in younger individuals.
So imagine being a young individual with anxiety. You've exhausted, you're isolated, you know, you've probably tried to self medicate, you're seeking psychotherapy, you have your pharmacotherapy that is chronic and it doesn't work well. And it might make your, you know, make your suicidality thoughts, if you have any. If you're experiencing worse, what are your options?
Very limited. So if you try all these, typically you're prescribed a benzo benzodiazepine, you know, something like Valium or Xanax.
And that's not approved. But for the acute or as needed reduction of anxiety, this is kind of the last resort. And guess what? Benzos work. They really work. They reduce your anxiety levels.
But there are downsides to benzos. Very well known.
Benzos are typically prescribed also as sleep inducers. So they reduce your anxiety by affecting your gaming system and they actually put you to sleep. That's how they work. They reduce the activation of your cns. They put you to sleep. So not optimal. You have anxiety. And there's more. Okay, they make you drowsy, you Cannot drive.
You cannot go out and do your normal activities uninterrupted. You're foggy. So you cannot take a benzo and play competitive sports. You cannot take a benzo and go take an exam. Well, you could, but, you know, you're probably not going to do as well as you could have done without the benzo. And there's tons of data supporting all this. This is very well described.
So here comes BNC210. Okay, here comes BNC to 10. So what we're developing is a medication that can reduce the anxiety levels. And that's, you know, experimental phase. So we have phase one, phase two data, we're currently in phase three, can reduce the levels of anxiety as much as a benzo, but it doesn't make you drowsy, foggy. And there is no addiction potential. That's the major downside with benzos. Okay. And so far we've tried. We've, we've looked at this profile and we've asked psychiatrists to give us an opinion, and we build a, you know, a market assessment of, of the opportunity. And this is huge. This is considered in, from, in terms of unmet need. This is considered the holy grail. So what are we looking for, for social anxiety disorder that is not approved? Something that acts fast.
You know, this acts as, you know, as fast as 60 minutes.
It lasts for five hours because that's a half life of BNC 210. It doesn't make you sleepy, it doesn't make you drowsy. And so far there's no evidence of addiction potential.
So this is, this is, and, you know, if you think about the social interactions, you can plan around your social interactions. You know, when you're gonna go out and have an interaction, you can take it and within 60 minutes. So far, our clinical data show us that there is a sizable reduction in anxiety levels as reported by patients. Okay. And this also almost mimics the anxiety reduction that you get with a benzodiazepine.
[00:13:50] Speaker B: There's a lot of talk lately in psychiatry circles around separation from placebo. And I imagine that this is top of mind for you, especially in a phase three. I'm curious how you're thinking about that.
[00:14:00] Speaker A: Absolutely. Whenever you work in a medication, the first thing is separation from placebo. Just want to make a note here for your, for your audience, you know, very, very important in actual clinical practice.
We love placebo because whatever we do as is added, so whatever we give, there's a narrative effect of an expectation for a therapeutic benefit to patients.
I Just want to highlight. You know, a lot of people see placebo as the enemy. No, placebo is a friend. So there are two things.
There are two things about the placebo effect, okay? So at times we try to, you know, develop medications, okay, that produce marginal benefit.
Like one of my mentors, early mentors, told me to Peters, don't worry. If you're working on a good drug, the good drug is going to reveal itself.
So, you know, separating from placebo shouldn't be that hard of a task when you're working with treatments that are associated with substantial and significant benefit. Rule number one. So when you're not just trying to separate minor changes, then the placebo effect should not be an issue. But what if you're working on something that is adjunctive? You know, it's still useful, it's still a powerful treatment, it can provide benefit, but, you know, the treatment effects are not so profound. And they. They. The placebo effect might. Might create the noise and avoid the separation. That's where the art comes in. And every company has experienced people that manage and make sure that there is no placebo effect. And there are two elements of the placebo effect, okay? There's the element of the placebo effect as felt by the patient, okay? So the patient's expectations of getting better.
And there is the bias introduced by the raters, the physicians that are rating the patients.
So you have to have strategies in order to ensure that you're not cultivating an expectation to patients.
Don't advert over promise. You don't advertise.
You train your patients appropriately so that this is an experimental drug, and you might not be realizing any benefit. But you also have to train your sites, your investigators to make sure that the process is, you know, how they approach the patient, how they treat their patient. Your patient is.
Is appropriate. And expectations are not cultivated in terms of outcomes. The second thing for the placebo effect is focusing on the investigators themselves, okay? Focusing on the quality of the investigator, on the training of the raters.
And then there are some even more sophisticated ways that you can utilize in terms of the actual clinical trial design to filter out the potential for placebo effect.
All these methodologies have a valid scientific foundation, but at times, you know, have proven problematic. So one way is to have a period of time where you're just administering placebo and you're just excluding patients that are placebo responders. So that's kind of like a very traditional way of managing the placebo effect.
This works in some occasions. In some occasions, it does and there are some more sophisticated methodologies, both for psychiatry and neurology, to filter out placebo effect. So placebo effect is. I just want to recap for, for, for our audience. We love placebo effect in clinical practice. It's a friend.
The placebo effect is real. It's biologically driven. There's a way that humans respond emotionally and physically to the expectation of getting better. It's part of our nature. And in clinical trials, there is this. The placebo effect is related with kind of the, the power of the. Of. Of a drug.
Okay. How much treatment benefit it can introduce.
And you can control it by educating your patient not to expect improvement necessarily, but also training your investigators and applying methodologies to reduce placebo effect in clinical trials. So a very complex question, but thank you for giving me the opportunity to elaborate on.
[00:18:52] Speaker B: Yeah, certainly, I mean, expectation bias, certainly so hard to disaggregate, especially in a world where you only really have subjective scores to go on, as is true in most of psychiatry right now. I've had Sean Singh over from Vistagen on the show and he expressed some of the particular challenges, let's say, with working with the population and social anxiety disorder. I'm curious, like, how do you think about, like this specific population and the kind of accommodations required to design, know a great trial and compelling research in sad.
[00:19:20] Speaker A: So the trials in SAD very much depend on our ability to execute on a task that mimics a social interaction that is causing anxiety to patients.
So it is an artificial methodology, very well accepted, very well studied. So we try to ask patients to talk in front of a trained audience.
In the confines of a clinical site, you come in the doctor's office.
So we bring them in, consent them, screen them, and then we ask them to sit in front, like all the tests, sit in front of an audience and rate their anxiety levels over a period of five minutes, which actually a period of two minutes. We call it the anticipatory anxiety.
So we asked them to prepare a speech and we asked, how anxious are you now that you're preparing the speech? It is quite, quite taxing what we're asking these patients to do. And these are patients that are. They are suffering from social anxiety disorder. As you can imagine, this is a complex endeavor. You know, it's an experiment that has many moving parts and a lot of nuanced pieces.
So, you know, programs that are. And by the way, the FDA actually likes it. Okay. And the. One of the. I mean, I've talked to the FDA on more than one occasions on this and they consider it a very valid proxy to, you know, an actual social anxiety, social anxiety event. Okay. And it's as close as, as you can, as you can get. Okay. If you want to go a step further, it's mostly a performance anxiety, but performance anxiety is a key component of social anxiety. Okay. It's not the end all be all because social anxiety has this anticipatory anxiety. So the most like patients feel anxious because of the anti sympathetory anxiety mostly. And that's what triggers to avoidance isolations rather than the task themselves because ultimately they will isolate, do nothing or do very little.
So you know, there are two types of approaches. You have to be able to manage the anticipatory anxiety and have patients do what they need to do and get them out of their shell and back into the society. And if you don't manage anticipatory anxiety, that becomes problematic. And the second step is to decrease their anxiety levels while they're out there performing, giving a speech, playing a sport, attending a family dinner, etc. Etc. So there are two components in social anxiety disorder. So the most important element for all companies, us, VistaGen, everyone that is working social anxiety disorder using an acute treatment paradigm, because there are other treatment paradigms that are not based on the public speaking task that we're asking the patients to perform is consistency, consistency training and evaluation of the sites on their performance and training and retraining, controlling variants.
And you know, it's that the, the kind of the, the, the fine print in, in, in the site manual and the training that you provide and the consistency and the monitoring that you apply to sites that is somewhat the secret sauce in, you know, for success in social anxiety disorders.
[00:23:19] Speaker B: Yeah. When I, when I think about the, like the operational challenge ahead of running a very kind of consistent study in social anxiety disorders with, with all the kind of setup you've just described, it does sound like an operationally complicated behemoth to kind of manage.
[00:23:34] Speaker A: It is conceptually. I mean I don't want to pass the wrong message to the, into the audience, but it's not more complicated than an image imaging like a complex biomarker study or an imaging modality that has to be applied across sites with the same type sequences or procedures and process, it's just another process, another procedure. But it's the consistency, the training, the monitoring. Ultimately it's not that difficult, I must admit, ultimately it's not that difficult, but it's the know how that I'm pretty sure all the companies that work in the space have developed that makes it eventually a lot easier and makes it almost routine.
So as the field evolves and you know, if we're fortunate enough to have 1, 2, 3, 4, 5 medications for acute treatment of social anxiety as needed treatment of social anxiety disorder, this will become, you know, part of, you know, our, our toolbox. And it's not going to be, you know, that hard. It's not going to be considered that hard any, any longer.
[00:24:48] Speaker B: Certainly, I'm sure you all benefit from each other's work kind of training and reinforcing and.
[00:24:54] Speaker A: Oh, absolutely. I'm so grateful to, you know, VistaGen and the hard work that I've been doing, you know, all these years. And I'm grateful to, you know, bionomics and non euphoria that are taking on the task of addressing this huge unmet need. I've always, this is a huge, very prevalent indications. I hope that more, more companies are going to become interested in this space. You know, migraine has 20, 25, 30 drugs and it's a third, like a third or like half or a third of the prevalence of social anxiety disorder. So there is room, there's room for, you know, a lot of innovation here, A lot of innovation. So I mean my message is don't necessarily be fearful or question, you know, the complexity of the program. Yes, it is complex. Not more complex than any other clinical trial.
[00:25:52] Speaker B: I'd love to maybe change gears a little bit here. So you've painted a really compelling vision for why social anxiety disorder has such an unmet need and is so imperative to resolve. And you know, certainly you had other guests on the show kind of talk to a similar vision. How do you think about the next indication why PTSD as opposed to generalized anxiety disorder, for example?
[00:26:11] Speaker A: Yeah, yeah, I mean that, that's a, that's a very, very good point, Brandon. So actually PTSD was the first indication for BNC to 10. You know, I just want to be very clear and straightforward. The team even thinking about BNC210 preclinically, that's what they were gearing towards.
So we have a series of preclinical models that point towards not only a broad anxiolytic effect, but an effect on threat avoidance.
And threat avoidance is kind of the backbone of ptsd. Okay, so earlier days we had positive data in generalized anxiety disorder and in a panic attack model with robust responses. And we've actually done head to head studies with benzodiazepines. But the totality of the data, if you look at PTSD, supports the development of BNC210 in this particular indication. So.
So we have the. So PTSD is reliving your trauma every day. Reliving for your audience.
If you think about ptsd, it's like a daily burden of reliving a traumatic experience over and over and over again. You have flashbacks, nightmares, intrusive thoughts of this unfortunate event. We call it index trauma. And this index trauma can be domestic violence, it can be a car accident, it can be a death of a family member, can be a toxic work environment.
You know, there's no ending. It can be military engagement. There's no ending to what can trigger PTSD in patients.
Okay, so this particular trigger and this reliving of this traumatic experience also causes depression, cognitive issues, avoidance causes irritability, aggression, trouble concentrating, trouble sleeping. So PTSD has, Based on the DSM 5 criteria, 20 different psychiatric symptoms that are captured through this structured interview called the clinician assessment of PTSD version 5.
It's a complex disorder with a level of severity that's unparalleled for the patients that are suffering. With BMC210, we've been able to demonstrate, both with clinical and preclinical data over time, that we could actually improve all the clusters, all the four symptom clusters of ptsd. One is intrusive thoughts, the other one is mood, cognition, the other one is avoidance.
And there is a fourth one, which is a more general anxiety, irritability, aggression. There are four clusters and we have data to support that. BNC210 can actually provide symptomatic benefit and reduce the total symptom severity in these patients. So it's not just administering an anxiolytic, a broad spectrum anxiolytic, it's delivering a medication that has the potential to reduce a lot of the symptoms. And what we saw and was surprising, at least to me, some things I was expecting. I was expecting, you know, effects on intrusive thoughts. I was expecting effects on avoidance and, you know, of course, anxiety, yada, yada. But we saw a very good response to depressive symptom severity in PTSD trial, supporting the notion that there might be an antidepressant element to the mechanism of action. And it absolutely makes sense because if you look at the expression of the alpha 7 nicotinic receptors is expressed exactly in the areas that control mood in human.
[00:30:28] Speaker B: So there's a potential expansion like roadmap here without committing to anything across a broader range of psychiatric conditions.
[00:30:36] Speaker A: I'm just going to start with a very harsh realization here for your audience that small companies have to focus. And we have a one of a kind data set in ptsd.
This is the only data set with a novel mechanism of action that has shown clinical benefit in a large late stage, potentially registrational trial. Okay. Because attune is potentially registration based on our interactions with, with the fda.
The other programs are psychedelics, okay, A category of their own.
They have a role.
But we're talking about, you know, an outpatient approach with a novel mechanism of action. So this is what we have, is very important to continue developing because as we said, patients don't have options.
It's just a no brainer for us to continue our work in ptsd.
There is a lot of potential and opportunity in anxiety disorders. Okay? And the number, and the numbers are staggering. 30, 40 million. I don't know if the numbers are just out of this.
We have data in generalized anxiety disorder supporting, very much supporting the development of BNC210 in that indication. We have data in panic attacks supporting. But you know, our stronger data set and our largest data set is social anxiety disorder. And you know, we tackled social anxiety disorder because, believe it or not, other than panic attacks, where you measure the number of attacks and severity of attacks, it has some objectivity in the realm of subjectivity.
So for social anxiety disorder there is also a task and a development path that is different. And it's different in a methodological way, but it's also different in terms of timelines and costs. So the timelines and the costs for running social anxiety disorder are shorter. And for a small company with kind of specific funds to allocate which shows social anxiety disorder. I was not with a company when this choice was made, but I completely support the choice that the previous management over at Bionomics made to move so into the space of social anxiety disorder instead of going, let's say after generalized anxiety disorders, disorder or panic attacks. So we have an indication that is based on chronic administration, that's PTSD, which is your typical 12 week trial placebo controlled based on an established scale called CAPS 5. And we have another treatment paradigm that is acute, dare I say, a Tylenol for social anxiety disorder, which may be. I mean, I hope your audience doesn't miss interpret my, my optimism here. We're still in phase three, we're still experimental phase, but there's a good parallel. There's nothing out there. And the development path is what I call, you know, short and sweet.
Short and sweet and cost effective. So that's why we chose social anxiety disorder and ptsd. As a company. Yeah.
[00:34:08] Speaker B: You go where the, where the data is the clearest, where there's the most unmet need, and hopefully the development complexity is the lowest. There's a triangulation, I'm sure.
[00:34:16] Speaker A: Yeah, yeah. And huge market. Yeah. As you said, unmet need, huge markets, and no innovation for 25 years. Plus.
[00:34:24] Speaker B: You know, it's been said on the show a few times that it feels like we're in a psychiatry and neuroscience renaissance. I'm curious, like, what do you think is driving this. Why all this action today?
[00:34:32] Speaker A: Oh, I've always dreamed about this moment, Brandon. I've been a neuroscientist more than I've been a neurologist. I've been in neuroscience for 27 years. I've been a neurologist for about, you know, 20 plus years. And I've always, when I, when I actually was being trained as a neurologist, I mean, I always dreamt about us having more opportunity to peek into the brain.
You know, our toolbox is what is driving this renaissance.
You know, we have modalities, imaging modalities, biomarkers, clinical trial methodologies from a psychometric perspective, better scales, better awareness.
So over the last 20 years, my job as a, as a neurologist has become a lot better because.
And a clinical researcher, a. Because I have a better insight on the brain's functions and a toolbox that I can use to interrogate the brain.
So that is the number one reason why we have been able to do more in neurosciences and develop better experimental therapeutics and put them to the test.
So that's the number one reason the unmet need is there has always been. But 20 years ago, 25 years ago, we were not able to diagnose us correctly, to monitor us correctly, or to apply experimental methodologies to study the brain, whereas now we can.
So thinking where the future of neuroscience is going, it's the ultimate frontier.
And we still have a long way to go in neurology and psychiatry. Understanding the brain's function, the circuits, the complex neurotransmitter systems. But we're making strides.
And whether there is a future where we can look at machine human interfaces and whether we can think about the unimaginable in neurosciences and restoring neuronal function in different conditions altogether is going to be achievable or not, I think the jury's out. But we are in a very, very good trajectory with the work that is being conducted today.
I cannot help but being optimistic about.
[00:37:15] Speaker B: Certainly, it seems like every week on this show I have another conversation about better understanding how the brain works, how to image the brain, the moas, precision biomarkers, all these kinds of things, new techniques.
[00:37:26] Speaker A: I haven't even touched on precision. I have not like precision. We can perhaps have a separate standalone conversation on precision and how precision can really change the trajectory of drug development, where this is an area, I think, especially precision psychiatry, that we definitely need to spend more time looking into this.
Precision neurology has, I think, surpassed precision psychiatry.
The genetics of some of the neurological conditions have been more straightforward compared to the genetics for psychiatric conditions, and that have made the neurology space take a small step forward in the precision medicine paradigm for treating conditions. Whereas in psychiatry, we're still somewhat inventing the path forward. So I'm looking forward to a future where there's definitely more precision psychiatry because no patient is the same.
I'm not, I'm not a lumper. I'm a definite splitter when it comes to the pathophysiology of diseases.
[00:38:45] Speaker B: Absolutely. I'm sure, I'm sure this warrants a separate conversation entirely because I, I know in your background you spent a lot of time with the genetics of Parkinson's, which I'd love to have a conversation around as well. But sadly, we don't have the time for today. Where I'd like to close here is maybe to bookend things. I had Antha Shaker over at UPMC on the show, and he said that neurology and psychiatry are converging and you happen to have a dual background here. I'm curious, what do you make of that?
[00:39:09] Speaker A: You know, I, I, I come from a, from a family of physicians and, and scientists. So my father was involved.
I mean, he was a trained neurologist and psychiatrist. So back in the day in Europe, the concept was united and unified. It became separate over a period of, I think, 20 or 30 or 40 years where the concepts of biological psychiatry and other psychiatry approaches were separated. And I would say for the last 15, 20 years, everyone is acknowledging the biological basis of psychiatric diseases.
So this artificial bifurcation happened simply because there were two schools.
One that was a psychoanalytical school that believed that everything can be solved through psychoanalysis and behavioral interventions and medications and treatments belong to another camp.
So psychiatry was bifurcated at some point. And I strongly believe that everything is necessary. But there's no doubt that there is a strong biological basis for psychiatry. You know, the psychiatric diseases are like any other disease of the central nervous system.
And with this realization, there has been a reconvergence of these indications. And as professionals, I'm a neurologist, but I found myself fascinated by psychiatric issues that the patients, the neurological patients faced, and vice versa. I have a lot of great psychiatry colleagues that are interested and have devoted their lives in treating their neuropsychiatric features of neurodegenerative diseases.
So it's one organ, very complicated, that forms the foundation for both psychiatric conditions and neurological conditions. And these divisions are somewhat artificial for a good reason. But I think the convergence is real.
And I think neurology and psychiatry and dare I say, part of ophthalmology, the principles are very similar. And, you know, that's. That's why you see some neuroscientists working in ophthalmology, psychiatry, and neurology interchangeably. I definitely have had the privilege of doing so, but, you know, the future is conditions of the brain.
[00:41:46] Speaker B: Well, certainly with some of these additional tools that you described kind of underpinning the renaissance, I think the convergence is all the more compelling. The more we understand, the more we can bring these schools together. Well, Spiros, thank you so much for taking the time. You've been so generous with your insights and your storytelling here. Really appreciate you joining me on the show.
[00:42:02] Speaker A: Thank you very much. I appreciate the invitation and looking forward to joining you on another episode of your podcast.
