Revolutionizing Lyme Diagnostics - Episode 341

he tested negative for Lyme in our first doctor's appointment because that was one of the first things that I thought of based upon his lifestyle. He was always outside. He was in the woods, multiple tick exposures, but tested negative and then went on to really receive a diagnosis of early onset Alzheimer's disease.

Welcome everybody to this edition of the Gladden Longevity Podcast. I'm your host, Dr. Jeffrey Gladden. And today I'm going to be joined by two really interesting women, Nicole Bell and Dr. Jennifer Miller. And they are actually cracking the code on tick-borne tick-borne illnesses and Lyme disease. If you have any interest in tick-borne illnesses or Lyme disease, you're really going to want to listen to this. They have a new diagnostic that they've developed that's, I think, a real game changer in this space, and I think you're going to be very, very excited to hear about this.

He went from saving hearts as a cardiologist to rewriting the entire aging playbook. Dr. Jeffrey Gladden believes 100 is the new 30, and he's got the science to back it up. This is the Gladden Longevity Podcast.

All right, Nicole and Jennifer, welcome to the Gladden Longevity Podcast. It's good to see you here.

Thanks for having us.

Yeah, good. So you're in the middle of some pretty interesting work over there in Raleigh-Durham, North Carolina. Nicole, do you mind just kind of introducing yourself a little bit in terms of what you do? And then Jennifer, maybe you can do that as well. Then I'm gonna have you share with the audience kind of how you got into doing what you're doing currently. So maybe we'll go with that.

Yeah. And I can introduce how I got into this as part of my introduction, 'cause it's really core to why I'm here. So my name's Nicole Bell and I'm the CEO of Galaxy Diagnostics. We are really working to create a new standard of care for flea and tick-borne pathogens and diagnostics. And, um, I have a long history. I'm an engineer by training, so material science and biomedical engineering. I've worked in medical diagnostics and medical devices for the second half of my career, always kind of in young growing companies with new cool technology. And I got interested in the tick-borne space for the reason that a lot of people do, when it hits you personally. In my case, it was— yeah, it was— in my case, it was my husband. He started presenting with a lot of mood-based symptoms, depression, anxiety, irritability, and rage. And then eventually I realized that he was also having significant cognitive cognitive issues. And we went to the doctor. He tested negative for Lyme in our first doctor's appointment because that was one of the first things that I thought of based upon his, his lifestyle. He was always outside. He was in the woods, multiple tick exposures, but tested negative. And then went on to really receive a diagnosis of early onset Alzheimer's disease.

Oh wow.

Which was—

oh yeah.

What age was he at?

He was 59 when we first started and 60 at the time of diagnosis. He's a little older than I was, but still otherwise in perfect health, um, doing all the things you're supposed to do for brain health and longevity, but declining pretty severely. And to make a long story short, it was another 15 months before we returned to tick-borne as a potential root cause, at which case I found out that he was not only positive for Lyme disease, but also for two common co-infections, Babesia and Bartonella.

Right. So tick-borne, right? Yep.

And so he— his journey didn't end well. I mean, he was in late-stage disease at initial diagnosis, and so we treated, but it was really quite a long gap between the onset of his disease and us realizing what the root was. So he ended up passing away in January of 2022. Oh, wow. Yeah, thank you. It's— I think a lot of people don't realize that tick-borne illness can have some pretty devastating effects when misdiagnosed and progressed.

Inflammation gone wild, right? And I'm sure that the neuroinflammation that comes from tick-borne illness, there's some interesting genetics around that also as to who's susceptible and who isn't, right? I grew up in the East Coast and I'd come home every night and my mother would pull the ticks off me and we'd go eat dinner. You know, it was that kind of a thing, right? So not everybody that gets a tick bite is gonna get Lyme, Lyme syndrome, let's call it. So yeah, but it's, it's certainly, uh, if you get a really big systemic full body inflammatory process like that, it'll accelerate everything. It'll accelerate heart disease, dementia, cancer, you know, you name it. Everything is, everything is fair game at that point. So yeah, that's interesting. So you went through that whole process and then obviously it had an impact on you.

Correct. And it was one of those experiences that you, you can't just go back to your normal life. It was really pretty altering and As I said, I'm an engineer. I've always worked in startups and small companies, and I was like, there has to be a better solution out there. And so, you know, we have the current standard of care is a 30-year-old test, right? There's got to be better solutions. So I started researching what was going on with different specialty labs and what was in the universities, and I came across this company called Galaxy, and I just really liked the approach of of not relying upon the immune response, which is, as you said, is complicated and, um, and can vary and is also delayed and misses early stage infection. And, um, Galaxy was really focused on direct detection and looking for markers, biomarkers, or DNA for our different tests that really show whether or not the pathogen is present. And so I called up the founders and got to know them a little bit, and then eventually realized that they had the science that I was reading in the research literature was there, and I— but really needed some help on the commercialization and strategy side. And so about 2 years ago, I helped figure out how to scale the technology and then became CEO. And one of the reasons that brought me to the company is the, the woman that's here with us today, Dr. Jennifer Miller. I mean, what you talked about, about the immune response, she literally did her PhD thesis on Borrelia and how it impacts the immune system. And so her expertise and that of, you know, the company and other founders was really what drew me because I, I believe strongly that science is going to provide the answers to these problems. And, and her expertise has really been quite impactful.

So Jennifer, let's switch over to you. That's kind of a natural segue there.

Yeah. So as Nicole said, I'm Jennifer Miller. My role is I oversee clinical and scientific operations at Galaxy. So I run the R&D laboratory. I also run the CLIA laboratory. And my background, I'm an infectious disease PhD by training. As Nicole said, I did my doctorate on Borrelia burgdorferi. I did a postdoc studying both the immunology and the genetics driving the host response to Borrelia. And I've spent pretty much my entire career tackling this problem. Understanding the dynamics between this pathogen and the immune system. And at Galaxy, I've really focused my efforts on being a translator, taking the innovations and the great ideas that come out of universities and translating them into commercially available diagnostic assays. And my time at Galaxy, I've launched 7 now, 7 different laboratory-developed tests, you know, some for Lyme, some for Borrelia, I mean, sorry, Bartonella, and some for Babesia. And we really, as Nicole said, wanna change the standard of care and and develop better tests so that providers and patients can get better answers.

That's, I mean, that's fantastic, fantastic work. Let's give the audience a little primer on Lyme and why it's so difficult and why it hides and why it's difficult to detect. And just walk us through that. Maybe give us like the 3, 4-minute synopsis on kind of where we started with Lyme and how we got to this.

One of the first things that is unique about Lyme is it's a spirochete. And Lyme spirochetes in particular don't like to hide out in the blood. So one of the first things they wanna do is get in and then they wanna escape. They wanna go and they wanna burrow into tissues and, and hide. And their morphology as spirochetes allows them to corkscrew, burrow in, and hide. And that allows them to do a couple different things that are very important for understanding Lyme, but also for the focus of, of our session here. It allows them to evade the immune system. But they're also going to cause destructive pathology. You know, imagine this burrowing into, you know, the tissue of the joint or, you know, in the brain even, you know, and, and all the damage that that causes. And so really this is how the pathogen plays hide and seek with the immune system. It doesn't produce destructive toxins. It, it doesn't do the things that you think about if you think about, you know, somebody with strep throat or a staph infection. Or, you know, people that are, that are dealing with things that are toxins like anthrax. It really causes damage in its ability to confuse and manipulate the immune system. And because the immune system gets confused and manipulated, patients develop inflammatory pathologies that are very, very debilitating. And, and even when the pathogen is gone, it can be very, very difficult for patients to recover.

So it's a really interesting situation, right? So you've got this spirochete, it gets in, it's burrowing into the tissues, that's causing local damage, which in and of itself is releasing, let's say, cytokines and debris into the, into the system, which is going to cause local inflammation, but it's also going to, the immune system is going to react to that also, right? So you're going to be spooling up sort of whole body systemic inflammation just from the burrowing process, right?

Correct. And as you, as you alluded to, you know, the stirring up locally and then expanding systemically, you end up with these, we call them feedback loops where one problem feeds upon another. And what happens is the inflammation signal amplifies and now the damage is, is becomes even more widespread, unfortunately.

And I think there's also two other things that I'd like you to comment on. One is, so you've got all this mayhem being wrecked. And then you've got an immune system that's pulled into this, and it's also— it can't find the spirochete, but it's also getting pulled into it in a way that is kind of exacerbating the inflammation, right? And then there's a genetic predisposition for people that are more prone to go down that path than people that are more prone to resolve the inflammation. Could you talk to us a little bit about how the— how the immune system gets sucked into that in the first place, and then the genetics around why some people have a persistent response? Sure.

With the, with the immune response, one of the first things that happen, okay, from a— you think about pathogen defense, okay? So when, when the spirochetes are transmitted, the cells in the skin are defective in their ability to respond. So right out of the gate, the spirochete gets in, it's in the skin, it gets into the circulation, it goes to the tissues, and the body says, okay, I see it, and it tries to make antibodies. Well, the Borrelia interfere with the follicles of the B cell and so the germinal centers are weakened. And so right out of the gate, the antibodies that are produced are either fewer or there's a lot of them, but their specificity and stringency aren't as good. And that's why patients are either delayed in making antibodies. Some patients never make antibodies, but other patients have this hyper IgM signature where all they're making are IgM antibodies and they're making a ton of them. And then that creates a destructive loop because you've got IGM antibodies in the periphery. So now all the T cells that, that talk to the B cells are gonna produce what are called helper T cell 2 type cytokines. And those cytokines drive inflammation. And so you're skewing the immune system away from cytokines that can be deemed protective, things that, that people have heard of like interferon gamma, IL-12, and now you've got IL-4, IL-6. You've, you've got, you know, chemokines and cytokines that are, that are telling the immune system react with inflammation. And in certain tissue sites that can cause production of other things that are feedback amplified and damaging, like type 1 interferons. And the reason I bring that up speaks to the genetic component that you mentioned. And it turns out that there are people that have variability in their IL-6 promoter genes, which are gonna make them more prone to inflammation. There's been a lot of studies done in mice that are starting to be recapitulated in people that certain people have genetic predisposition to hyperinterferon activation. And, and a place where this has been seen is obviously with viruses, but also with things like rheumatoid arthritis. And so what I used to tell people is an easy way to think about it is, is Borrelia does damage by tricking the body into thinking that it's having an autoimmune response. And of course, autoimmune responses can be very, very destructive and In people, there are immunological and genetic drivers that unfortunately do predispose some people to being more susceptible to these types of infections. And we're now understanding that people that are, that are more elderly are more susceptible. Women that have had hormonal changes, perimenopause, postmenopause, tend to be more susceptible. And so there's a lot of things that happen genetically, immunologically, environmentally that can take this pathogen that, that was already a problem and, and it's just feedback amplifies the damage and destruction.

Right. So it's kind of like the spirochete gets in and then is attacking these B-cell centers, which are kind of your ammunition, you know, correct, distribution and production sites. And now you're making bad bullets and then you're blowing up stuff in the, you know, just randomly in the air, right? It's not really targeted.

That's a good analogy.

You got fireworks going on and then the body's reacting to that, right? And so it's, it's kind of this chaos that develops So with, with all that chaos, there are genetic predispositions that predispose and potentiate those responses so that people end up in this really very dark situation, Nicole, kind of like your husband, unfortunately did. And then there are other people that are able to resolve this also, right? That, that can resolve it. Talk about, talk to us about resolving it. How does it actually get resolved in the people that do resolve it? Because not everybody ends up with, with long-term Lyme, right? And it was a 20% post— with something like that, 25, somewhere in that neighborhood.

So absolutely. But part of what, what helps with resolving is timing. And Nicole alluded to this. It took a very, very long time for Russ to get an accurate diagnosis and the clock was ticking and the damage was done. So I always tell people the first key, your best shot is getting an accurate diagnosis quickly. In order to have that, you have to have an idea that you have Borrelia and not Bartonella, Babesia, the flu, COVID. And you have to catch it early. And so if you catch it early, within the first— varies from person to person, but certainly the earlier the better, within the first couple of weeks even. And you can have appropriate therapy. For some people, it's antibiotics. For others, herbal regimens work. And you buy your body time to mount an immune response in a supportive environment, and then you're capable of mounting that immune response, right? Those that resolve it will, will mount an effective, specific antibody response, okay, that, that allows them to develop the antibodies that are needed to help clear the pathogen. And because they don't get these danger signals amplified, either due to delay of diagnosis and treatment or genetic predisposition or environmental issues, they will go on, you know, and, and clear the infection. Exactly. But, but the problem is And you caught it in what I was saying, there's so many if-then statements there, right? The system is rigged.

Yeah.

Well, and I think somebody, I mean, somebody like my husband too, I mean, he, it wasn't like he just recently got a tick bite and then he was diagnosed with Alzheimer's, right? He had likely had this pathogen on board for over a decade. And, and finally, you know, the compilation of Borrelia, you know, Lyme, Babesia, Bartonella, he also had heavy metal toxicity with high levels of lead and mercury. And so all of these confounding factors kind of built over time and led to this chronic disease state. And so even if you don't have a genetic predisposition, the other exposures, the other pathogens, the other environmental toxins can all build to create a perfect storm, you know, per se, to, to really cause some pretty significant issues.

And sometimes it happens quickly and other times it's, it's sort of death by a thousand cuts, you know. You'll have something and you're a little bit immunocompromised, and then you get something else, and then all of a sudden, wham.

Yeah, that's a good analogy, death by a thousand cuts. You know, it's interesting, when we think about diagnosing it, we're typically looking at serology, right? Like, what antibodies are present? Is it IgM? Is it IgG? We're not really characterizing the quality of the IgG or the IgM, right? But we're looking at the levels of those. And then there have been people that have tried to look for spirochetes and things like that, But you've developed something that sounds like is a bit of a game changer in terms of being able to accurately not only detect Lyme, but the other tick-borne pathogens that we've rattled off here and sort out that, that soup right from the get-go, which I, you know, once you have the precision of that, then all of a sudden the way we think about it in general is you have more leverage on the situation to be able to go after what you need to. So walk us through the diagnostics that you've developed that enable you to have that precision. And then based on the findings of those diagnostics, what become the changes in the therapeutic approach? Because it's not the same for everybody, right? So, yeah.

Well, I'll start and then Jen can jump in. I mean, the first thing is, yes, the current diagnostic standard of care looks at antibodies. And as Jen so eloquently put, that's super complicated, right? Because it depends on the individual and, and what other exposures they might have. And then the other issue is, is that as she mentioned, Lyme doesn't like to be in the blood, right? So blood isn't necessarily the best sample. And so the microbiology of these pathogens really matters because they're stealthy, they're tricky, and so what you're going after is important. And so for Lyme disease, for Borrelia, what we do is a completely different approach. So instead of looking at blood, you know, if you look at the microbiology of the pathogen, one of the things that it does is it's constantly shedding surface, you know, part of its cell wall. So either proteins or, you know, components of the structural cell wall into its environment. And over 40% can be shed when the cell divides, right? And so that gets left into the environment in various forms. They actually get cleared, a significant amount gets cleared by the kidneys and aggregates in the bladder and excreted in urine. So the approach that we take is very different. We're actually looking, we use urine as a sample because this is a great matrix and there's been a wealth of information that shows this is useful for diagnostics. And we concentrate it and then use that, those, you know, those biomarkers and detect them in the urine to determine whether or not the pathogen is present.

So it sounds like you're almost looking at the proteomics or something analogous to that, right? Uh, in terms of what, what's being released from the organism. You know, we, we use proteomics and transcriptomics and things like that in other parts of our practice, whether it's related to, to cancer or even in the aging process, there are things we can learn there that can be very helpful. So it sounds like in the place that you're working, you've decided, look, antibodies aren't really gonna help. It's hard to actually see or find the spirochetes because they basically have burrowed in like, uh, you know, like moles underground. And yet at the same time, they are shedding proteins that are specific to them or structural components that are specific to them. And you can tell me what structural components they are or whatever, but from that, because it's aggregated in the urine, you're able to go in and detect their presence that way. Can you get from that, can you get a sense of how severe the infection is? Like, what is the concentration of these guys? Is it, does it correlate that as well? Or does it give you, you know, there's, there's different kinds of Lyme also, right? There's different kinds of these diseases, right? And so can you, how fine, how fine can you get here? Can you like, say, oh, well, this is this version of that and this is how much we have, or, or, or is it more qualitative, or how do you see that?

So generally the tests start out qualitative. However, with continued work and research and clinical validation and clinical utility, you certainly have the potential to measure, let's say, the amount that's being released.

Mm-hmm.

Then the question becomes, how does that correlate? Right? You know, how much, how much of what you're detecting, let's say in the urine, how does that equate to the, health and immune status of the patient, how does that equate to, you know, and the burden.

What's the burden?

Exactly. Where the burden is other places in the body, right?

Mm-hmm.

Is something that can be looked at. It's, it's just a bit trickier in, in people. Certainly in mice, and I would never argue that a mouse is a human being, but certainly in mice, there's, there've been studies that have shown that you can detect, you know, Borrelia proteins and at times active Borrelia in the urine. And from a qualitative standpoint, what we used to do experimentally when we were doing mouse studies is sort of the more you have is sort of indicative of the more, you know, the higher the burden someplace else, right? Because it was being cleared. But in people, that's tricky because you'd have to, you'd have to have some way to equate what's in the urine with burden elsewhere when you're talking about tissue sites that are perhaps difficult to sample and, and you can't really measure them in the blood per se. And so that's why it, it, it's tricky. Yeah. But, you know, as, as work evolves and we learn more about you know, and you brought it up, proteomics, transcriptomics, we learn more about the signature of the pathogens and what that might mean. We certainly might have the ability to kind of correlate, you know, the amount of, let's say, a particular pathogen signature with something that might tell us more about its burden or at least its activity in a particular tissue. And certainly there are people doing, doing work on that, but those studies are at this point in time, preliminary.

So do you do any genetic testing on the people that you're testing also? In other words, you end up connecting the dots on, we're finding this in the urine, we're seeing these organisms, we see genetically they're predisposed to this kind of response. Is there something where you're putting those pieces together to come up with a therapeutic recommendation like, this person would benefit from the following?

We are not, but, but others in the field are gathering that information. You know, there's definitely some very nice research and clinical trials going on where, where people are sampling and, and looking from a research perspective at what is present and then correlating that back to, you know, what's going on with the host. You know, how is the host feeling? What else do they have going on? You know, one study that comes to mind is the Maestro study being run out of MIT. It's taking this type of approach.

But in terms of treatment, you know, the, that's an important distinction too is, you know, Borrelia and Lyme is not the only thing that ticks carry, right? And so the other thing that's important to understand is these co-infections. And so again, the microbiology matters. And when we look at common co-infections, so we have another test which is bloodborne because some of the other pathogens are in the blood, albeit in low quantities, right? So you still need to use advanced techniques, but blood is a suitable matrix. And so we have other testing which— where we have a multiplex test for what we call the 3 Bs. And so it's Borrelia, Bartonella, and Babesia. And you might say, well, why Borrelia? You just told me that it's not in the blood. But that's Lyme Borrelia. Actually, relapsing fever Borrelia can be in the blood. And so generally when we pick it up, it's going to be a relapsing fever, not because we'll be able to pick up a Lyme Borrelia if it's in the sample, but just odds will say that, you know, that's less likely with Lyme disease. And so we have tests that look for those pathogens, and that's important because the treatment for Babesia— and then going back to your treatment question— the treatment for Babesia is completely different than the treatment for Lyme disease, right? Babesia is a parasite, and the treatments are more like what you would see in malaria. And so it's very important to understand what's on board.

Well, and even with Bartonella, the combination of antibiotics that you would use is, is going to be different, different most of the time than what you would use to treat Borrelia also. So as Nicole said, it gets very nuanced.

Yep. And I think one of the problems that, that certainly patients face, but also clinicians face is only getting partial information, right? Because you've gotta, I mean, if you can get your arms around really what's going on, you can basically start to treat things in an effective way. So I guess it comes down to the recommendation for the testing. So if, we were going to do testing, would we basically do both the urine collection? And one question I had was whether that was a 24-hour urine collection or whether it was a spot urine. But are you doing the urine collection as well as the blood at the same time to make sure that you're getting your arms around what's there? Or how do you guys think about that? Because time is kind of— yeah, important here, right?

Yeah, we would recommend doing both the urine and the blood-based test, right? Because urine will tell you the status with Lyme, and then the co-infections would be covered in the in the blood-based test. It's not a 24-hour collection, it's a single collection for the urine and, you know, in one tube for the blood-based test. And then we also do some serology testing here specifically for Bartonella because we have a lot of experience with that pathogen. And so, well, you know, as a lab, we bundle together our offerings to make it make sense. But I think there's evidence in the literature that you can do other pathogens in urine, but that's a little bit further along. So I think over time we'll expand the opportunity on both the urine side and the blood-based side by adding more pathogens and more testing that provides additional color.

So another question I would have is, and you may not be doing this, but it seems like the other piece of the puzzle here would be to understand what's the status of the immune system.

Yep.

Right?

Like what are the cytokine levels? What are, you know, what's going, how was the IgM? What, what are the antibody levels? Right, for that matter, right? It seems like all that would feed back together into a more cohesive whole. Is that so? Are you doing all of that testing too, or are you— we have to go elsewhere to get that and then marry it up ourselves? How does that work?

So right now we're not doing that, but definitely one of the biggest directions we want to go in, in the near future, because we want, we want to be able to provide information that, that covers both the pathogen and the immune system within a single sample, at a particular unit in time.

Yeah, I see a real, I see a real commercial value in that, Nicole, as you know, because this, you're commercializing this. But really, one of the problems in medicine, quite honestly, is that there's a lot of friction in not only the getting of the data, but then the integration of the data, right? So if you, if you can go to a place where you can get everything that you're, you know, 90%, 95% of what you need in one fell swoop, that's very appealing. For people, right? And it's very appealing for patients, right? Because it's like, oh, I can go here and really get this sorted out. I don't have to piecemeal my way through whatever, right? So it's, so that's your trajectory, it sounds like. Uh, is that— it is. It is.

This has been Dr. Jen's dream since her PhD thesis.

All right. Well, Jen, I'm just catching up to your dreams now. So, okay.

Yeah. Well, that's very cool.

It's very cool. It must be very exciting for you to be doing this. You're clinically available now. Is that correct? —these tests are CLIA-certified? They are. Yeah. Okay. Yeah.

So we have a CLIA laboratory. We're based in North Carolina. We regularly work with providers to provide information, and we've got an active R&D program that's, that's going. So there's always new things that we're working on and, um, and developing. Jen's team is fantastic. Yeah.

No, I can tell. I can tell.

Yeah. And a key part of what we do, and Nicole alluded to it, is, you know, we have a very, very good VP of sales that's very good at reaching out to our providers and soliciting feedback from them because we really want to be responsive to the market. We want to develop tools that providers actually want and need and can use, and we want to learn from them so that we can, you know, refine, iterate, improve, and really better understand, you know, how to get them the information that's needed in the timely fashion that they needed to be able to make a decision.

So speaking as a clinician, I'll tell you what my take on that would be. Would be if I can go one place and I can actually, you know, understand what's in the system, right? Then I can understand how the immune system is responding to it. Then I can also understand what's the genetic predispositions for this particular individual, where are they particularly vulnerable? And then out of that, I can get what I will refer to as nuanced recommendations about doing this in this sequence, or these are the things that are likely to calm the nervous system, or not the nervous system, but the immune immune system while we're going after the, you know, the pathogen itself, that kind of thing. Putting that together into a system is really very appealing as opposed to just data points, right? When you can integrate it into a system and a thought process with a sequence of steps, then that's— and you're probably, I'm probably repeating things you talk about all the time, but I'm just catching up to you. But I can just tell you in the market, because this is really a quagmire. With Lyme. You know, people chase their tail on it all day long, quite honestly. If we had something like that, it would be, it'd be massively helpful.

So yeah. And I think the piece that's been missing to pulling that all together is the direct detection, right? Because, because the immune system, because it's telling you exposure and not active infection, it's too hard to untangle that web if you don't know exactly which pathogens are on board. And so That's why we're kind of starting with the accurate direct detection, making sure those tools are great. And then, but as we've talked about over time, we absolutely intend to kind of layer these things on so that we can expand the clinical knowledge and provide those tools to providers.

Yeah, that's super exciting. So right now, do I understand that you have two tests available, a urine test and a blood test? Is that, or is there more?

Those are for direct detection. And then we also have Bartonella serology for the top four most common species of Bartonella. Which is way more common. We haven't talked a lot about Bartonella, but it's way more common than I think most people think, just because the vector, the number of vectors that it has and the exposures, like, we're talking about ticks, so obviously they're one vector.

What are the, uh, what are the other things that— how else do people get Bartonella?

Yeah, so if you Google Bartonella, right, you come up with cat scratch fever, and that's the acute form of the disease. But just like in Lyme, not everybody gets that really strong acute reaction when they first get infected. And Dr. Jeffrey Gladden really has showed, and over the course of his, you know, decades doing research on this pathogen, is that a lot of people develop these complex chronic symptoms. And, and just like what I talked about with my husband, some people may have the pathogen on board, but it doesn't become an issue until they get another infection or they get something else going on. It's kind of one of those opportunistic infections that can flare and buddy up with these other pathogens and cause some major damage. And it's been associated with a lot of mental health issues. So over at NC State where our founder is, they've done studies that have shown the linkage to schizophrenia and psychosis, and it's been linked to PANS/PANDAS in kids where they have serious OCD and sometimes violence and rage. It's, it really, again, you know, it can wreak some havoc with cytokines and inflammation and in it, all three of the pathogens that we work on cross the blood-brain barrier. And so they can have a real impact on mood, cognitive state, and behavior.

It seems like one of the common denominators in all that related to the neurological findings is really the neuroinflammation, right? The brain inflammation. Yes. Yeah. And then that affects people different way, whether it's rage or OCD or, you know, ADD or what, whatever it is. So do you guys in your, you know, scope of what you're building, do you see yourselves starting to look at inflammatory markers also that are associated with brain dysfunction, or is that part of it? Yes. Yes. Okay, great. Yeah.

And obviously, I mean, Alzheimer's is near and dear to my heart because of my experience with my husband. And I think— and we just see that some of the most difficult cases, there's that neural inflammation piece. And so, and, and honestly, just as a follow-up on my husband's journey, I, I donated his brain to science, and I now have images of Borrelia in his brain as well as PCR evidence of Babesia. And so there's real science there that's been emerging over decades, and I think it's going to help a lot of people when we can pull all these pieces together.

Absolutely. I mean, it might— there might have been Alzheimer's, but there was a lot of things potentiating it, right? It's kind of the toxic burden that we're talking about. The toxic burden builds up to a point it overwhelms the physiology's ability to compensate, and then, you know, next thing you have disease states, right? So Well, congratulations on the work you're doing. It's spectacular, quite honestly. I mean, we've been waiting for breakthroughs in this area. I will say that the last person we had with Lyme or with tick-borne illness came to us with alpha-gal, actually, which you may be familiar with, right? So it's a young Alabama athlete, a woman who went to a summer camp and then got a tick bite and then ended up with alpha-gal and then had to drop out of her track scholarship because, you know, accelerated heart rates and anxiety and, you know, all kinds of stuff. So we were able to kind of, you know, deconstruct that for her. We didn't, quite honestly, didn't know a lot about Alpha-gal when she came to us, but we kind of go down the rabbit hole on things and we were able to figure it out. And now she's back, you know, doing quite well, starting to, starting to run again. But it takes, it takes kind of a really concerted integrated effort to figure these things out. It's not just like, I don't know, a strep throat and you give, you know, an antibiotic and pretty much done, right? It's not like that at all. It's very, very complex. So, well, it's beautiful work you're doing, Jennifer and Nicole. I see your, your contribution as well. So good stuff. How do people get a hold of you? Where do they find practitioners and all that sort of thing? Yeah.

So the best place to start is our website, which is galaxydx.com. Um, and we have a lot of information. You can sign up with an account, but we also have a clinical learning center, which is really geared towards providing a lot of tools. I mean, we're really through our partnerships with a lot of our university collaborators, we're really on the front lines of the emerging innovations in the space. And so it's a great vehicle for people to stay up to date, to get basic training of kind of what these tick, tick-borne pathogens can do, like what signs and symptoms to look for, you know, the specifics of when to think one pathogen for the other. Those are all available on the Clinical Learning Center. And we also have patient resources for people who are interested because as I think we know in chronic illness, a lot of times the patients have to take such an active role in in their own health journey because the solutions are not readily available.

Yeah, absolutely. Which we're working to change. Yeah. And you will. And you will change. You're well on your way. All right. Well, great. Well, thanks so much for spending time with us.

Thank you. Thanks for having us.

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