We work on a fundamental mechanism for brain health that clears insoluble metabolites, debris, and exoomes that are in between the cells, in between the neurons, the interstatial spaces of the brain. This clearance mechanism deteriorates with age allowing the deposition of metabolites that trigger inflammation induce a series of pathologies that are seen in neurodeenerative disorders including Alzheimer's disease. So Alzheimer's doesn't suddenly appear all over the brain. It happens in a step-wise manner. So in this area shown here in orange, the medial temporal lobe, that's the first place where plaques, tangles, and neurodeeneration occur. It takes about 5 years for the disease to get going and it turns into a self-perpetuating pathology that spreads first to the adjacent limbic areas and eventually to the entire cerebrum. It's a bit like a campfire that turns into a a wildfire. No other animal gets this disease and it always starts there in humans. So what is it about the human brain that allows this to happen and can we stop it? Well, it has to do with a housekeeping function, right? The brain clears the interstatial spaces by making cerebrros spinal fluid as the interstatial fluid. It doesn't have a lymphatic system. It does this instead. So it makes about a pint or half a liter a day in these four chambers shown here in blue. Right? The CSF moves slowly out through the brain picking up these metabolites and debris until it reaches the outer margins and the subacoid spaces around the brain. Now, depending on where it is in the brain in different neighborhoods, it gets rid of the CSF slightly differently. All right, the area where Alzheimer's begins here in the medial temporal lobe, right? It goes forward to the surface of the temporal lobe, then goes to the front. There it meets a rudimentary funnel made by the lateral olfactory strea and it follows that along. It follows it the alactory system down there and over here to right between the eyes and that's where it leaves the brain. Right? Separating the nasal cavity and the brain is this funny bony structure here called the cribopform plate. Right? It's got two little grooves there. And these holes or apertures accommodate the odor receptors that are picking up smell signals in the nasal sinus and they bundle together into cranial nerve one and they go up to the brain. They're oldactory bulbs sitting above there like two little sausages. Now around those nerves are little channels where that metabolite laden CSF is draining the other way. Okay, we looked at over 600 cribform plates in people and here's an age comparison. On the left, people under 55 and people on the right 65 and over. This is a heat map showing the probability of an aperture occurring in these people. And you can see there's a a much uh a reduction in that in those. There's a a paracity of the cribopform plate that really starts to deteriorate around 60 and then it picks up steam. So in effect what we have if you look at the gray bars these are people 55 and younger 65 and over and Alzheimer's patients all 65 and over right you notice it goes down so it seems the Alzheimer's patients are just farther along in this aging process than the other subjects okay so the effect of that is there's less CSF going through the cribform plate okay so the the CSF starts here in the medial temporal lobe right so this is the important area comes out of the ventricle goes to the front and it follows the alactory strea bulb and here's the cribopform plate it can't get through there the result is of that is less flow there's less flow in there there's less clearance and it happens gradually with age so there's less and less clearance until you hit a tipping point so what we have is really a plumbing problem and the straightforward solution isn't a drug it isn't cell therapy It's just to put a little shunt in there so the CSF can get out. So we do this as a minimally invasive outpatient procedure. It takes about 5 to 10 minutes to put it into a patient. So here in the nostril neurosurgeon makes a little incision. We put a guide tube up to the cribform plate. Then everything's done through the guide tube. They make a small hole. They put in the inlet up here shown in black. It's actually white but uh in there. And then that tube comes down there. They take the guide tube out and they connect the end of it to a flow regulator because we can't just have unregulated flow of CSF. There would be headaches and maybe infection. So, we put a little flow regulator. I have one that's made of anodized titanium. And this is it there. Right. This fits in and it goes under the mucosa. So, it's all inside the body and you get a slow drip drip drip. So it's basically enhancing this flow. Taking someone who's 75, it's not flowing very well, and taking it back to when they're 25 and it's flowing very well. So you're getting better clearance. So the patients were going to put this in first have something called mild cognitive impairment, right? It's the earliest stages of Alzheimer's disease. It's before the the the horses left the barn, before the pathology spreading. So the neurons in that medial temporal lobe, they're basically in a slew and they're trying to survive. One of the things they do is they sort of turn off their synapses. They don't put as much energy into synaptic transmission. The synapses are still connected. So if we put this in, suddenly the slew is cleared up. Those synapses should recovery. So we expect patients to recover cognition in 3 to 6 months, right? Versus the control subjects that are going to still stay bad and gradually get worse. So if we look a year later, we should be able to see what's the story, right? When we do a pivotal study probably 140 people alto together we'll also follow those subjects for another two or three years because those control subjects they get worse MCI and eventually they get Alzheimer's disease versus the people who got the device they're not only not progressing but they've probably gotten a little bit better in their cognition. So then we go to the FDA and we say we want a second indication for Alzheimer's. So first soon on we say well we want an indication for MCI and then later for that. So we've got our ducks in a row right we've done the manufacturing the FDA we've had discussions with our good friends at the FDA we've got the business development the clinical and we're getting ready to do our first clinical trial in January February 2026 it'll be in Palm Springs actually Rancho Mirage which is the wealthy part of Palm Springs. There's the uh famous Eisenhower Medical Center. Our chief medical officer just took over neurosurgery, in fact all of surgery at Eisenhower and um so we're going to do the first few patients there, the 15 patient uh pilot study and then once we've established after the first few patients, we don't have to do the whole study. We just have to show that that it's safe to put this device, how we manufacture it and clean it and sterilize it, safe to put into people. We can start doing our pivotal studies. All right, we'll do also another site in Santa Clara, California, which is the Bay Area. Maybe one in Houston, one in Vancouver, where I'm originally from. And then maybe one in Montreal. In Europe, in the UK, we'd like to do sites there, too. And also, we have a strategic partner we're developing a relationship with in Japan who will help us with that. Uh, Australia is also very friendly for for clinical trials and India and China as well. So, this is sort of our strategy. you want to get to 140 and 50, but it helps us to have more data in more places, particularly like Japan, you need to do a study on the Japanese population to uh to get approval for that. Okay. So, here's our here's our market. The total addressable market for Alzheimer's is enormous. So, here's 1, five, 10, and 20% adoption of this in the patients at that stage. Okay? And you can see it's billions of dollars here. But what we're really doing is tapping into a basic brain health mechanism. So we can use this for other things. We can increase the flow through of CSF for the debris that occurs in stroke maybe improve stroke. Normal pressure hydrophilis which is I I don't have time to talk to that but it's a CSF disorder. Frontal temporal dementia. Bruce Willis has this. If you noticed in the earlier one where I had the cross-section there was a little part of the green that comes from the frontal lobe up top. We think it's the anatomy is very similar. We think it's very related. And people with Down syndrome who have sort of a pugnose and dis misshapen cribopform plates, we think that might also benefit them. And then there's long COVID. Remember when you got COVID, you have the problem with the sense of smell. And some people the smell doesn't come back and they start to get cognitive problems. They can't remember things. They can't do things that are similar to early Alzheimer's. We'll find out in four or five years if a number of those patients start turning into Alzheimer's patients, but hopefully we'll be in the successfully in the clinic at that time. So, it's a potential market for our device. And then brain aging. It's such a small innocuous device. We could put it in other parts of the skull to sort of draw through increase CSF clearance in different parts of the brain. So, really, we've got multiple shots on goal with this. So, even if Alzheimer's is h it's successful, it's not great. Although, I'm pretty sure this is going to work. um we have other shots that we can do. Okay. So, right now we're we have money to get into the first two patients, but we don't want to run out of money in our first uh uh pilot study. So, we've got uh you know, we want to raise another $5 million to make sure we get through that. We have um we've raised 5 million. We've been very frugal about our money. Uh we have 20 investors, three billionaires. We have another two waiting in the wings. It may, you know, once we hit clinical trials, we have clinical data, it becomes a different ballgame. So, smaller investors might be priced out by those guys later on. But once we start having some safety data that our device is safe to put into people and we start we want to do the efficacy studies, um, we'll probably do a 20 to$50 million series B round. But that's that's kind of where we stand. myself. I was a PhD neuroscientist. Uh worked in a bunch of different places. Was a professor for many years in med school and this spun out of my academic lab. Uh our chief medical officer Jab Sadiki is MD PhD road scholar neurosurgeon uh very famous skullbased surgeon. He's been working with me on this project for a very long time. Our our third one is Ned Shadic. He's um an MBA, Harvard MBA, former hedge fund manager, ran four billion dollars for Putinham Investments before it was acquired. Then he retired and he's sort of working on a fractional basis with us. But uh that's sort of us. I'm here for the rest of the conference. If you'd like to chat with me, I'm available. Love to chat with you. Thank