Great to be here, and great to see you. So many people here, actually. So our mission here is to make it possible for Alzheimer's patients to live an independent and active life. We have about 50 million people in the world living with Alzheimer's disease today, and we're expecting this number to double over the next 25 years to about 100 million. Of course, this comes with an enormous burden to society, but also with an enormous cost. We're estimating the cost currently for Alzheimer's disease to be about $1.3 trillion, representing about 1% of the global GDP. Obviously, the market is also growing. What we see is a CAGR of 8%-12%, and we have a potential of about annual sales in the excess of $12 billion for a true disease-modifying treatment. So what are Alzinova? We're a Swedish biotech company. We're based in Gothenburg, founded in 2011 as a spinout from the university. Anders Sandberg, one of the co-founders, is still with the company as our CSO. We believe we have a very innovative science and an IP technology that makes it possible for us to make disease-modifying treatments for Alzheimer's disease. We have two different candidates. We have a vaccine or an active immunization called ALZ-101 that is Phase 2 ready. We also have an antibody, ALZ-201, towards the same target that is in the preclinical stage, and we're planning to take this into the clinic, pending financing, of course. We're listed on Nasdaq First North. I'm going to start with this one. Just to talk about one of the advantages we have with our potential treatment. The treatments we have on the market today, the first two disease-modifying treatments, actually, for Alzheimer's disease, require IV infusions, and the patients need to come into the hospital or the clinic about 26 times or biweekly to get these injections or infusions. It takes about an hour, and the cost for society here is about $15,000, excluding the cost of the drug. With our treatment and what we see from our Phase 1b data now, it's, of course, a vaccine, so we will only have a simple intramuscular injection together with an adjuvant. It takes 10 minutes. We need to do it three times a year, and it can be done at home in a clinic by any primary care setting. The cost for this will be 2% of the cost for the other treatments, right? Now, of course, I need to mention that there are subcutaneous injections available now with Leqembi, for instance, and however, this comes after 18 months of IV infusions, and it's going to be weekly treatments. So we still have an enormous advantage here, of course. So our business model is based on the fact that we are going to develop this, of course, to show efficacy, safety, and tolerability in patients with Alzheimer's disease coming up in a Phase 2. We are planning to partner with big pharma, preferentially, of course, before the Phase 2, and this is something we're working really hard on. Our income is a classic model: upfront milestones and royalty payments. So what is it we're doing? Some of you might be familiar with the amyloid beta pathway, where the current treatments that are on the market are active. We have amyloid precursor proteins that, for some reason, start to aggregate in the brain. These are called amyloid beta 42, and they are accumulating as insoluble stable plaques in the brain. These plaques have been known for 100 years. We know that they are part of driving the disease, but we don't know how important they are. Now, there are many other types of amyloid beta 42, and it's been shown for the last 10 to 15 years that there's something called A beta 42 oligomers that are really toxic towards the brain. We have shown this in cell extracts from Alzheimer's patients and put that to neurons, and we can see that they are killing the neurons. We can remove them, and we see a much better outcome. Obviously, there are other groups in the world that also have shown the same type. Now, the problem with these oligomers is they are very unstable and soluble molecules, so it's been extremely difficult to use them in drug discovery and development. Our team has been able to stabilize them by introducing a disulfide binding in these peptides, stabilizing it in its oligomeric form, and we can use this for drug discovery. Now, of course, we're working with an active immunization here, which means that we are driving the body to produce the antibodies instead of passively injecting them. This, of course, means that we can have a long-lasting immunity. We will have good patient compliance because of the dosing only three times a year, and it also takes up the opportunity, of course, to have preventive treatments for people that have yet not developed Alzheimer's disease, and this is, of course, something we'll look into the future. I'm not going to spend time talking about the monoclonal antibody. I mentioned it's in the preclinical state towards the same target. We have done a Phase 1b trial. We finished this in the spring this year. It was 32 subjects, and we had three arms in the first part, Part A, continuing into an open label on Part B. Altogether, to take this shortly, the patients were in the study for about two years on active treatment. The primary endpoint we looked at here was safety and tolerability. Obviously, it's a Phase 1b study. We also looked at immunogenicity, obviously, for something that is a vaccine. And then we had some explorative endpoints, importantly looking at cognitive readouts, but also on biomarkers. I should also mention that in this study, we had patients that were mild cognitive impairment or mild AD, where the majority were mild AD patients. So with respect to the outcomes, first of all, we saw that we have a very safe and tolerable treatment here. The only real side effect we saw was the injection site reactions, which were the same in the placebo and the active arms. For the immune response, we saw a very robust, long-lasting, and importantly recurrent immune response, meaning that we saw a fast response coming up after the booster injections, indicating here that we have an active B cell immunity. We also measured the IgG levels in the brain and saw that we have expected levels 0.3%-0.5%, which should be sufficient to drive what we are looking for here. On the explorative efficacy endpoints, we used a scale called ADCOMS, which is an established scale. It was developed by Eisai for the Leqembi trials, and what we could see here is that the patients that were on active treatment for the duration of the trial remained stable in their disease states, indicating that we are able to halt the disease progression. We should take into account, of course, that we have a small number of patients, and we need to prove this in a bigger patient population in order to have significance here, of course. Further supporting our data was that we looked at biomarkers, of course. An important biomarker here is called neurofilament light. It's a biomarker that is known to be affected in many neurodegenerative diseases, including Parkinson's disease. We could see that this biomarker is correlating with our cognitive data, indicating that we have something that works here. In addition to this, we made a discovery where we saw that in healthy elderly individuals, they have naturally occurring antibodies towards our oligomer. Then we looked in young people. They have none. When we look in the Alzheimer's people, they had very low levels of these antibodies. However, when we use our vaccine approach, they come up to the same levels as what we see in the healthy individuals, indicating that Alzheimer's disease might be driven by an immunodeficiency in a part of the population. This is something that we will explore further in collaboration and look more into. Something I also need to mention is the ARIA-E events that we have seen with the current treatments on the market. There is something called ARIA-E, which is a form of edema in the brain that is very frequent with the current treatment. We don't see any of this in our trials above background levels. So we feel confident that this will be a treatment that will not have limitations in the populations when we get to market, which is in contrast to current treatments where we have a limitation for patients that have double copies of the APOE4 gene. So what is it that we do now? Well, we are, of course, preparing for the Phase 2 trial. What I think is most important to point out here is that we had the IND cleared two weeks ago. We are awaiting Fast Track, and the EMA submission is in progress. We, of course, had the study design and protocol in place, and we have selected the CRO, who is on standby now. We are still working hard on extending our IP rights, and the drug substance has been released. Drug product is awaiting release and will be ready before we get to the clinical trial. So again, path to market here is to find a strategic partnership and help us take it all the way. And I think I'll stop there. Thank you so much, Tord. We have got quite a few questions for you here, actually. Which partners and investors are you targeting at the moment, and when do you expect to reach new agreements? I mean, yeah, obviously, I can't talk about the partners. I know, but I have to ask you because someone said to me. Yeah, yeah, we get this a lot, of course. I think that it's an interesting question. I think we are working as hard as we can. We are talking to people all the time and different companies, but I can't say anything about where we are. It's also not our decision, right? I mean, we can only present what we have and keep pushing the discussions. If somebody wants to do it, it will happen. Turning then to the more clinical side of things. Thanks. There's a question here about how ALZ-101 actually crosses the blood-brain barrier. How does it work? The antibodies, you mean? How does it cross the barrier? Yeah, there's a lot of theories around that, I suppose. And I think there's passive and active transport that can be involved. We don't know exactly how this happens. We think maybe in Alzheimer's patients, there can also be some leakage in the blood-brain barrier that opens up for further transfer, which is also a possibility. But we do know that we get in there, and I think that that's the important part. I think we have an advantage since our oligomer is very sparsely expressed in the brain. There's few of them, right? And so the antibodies that we have are very specific and will bind to those oligomers in there. Someone's asking for some more information on the Phase 1b study. What was the outcomes in regards to clinical symptoms of Alzheimer's disease or the progression of the disease? Yeah, I mean, as I mentioned, there's only 32 patients in the study, right? For the active arms, I think that what we see is that they really don't move in disease progression. Now, we have to keep in mind that there's a huge variation, of course, between patients, right? So that's why we can't say for sure that this is true, right? We need to see it in a bigger patient population. But we see that it's trending in the right direction, and I think that is supported also by the biomarker data we have and also by these findings with the naturally occurring antibodies that indicate that we are on the right track. You mentioned the size of the patient population here, and someone's asked how many patients are needed in a Phase 2 in order to produce significant significance. Good question. We have designed the study with 240 patients. So we will have three arms, placebo and two active arms. How early should the patients start the treatment, and what are you expecting in terms of cost? I think, yeah, the cost, I mean, it's very hard. I think that we will have to look at comparable pricing for other drugs, right? Where I think that it could be a win for the society is, of course, that we can reduce the cost for injections and infusions, this type of thing, right? So when it comes to the drug price, that has to be negotiated in all markets as we always do. As you always do. Yeah. I think that was everything I had for you today. Thank you, Tord. Thank you very much.