Right. Thank you very much. It's my pleasure to be here today. My name is David Gray. I am the Chief Science Officer at Vigil and honored to be representing our company as we talk about what we're doing in neurodegeneration to advance these important treatments. Just as a reminder, forward-looking statements will be made as part of this presentation. So Vigil is a clinical stage microglia-focused therapeutics company. What we're focused on is developing novel treatments for patients who suffer with both rare and common neurodegenerative diseases. As I mentioned, we do that by focusing on microglia. These are the key immune cells. These are the key components of the brain's immune system. And we have initially focused on TREM2 as a modulator of microglia. TREM2 plays a very key role in establishing the character of microglia and their response. Microglia play this incredibly important role within the brain in maintaining the health of the entire brain through a number of functions, and TREM2 plays a really key central role in that. Now, we're unique among companies in that we have both a monoclonal antibody TREM2 agonist as well as the small molecule TREM2 agonist. These are differentiated molecules, and we've positioned them appropriately in two indications, as I'll discuss later. Ultimately, as a company, we believe strongly in a precision medicine approach. And specifically, we focus on diseases where there's a clear genetic association between microglia dysfunction and the disease. Now, ultimately, our strongest asset at Vigil is our people. We have a very experienced management team that has depth across all aspects of drug development, and we work together really well. We've been able to, as a group and working together with the rest of our Vigil colleagues, we've been able to deliver on all of the milestones that we have set for ourselves during our brief 4-year history and have accomplished quite a lot, as you will see. Looking a little bit more closely at microglia, these are beautiful cells. They're distributed throughout the entire brain, and they have a number of functions. You can see on the left illustrated, these are all important aspects of maintaining the brain's homeostasis and the health, and they're able to adapt to different things depending on what's going on in the environment. One of the core aspects of microglia is that they play a surveillance function. So under normal, healthy circumstances, constantly surveying what's happening within the brain environment, looking for sources of trouble. That trouble could be infection, it could be a dying cell, it could be amyloid plaque developing, other sources of inflammation. All of these are things that microglia is looking for, and the mediator of many of that sensing is the TREM2 receptor. TREM2 is expressed on microglia, and it is able to sense those different types of damage. And when it does so, it triggers a change within microglia that converts them into a neuroprotective phenotype that's able to respond to, isolate, and in many cases, eliminate the sources of damage. As I mentioned, we focused on TREM2 for our initial clinical programs because of this central role that it plays in modulating the character of microglia. Now, we've been able to identify several diseases that meet our precision medicine criteria, and specifically that we know where there's a very clear involvement of microglia in the disease. Starting with our monoclonal antibody program, we've positioned that in a disease called ALSP, or adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, or ALSP. This is a disease that is clearly a primary microgliopathy, and I'll describe more about why that's the case in a little bit. Now, we believe that from success in this initial indication, we will be able to build into other adjacent rare microgliopathies. These are all diseases where the blood-brain barrier is compromised. That sets them up well for engagement with a monoclonal antibody therapeutic. Now, we also have a small molecule TREM2 agonist, and our initial development there is in Alzheimer's disease. Once again, there's very strong genetics that associate Alzheimer's disease with microglial dysfunction, specifically at the TREM2 level. Ultimately, this entire space is extremely exciting and important. We know that neurodegeneration has emerged at the neurodegeneration across all different types of neurodegeneration often features various kinds of dysfunction in the brain's immune system, and many of them feature data that implicates microglia. So there's a tremendous amount of opportunity building upon the science and the capabilities that we have. In just a few years, we've built a really exciting pipeline. So I'll take a little bit of a minute here to describe. Starting at the top, we have iluzanebart, which is our TREM2 agonist monoclonal antibody. I'll refer to it as IBART for short. This is a program that, as I mentioned, we're developing in ALSP, and we're currently in phase II with that program. Down at the bottom, you'll see in purple, we have indicated a natural history study, and that is a really important component of our ALSP program. We are the first company to be studying ALSP in a therapeutic sense, and we also need to learn a lot about the disease. That's where the natural history study comes in, and I'll talk more about that interplay in a minute. But both those studies are ongoing. We also have our small molecule program, which is currently in phase I SAD-MAD study in healthy volunteers. From a data readout perspective, this is a really important year for us. We will have additional data from our IGNITE study, which is the phase II study in ALSP with iluzanebart later in the third quarter of this year. And we will have data in the middle of this year on the small molecule within the healthy volunteer SAD-MAD study. So both moving those programs forward, and we're really excited about that. Looking a little bit more closely at iluzanebart, over the last four years, we've learned a lot about this molecule, about this antibody. One of the things I want to highlight is that through our phase I study in particular, but also preclinically, we've established this molecule is very safe and well tolerated, has excellent PK, which lines up to once-monthly dosing, which is the regimen that we're using in our phase II study. We were also able to establish within that phase I study that we see engagement of key target biomarkers that indicate target engagement as well as engagement of microglia in general. Those biomarkers allowed us to select our doses that we're using in our phase II study and really set us up well for success. Now, let me take a minute to talk about ALSP. This is a disease that many people are not very familiar with. It was identified. The linkage to the genetics was identified just a little bit over 10 years ago. ALSP is caused by mutations in the CSF1R gene, which leads to problems with the CSF1R protein. Now, that CSF1R is a really important trophic factor. It's expressed on microglia, and when it's not functional, this leads to issues with survival of microglia as well as their overall health and function. Because of that CSF1R deficit, we see ultimately a number of whole brain changes and impacts that ALSP causes. A little bit unique among many neurodegenerative diseases, the symptoms really don't appear until the 40s, and there isn't evidence of pathology prior to that. However, once the symptoms do start, the disease is extremely aggressive, causing whole system impacts and within six - seven years, death. Initial presenting symptoms can be a little bit varied. They can include cognitive symptoms, executive dysfunction, issues with motor function, for example. And for that reason, ALSP is often even still misdiagnosed as other neurodegenerative diseases that have some similar presenting symptoms, including AD, FTD, and MS. The diagnosis itself is quite straightforward at this point. There's a simple genetic test, which can be used to definitively confirm the diagnosis, but there are no approved treatment options available at this time, neither for modifying the course of the disease nor for symptomatic treatment. Because it's an autosomal dominant disease, individuals who are carriers have a 50% chance of passing the disease on to their offspring. Now, we still have a lot we need to learn about ALSP, but we've been now over two years conducting ILLUMINATE, which is our natural history study. This is our opportunity to learn about the way that the disease progresses and evolves over time, and importantly, the way that certain biomarkers behave and could potentially be used. Our strategy here is to try to enable an accelerated development and approval strategy for ALSP with iluzanebart, and ILLUMINATE plays a very key role in that. It's designed as a 36-month study enrolling up to 50 individuals, and we are, of course, looking at clinical measures that we've included within the study as well as functional measures. We also have volumetric MRI assessments and assessments of CSF biomarkers, notably NfL and soluble CSF1R. All of these in order to learn about potential endpoints that we could use for clinical study, as well as to learn about the disease. Now, I'll just give you a couple of examples of things that we've learned from our natural history study. Shown here on this slide are three biomarkers that we've collected from CSF in ALSP patients. On the left, we're looking at soluble TREM2. The reason we're looking at that is this is the target that we're using to modulate microglia within ALSP, and what we see is that the target is present, which is what we're looking for, so that's a good sign. You can see that the levels of the target are pretty similar between the ALSP patients, which are in purple, and the healthy control reference set, which is in blue. Now, when we move to the middle panel, obviously, this is now very, very different. We're looking at soluble levels of CSF1R. This is the affected protein in the disease, and we clearly see that effect and that impact when we look at this data. So there's a very marked loss in soluble CSF1R that you can see in the symptomatic ALSP patients. This is also actually present in preceding stages of the disease. And because of this and other data, we clearly can understand that soluble CSF1R has emerged as an important biomarker for looking at disease pathology. And then finally, on the right, we're looking at NfL levels in the CSF. Interestingly, these levels are normal in prodromal ALSP, but once patients become symptomatic, there's this tremendous increase. You can see, again, this level of NfL is essentially as high as any neurodegenerative disease that we know. So very, very aggressive loss of axons within the neurons that we can see using this biomarker. So all of this positions us very well to be able to look at these biomarkers when we look in our phase II study. From a drug development perspective, one of the things that is also really exciting is that we're able to start to establish correlations between changes that we see on clinical measures and changes that we see on unbiased biomarker measurements. This particular slide focuses on volumetric MRI, and let me just walk you through the data a little bit. When we look at 12 months, on the x-axis at the bottom, we have changes in a cognitive scale, which is the MoCA score. This is a great cognitive test, and worsening is going to be to the left on the x-axis. As we look at the relationship between worsening on that cognitive scale and worsening on these volumetric measures, we see that there's a highly statistically significant correlation between those two types of measures. This is exactly what we would want to see in terms of being able to enable something like MRI for use in an accelerated approval scenario. Earlier in our development, we did discuss with the FDA the potential for MRI to be used as a biomarker in that context, and they left the door open to that. This kind of data is what we need to bring and to be able to show that those relationships hold and can be predictive. So on the left, specifically looking at ventricular volume change, you can see the correlation. On the right, that also holds for looking at loss of gray matter volume, where worsening would be loss of gray matter going down on the y-axis, and again, we see a really nice statistical correlation at 12 months. All right, so that sets us up to talk about the phase two study. Just briefly, this is a 12-month study. We've been able to enroll 20 patients, which is more than the 15 that we had originally targeted. The primary endpoints of the goals of the study are safety and tolerability. We're looking at PK, but importantly, we're also looking at the same biomarkers that I just discussed that we have in our natural history study. And these include pharmacodynamic measurements such as NfL, soluble CSF1R, as well as the MRI measurements. The criteria to be in the study, the patients have to be symptomatic for ALSP. We're targeting those that are earlier in their disease state, mild to mildly moderate, and they, of course, have to have the CSF1R gene mutation confirmed. There are two parallel groups, cohorts in this study, a 20 mg/kg cohort and a 40 mg/kg cohort that we're studying both of those doses. Now, in November of last year, we did share initial interim data from this study looking at six patients who were treated for six months at the 20 mg/kg dose. What that data confirmed is that we continue to see good safety and tolerability with this antibody. We continue to see the pharmacokinetics that we wanted to and expected to see, and we also saw durable effects on microglia activity biomarkers that we had measured in phase I. More importantly, I think, we also, all of those six patients were previously in our natural history study. And so while it is a very small data set, we did have data on each individual prior to entering treatment in terms of what their progression looked like on some of these biomarkers, like on MRI, for example. What we're really encouraged to see is that for many of those individuals, we do see that the rate of change that they experienced while on iluzanebart was slower compared to what they had prior to entering treatment. We also see directionally consistent for some patients that are consistent with the treatment benefit. So again, small data, but really encouraging to set us up. And then additionally, I think very importantly, we're seeing increases in soluble CSF1R within the CSF. And as you recall, this is a biomarker that's significantly affected. We see very, very low in patients. So to see that go up and given its linkage to disease pathology is very encouraging. Now, we're really grateful to all the patients and their families and to the investigators and their staff who contributed to both of these studies. I want to say that we learned a tremendous amount from them, and one of the other important roles that they play is in helping to educate the FDA around this disease that is a new disease. In January, the patients organized a patient listening session. They got very excellent engagement from the FDA around that session and participation. They were able to express the challenges and the unique aspects of ALSP that they face. And from the questions that the agency asked, it's apparent that they understood those challenges and can appreciate some of the ways that those will impact development. Again, all of this feeding together with the data from both of these studies and these kinds of education feeding into our ability to develop and ultimately align on an accelerated approval pathway, which we'll continue to work on. Our goal always as a company has been to be a valued and contributing member to the ALSP community in which we work. To that end, we learn what are some of the gaps and what are some of the challenges that they face. One of the things that came up in that investigation was access to genetic testing and availability of genetic testing, and we were able to respond to that by introducing ALSP Aware, which is a no-cost genetic test that we make available along with counseling to individuals and affected families, as well as to healthcare providers who may want to confirm or rule out an ALSP diagnosis. All of this really is because we want to bring therapies to ALSP patients as quickly as we can, and we focus very much on strategies that will enable us to get there quickly. I want to talk a little bit about prevalence. There's not been really good data on this, again, because it's a relatively new disease with a lot of misdiagnosis. But very recently, we do now have a lot more information about the prevalence, and let me just quickly mention a few of those. Dr. David Lynch at UCL in London did an analysis of the UK Biobank. Within that analysis, he was able to show that the frequency of pathogenic ALSP mutations is 281 per one million. And so if we extrapolate that to the U.S. and E.U. populations, we get 94,000 and 145,000 respectively. We can then bolster that general understanding about the frequency of these mutations with what we see in other settings. So with additional data now globally coming in from Japan and U.K., the average in terms of patients that are seen in adult leukodystrophy centers is about 16% of those are ALSP patients. And finally, several studies that have looked at misdiagnosis have established 0.3% and 0.5% respectively of those in those studies were actually ALSP that were misdiagnosed. So if we take all of that together, it all points to a U.S. prevalence of at or greater than 19,000 and a correspondingly higher number in Europe. Very significant opportunity, and there's a lot of the way we look at it, there's a tremendous opportunity for us to impact the patients that are suffering with this disease. So moving on to our small molecule program, which again, we're developing for Alzheimer's disease. We and many experts in this area really consider that harnessing the immune system and engaging the immune system is the next frontier in Alzheimer's disease treatment. This is among other reasons because this type of approach has the ability to go beyond targeting just a single toxic species and engage the potential of the immune system to respond to the multiple different contributors to AD progression. Now, TREM2 also fits in our precision medicine strategy because there is a clear causal link between loss of functional mutations and risk in AD, as well as faster progression in AD for those carriers of these mutations. There's also additional data that higher TREM2 is associated with slower progression in AD, which is favorable when you think about a therapeutic. As I mentioned before, TREM2 is this critical pathology-sensing receptor on microglia. And this role is one that we're basically taking advantage of in terms of our therapeutic approach. Again, activation of TREM2 signals a switch within microglia to convert into a neuroprotective state. And so our therapeutic hypothesis is to activate TREM2 with the TREM2 agonist and engage that neuroprotective capability. All right, so VG-3927 is a really special molecule. This is an orally bioavailable, highly brain-penetrant, highly selective TREM2 agonist. And again, we're developing for Alzheimer's disease. There's a number of specific attributes that lead us to select this molecule, as well as this modality, as well as specifically this molecule, and I'll take you through some of those here. Among the more obvious ones, a small molecule has advantages in patient access and dosing, has advantages in ability to combine with other therapies, and ultimately flexibility. I want to focus on one that is maybe not as apparent, and this has to do with ARIA risk. So we don't know exactly what the reasons are that ARIA is seen with the currently approved therapies. However, one commonality that is present between those therapies is that they're all antibodies that have their Fc component that can engage with the immune system through intermediacy of the Fc. And that potentially may be a contributor to ARIA. There is data and thinking that the immune system may play a role, especially with very high concentrations of antibody in the vasculature. And to the extent that that's true, the small molecule acts completely differently. It acts at a different place within TREM2, and it does not have an Fc component, so we would avoid that. Now, it may turn out that ARIA is just a consequence of clearing plaques from the vasculature, and in that setting, the clinical strategy is to either discontinue or to lower dosing. Even in that case, a small molecule does have advantages in terms of the flexibility and speed at which you can implement that type of mitigation. The other thing that's really important is that this is a differentiated molecule relative to the antibody. I will take you through some data that one piece of data that highlights that, but it has a unique mode of action, and that is something that we're really excited about. One of the examples of how this different binding of the small molecule and the way that it interacts differently with TREM2 plays itself out functionally is shown on this particular slide. Starting on the left, what we're looking at here is the activation of TREM2 in vitro. The very lower left is this natural agonist. In this case, this is sulfatides, which is a component of the myelin sheath, and it's also a ligand for TREM2 that signals that there is some damage that needs to be responded to. You can see that VG-3927, which is our small molecule, is a more potent agonist of TREM2 in this system. But when we combine VG-3927 and sulfatide, we see this really impressive synergy in the light blue. Now, why would this be important? So I'll illustrate that with a cartoon on the right. We know that when we have these types of damage, and we'll illustrate that with a plaque here, that the presence of the TREM2 natural ligands, the ones that signal that there's damage, are higher in the local microenvironment around these types of pathology. So what we would expect is that there would be a concentration gradient of these ligands that would increase as you got closer to the site of damage. Because of the synergy that we show here on the left, we envision a type of spatial specificity and enhanced efficacy that would potentially be very important when we think about therapeutic index and we think about efficacy. So we're very excited about this property, as well as other properties that specifically are because of the way that the small molecule interacts differently with TREM2. Now, I think I mentioned briefly that the field, one of the reasons for excitement of harnessing the immune system is for this broad potential to go beyond single toxic species. Within our labs, we have a multicellular system that includes astrocytes, neurons, and microglia, and we're able to assess the impact of VG-3927, as well as other things in this system that now includes all the cells. What I'm illustrating here is that when we look across different elements that may be important within a disease like Alzheimer's, we see that VG-3927 impacts broadly across all of those in a favorable way. We see reduction in multiple potential contributors to pathology, including reduction of a number of inflammatory cytokines that are shown in purple. We see reduction in GFAP, which is a marker of astrogliosis. We see reduction in TAU and NfL, which would be markers of nerve degeneration. And so that breadth of potential is extremely exciting for the mechanism in general and specifically for VG-3927, which does this so impressively. Now, we have an ability because of our previous experience with iluzanebart, we have an ability to build upon that when we are working on VG-3927, and we're indeed doing that. So within our phase one study, we can implement, for example, soluble TREM2, which is a target engagement biomarker that we measure in CSF. We measured that with iluzanebart. We're now able to measure that in the phase one study with a small molecule. And we have other biomarkers that we measured in that study as well. So implementing some of that synergy, we continue to advance that forward, and we look forward in the middle of this year to being able to share interim data from this phase I study. Now, once we have the dose locked in, we plan to move into an Alzheimer's disease cohort within the context of that phase I study. This will be a biomarker study, and the specific purpose is to look at biomarker responses in AD, and we will include individuals that have some of these genetic components that we talked about, so TREM2, loss of function, as well as other genetic indicators that we think are relevant. Using that data, we think that will help us to inform our larger planned phase II study, which would come after that, and make sure that we're using the data and what we can understand about biomarker response to optimize our patient population and selection. So looking ahead, the exciting future for Vigil. As I mentioned, we've been able to identify multiple indications where microglia dysfunction feature very prominently. I mentioned those today. We also have additional programs that we've built that take advantage of our expertise in microglia. They're not TREM2. And taken all together, we're very confident in our ability to take our precision strategy, align the right target, the right modality, and the right indication, and continue to build upon the emerging science in this important space, again, harnessing the immune system productively to treat these diseases. Just to recap the key milestones for us this year, in our iluzanebart program in the third quarter, we'll have additional phase II data. And on the VG-3927 small molecule program, at the middle of the year, our interim analysis from the healthy volunteer phase I study. Maybe just a final word on where we're at. We've seen from success in other disease areas, notably oncology, that the body's own immune system is a very powerful therapeutic when properly directed. Recent advances in neuroimmunology have showcased that that is also possible within the brain and that we can use that same general type of approach and build upon productively directing and engaging the body's own immune system within the brain to treat neurodegeneration. Our strategy, our expertise, and our programs themselves position us extremely well to take advantage of the emerging science in this area and to bring important new therapies to patients who suffer from neurodegenerative disease. Thank you.