Good afternoon, everyone, and thank you for joining the 2025 HC Wainwright 27th Annual Global Investment Conference. I'm Dr. Jade Montgomery, an Associate Biotech Research Analyst at the firm, and I'd like you to please join me in welcoming Neil Berkeley, Chief Business Officer and Interim Chief Financial Officer of Alector. Neil? Thank you. First, thank you for having me. I appreciate it. As I was just introduced, I am the Chief Business Officer and Interim Chief Financial Officer at Alector, and very happy to be here to tell you a little bit more about Alector. Before I get started, I need to do the obligatory forward-looking statement. I could be making forward-looking statements, and I refer you to the disclosure here in our SEC filings about this. Alector is an exciting clinical-stage neuroscience company, which I believe, and which we believe, is positioned to drive both near-term and long-term value. We are focused on addressing neurodegenerative diseases by removing misfolded proteins, replacing dysfunctional proteins, and restoring dysfunctional immune cells and neurons. We have, as I mentioned, a late-stage clinical pipeline with a phase 3 program that is reading out shortly. I will tell you a little bit more about that for frontotemporal dementia, a phase 2 program in Alzheimer's disease, and a robust early-stage innovative pipeline where we are leveraging our Alector Brain Carrier platform, which I will also tell you a little bit more about. We are well-resourced and have a global partnership with GSK on our two lead programs. Here is a quick look at our pipeline. As I had already mentioned, we have a robust pipeline of late-stage clinical assets, as well as multiple preclinical assets, the majority of which are enabled by what we call the Alector Brain Carrier, and we will talk a bit more about that. Specifically, drilling down a little bit on our clinical programs, latozinemab, otherwise known as AL001, is in development for frontotemporal dementia with patients with granulin mutations. We have a phase 3 pivotal trial with results expected by the first half of Q4. We have Breakthrough Therapy, Fast Track, and Orphan Drug designation on this, and are very excited about this readout, and I will tell you a bit more here in a minute. AL101 is an Alzheimer's program in a fully enrolled phase 2, 76-week trial, and completion of this trial is expected in 2026. On the research side, as I mentioned, we have a robust pipeline of early-stage assets, most of which are enabled by our brain carrier technology, the Alector Brain Carrier platform. We have a beta program using the ABC platform, a G-case program using the ABC platform, as well as some earlier stage siRNA programs with Tau being the leading program here, leveraging our ABC platform. Digging in a little more on the Alector Brain Carrier (ABC) platform, we have spent many years developing this. It is a TFR platform, but it is what we believe to be one of the most versatile platforms and is very adaptable, tailored for the type of cargo that we deliver, and is tailored for each program and each payload from a developability perspective. We are delivering antibody cargos, enzyme cargos, and nucleic acid cargos and have multiple versatile configurations with this platform. We've clearly demonstrated using some tool compounds, deep penetration in both non-human primates as well as rodents, and here's some of the data with the non-human primates being on the left and the rodent data being on the right. We've also demonstrated improved serum half-life, improved brain penetration, as I had said, as well as safety. Starting on the left, this is serum half-life tested with a serum half-life shown with improved antibody cargo, and we as well have shown uptake in mouse, which I showed on the previous slide, but we've also shown improvements compared to comparator TFR binders and reticulocyte activity, which is a leading indicator for anemia. Now turning to the progranulin franchise to dig in in a little more detail. Progranulin is a very well-known genetically validated target for multiple different neurodegeneration diseases. In patients who have a homozygous knockout on this, it's a very severe disease of early onset. In heterozygous knockouts for patients that have 50% of the normal levels of progranulin, they typically will develop progranulin, or they will develop frontotemporal dementia (FTD) at some point in their life. In non-coding mutation, there's an increased risk in ALS, Alzheimer's, and Parkinson's disease. We are addressing this by targeting Sort1, and by doing so, we are blocking one of the primary degradators of progranulin, which therefore elevates the levels of progranulin in humans. In our phase 2 open label trial in FRONT2, we clearly demonstrated elevation of progranulin in FTD patients to levels seen in healthy volunteers. As you can see here, both in plasma concentrations as well as in CSF concentrations, we were able to elevate progranulin levels back to the normal range, which is what can be seen in the gray boxes. In our FRONT2 trial, we were able to restore or reduce GFAP, which is another biomarker of disease for FTD, and we were able to restore this back to non-symptomatic levels for these patients as well. This is another important biomarker in our INFRONT2 open-label study. Finally, in our INFRONT2 study, we were able to show data against matched historical controls that demonstrated what we believe to be a slowing of annual disease progression by approximately 48%. This is as measured by the CDR, the modified CDR, which has been modified to reflect more of the FTD patient population as opposed to the Alzheimer's population. This will be one of our co-primary endpoints for our phase 3 study, which is an ongoing 96-week, placebo-controlled trial with 103 symptomatic and 16 at-risk FTD patients. This again has, as I mentioned, as a co-primary endpoint, plasma progranulin, as well as the modified CDR, which again has been modified to reflect some of the behavioral and potential speech differences that FTD patients exhibit. We will also be measuring several other secondary clinical outcome measurements, as well as exploratory endpoints in this trial. This trial is reading out in the first half of the fourth quarter of this year. Turning now to AL101, this is again another progranulin program. In this case, it's looking to elevate progranulin as a protective mechanism for Alzheimer's disease. This is currently in a phase 2 trial that is fully enrolled, being operationalized by our global partner GSK. That's a 76-week trial, and it's expected to complete next year. Here is a bit more on that. Again, 76-week trial, we're testing two different doses against placebo and have multiple primary and secondary endpoints, which we'll be looking at as part of this trial. The trial will complete next year with data to follow sometime at the end of next year or the beginning of the year after. Touching a little bit on the GSK deal, this was a very great deal for us, very solid upfront and potential milestones. Importantly, this is a 50-50 profit share and co-commercialization for both programs, AL101 and 101, in the U.S. Outside the U.S., GSK will be in control and it's a tiered royalty, double-digit tiered royalty economics. There are significant milestones on first commercial sale, and we are working very closely with GSK on both of these programs and will continue to do so. Now turning to some examples of our earlier programs, specifically talking about our Alector Brain Carrier platform brain-penetrant anti-Aβ antibody for Alzheimer's. As you all know, amyloid beta is an important disease target for Alzheimer's and has been for many years. The most recent programs have shown some success and are starting to demonstrate the importance of this target in this patient population, but unfortunately, they still have some limitations. They have some safety risks, there is some monitoring and uptake limitations, as well as just being able to get this drug to the patients. There are many companies, including us, or not about many, but several companies, including us, who are trying to address these issues by using blood-brain barrier platforms. We are developing ADP037 ABC with the target of increasing and having a very robust efficacy, doing sub-Q administration right from the start. We are looking to improve the overall safety of the A-beta approach, decreasing ARIA, hopefully limiting the anemia with the BBB programs that are out there now, and eventually moving to a prevention therapy. We are doing this by focusing on four specific things. We are focusing on selectivity. We have engineered a very high affinity fully human antibody that selectively binds A-beta plaques. We are trying to make a much more potent program or a potent asset by having a fully active constant region and enabling recruitment of the myeloid cells to the plaques. We are using our platform and the tunability that I mentioned before by specifically binding a unique epitope, tuning the affinity, as well as other aspects to try to make this safe and minimize the hematological adverse effects. Lastly, like I said, right from the start, we are looking to be sub-Q with this program. It is just some quick data just showing good uptake in human brain epithelial cells. This is a robust uptake of our program or of our asset. We have shown in both in vitro and in vivo models effective reduction in plaque and A-beta. Moving on to our Alector Brain Penetrant G-case enzyme replacement program, ADP050 ABC for Parkinson's disease. Just to start, for those of you who are not familiar with the GBA gene mutation, this is a mutation that reduces G-case enzyme activity and ultimately results in toxic substrate accumulation, which affects multiple diseases, including Parkinson's, Gaucher's, and Lewy body, all of which mutations in this gene are directly related to disease. There are no therapies currently to restore G-case that are brain penetrant. The only active G-case therapies are for Gaucher's and are not effective for the brain neuropathic versions of Gaucher's. We used our platform to design what we believe to be an ideal product for the neuropathic effects of G-case mutations. We have a very potent G-case, which is stable. Tuning our TFR platform to overcome some of the limitations or some of the potential safety issues of TFR platforms around anemia, and doing this by silencing the FC domain, as well as tuning the affinity. Just like the anti-Aβ antibody and all of our other programs, we are looking to go sub-Q right from the beginning. Here is some data on the left side, just showing you that we have a very active and stable G-case, which is much more active and stable than the wild type. We have shown a 10 to 100-fold elevation in G-case activity in the NHP-CSF. Excited about this program as well and the potential that it could have. To summarize, Alector is focused as a neurodegeneration-focused company, which is driving towards both near-term and long-term value inflection points. We are delivering on our late-stage pipeline in conjunction with our partner GSK. We have an exciting phase 3 reading out in FTD in mid-Q4 2025, and our AL101 phase 2 Alzheimer's study will complete next year. Coming right behind it is a host of different Alector Brain Carrier-enabled programs, including an anti-Aβ antibody and Tau program, as well as a G-case program. We continue to be very excited about what we are doing. We have a great team, and we have the resources to execute on these programs and remain well-resourced. Thank you very much.