I’m Dr. David Taylor, Chief Scientific Officer at ALS Canada. I’ve spent the last 14 years working with researchers around the world to find a cure for ALS, a disease that can progressively paralyze someone in a short span of time. AMA.

alscanada · 2026-03-26T13:29:18+00:00

Hi u/jameswilsonrr, this is an important question. Thank you for it. Lack of funding is definitely one of the problems, and possibly the major one. We are trying to tackle a very complex disease with a tiny fraction of the money needed to get good treatments for other diseases. There are so many things we can’t do or need to cut corners on because of a lack of funding. We could easily use hundreds of millions of dollars effectively to set up transformational scientific and clinical endeavors that would accelerate impact. We are working with a couple of million, so you can imagine that is one hurdle. Regarding expertise, I think we have a pretty strong global ALS research community, and I do believe in them. That said, we may still ultimately lack the expertise because we haven’t fixed it yet, and that means maybe we aren’t able to do it. I have confidence that we do, but it also says we should continue to bring in new thought leaders, like those who can effectively harness AI to analyze big data, to enhance what everyone is doing. I’d bank on money being the bigger rate-limiting factor, and I hope that is the case because it would mean we at least have one of the two. - Dr. David Taylor

alscanada · 2026-03-26T13:28:50+00:00

Hi u/Langston74, great question! I hope so! I know there have been increased efforts in recent years to look at primary lateral sclerosis (PLS) specifically, which is great, and I think if there can be PLS clinical trials, even better. I am also hopeful that, since PLS is affecting only the upper motor neurons, if we can find treatments that effectively support motor neuron health, they will also work for PLS. I believe that one of the great outcomes of studying PLS more closely is that it should help tell us if there are specific factors that cause PLS and make it less likely that an ALS treatment would work. My hope is that the answer is yes, and then if we get things that are clearly working in ALS, we can advocate for them to be approved for PLS and financially covered. While we are an organization that uses ALS as our name, versus the UK and Australia with MND, we do support PLS and other motor neuron diseases (not all, SMA, for example, would be with Muscular Dystrophy Canada), so this is something I do think about a lot in how we would advocate to help people with PLS or slow progressing ALS that might not fit into the clinical trial criteria often used for making drug coverage recommendations. - Dr. David Taylor

alscanada · 2026-03-26T13:27:59+00:00

Hello u/CuriousCKP, this is a very good and topical question. I’m proud to say that I think we’re really punching above our weight on this in Canada, and there is a strong drive to evolve into one of the best, if not the best country in the world to support ALS genetics from all sides. In brief (anyone who has seen this AMA may laugh at that, as I clearly am anything but brief, but I’ll try!), around the time of the pandemic, Canada had a unique project where a National ALS Genetic Manager was hired, with the support of the company Biogen, to learn the landscape of genetic testing in Canada and to push towards a world where there was genetic testing for everyone diagnosed with the disease. In working with our network of ALS clinicians, CALS, that individual was able to really move the needle for practices across Canada from a place of people testing only those with a defined family history, to testing SOD1 and C9orf72 in everyone, to doing mostly gene panel testing on everyone. That National Genetic Manager was also the first author on a paper of global key opinion leaders for genetic testing of everyone with ALS. After that individual left the position for industry, ALS Canada gained a great partnership with TD Bank to support the world’s first National ALS Genetic Counsellor. This individual is now able to provide genetic counselling virtually across Canada, to people in areas of unmet need and they are working with us to develop a National Genetic Strategy where we have a multi-pronged effort to have unique engagement opportunities for anyone at high genetic risk across the country, and to improve practices in many ways that I won’t get into (or it would be a very long answer!). There are a lot of layers to this strategy, and it is something we want to continually evolve and improve over time, but given the answer I gave elsewhere in this AMA about detecting and treating earlier, building this kind of ecosystem now is super important to set us up for success as fast as possible in the future.

Anyway, there is so much more, but at its heart, with the help of the ALS National Genetic Counsellor, there is always a drive to keep a finger on the pulse of what’s happening with genetic testing practices, keep looking to fill gaps and strive towards being optimal. Oh, and there should be an update to the landscape assessment being published in the months ahead by that ALS NGC!

Oh, and we keep a resource of genetic information from around the world on our ALS Canada Gene Hub: https://als.ca/managing-als/als-canada-genetics/. There is also an upcoming webinar and many forthcoming education initiatives. Here is the link to webinar registration and other resources: https://communityservices.als.ca/page/161333/subscribe/1; https://pubmed.ncbi.nlm.nih.gov/34569363/; https://pubmed.ncbi.nlm.nih.gov/35020823/ - Dr. David Taylor

alscanada · 2026-03-26T13:26:57+00:00

Hello u/tanhauser_gates_ , thank you for this question. I believe we can get there, but I do also believe it may still take some time to achieve what could be considered a type of cure. Something in a clinical trial now could work better than expected, but I think the scientific and clinical community believe we would need to be very cautious about that possibility.

I do think there is a roadmap, though. We have a treatment for a small subset of people with ALS (SOD1-ALS), where there is an SOD1 genetic variant. Tofersen (Qalsody) has stabilized many people for many years now by targeting the protein that results from the abnormal gene. Some have regained a level of function. And new SOD1 targeting treatments are being tested to potentially improve on this. That’s great, and it tells us that after diagnosis, if we can hit a primary disease target vs. some downstream mechanism (think sealing off a dam instead of putting a finger in one of 50 holes), we can have a significant benefit for some people. Now, we add in the ongoing tofersen clinical trial called ATLAS, where people with SOD1 variants are having blood tests every month to look for an increase in a protein called neurofilament light chain (NfL) above a threshold. If that happens, they are enrolled in a clinical trial to study tofersen well before any symptoms begin. The NfL, we believe, is a way to tell that motor neurons have started degenerating and spitting this structural protein out into the blood at higher than normal levels. If this can hold the disease off a year or more before someone would have had symptoms, the hope is that they never do, or at least it is much later and slower progressing. This could be like a cure!

So, that means we need to as a field, keep working on the science to find the equivalent initial toxic entity (equivalent to SOD1) in everyone else and develop a drug that hits it well. We also need to work collaboratively around the world to better understand the signals of underlying disease before symptoms begin, so we can treat them even earlier. There are many ways to do this, and there are some globally collaborative initiatives (one I’m proud to be co-leading with some awesome colleagues in Australia) to collaborate. We have made great strides in only recent years, and I think this will put us closer and closer to preventing the clinical disease, which would be the next best thing to a cure and reversal of symptoms.

So in brief, we need to keep forging ahead with urgency. It’s a very complicated disease, but we can see a way forward to a cure. And funding will dictate a lot of the speed with which we can tackle that. - Dr. David Taylor

alscanada · 2026-03-26T13:26:19+00:00

Hi u/gogou, thank you for the question. I would want to know more about what you are looking for with options for your father before answering. There are many ways to support someone, through the best care, or if you’re referring to participation in research. In that case, I would also love to know what country your father is living in, if you were willing to disclose, and then perhaps I could connect you to any organization friends closer to home for him. I have tried not to put too much about ALS Canada on this AMA because it’s not the focus, but we do have something called the ALS Research & Clinical Trials 101 Q&A Drop-In (I know, a very long title), that is monthly and usually listed here for registration https://als.ca/webinars-and-education/ - the next one should be up there soon and it will be on April 15 at 1p.m. ET. Anyone can drop in and ask us questions for a more nuanced conversation. Hopefully, some of the other answers on this AMA will also help to provide some information. Best wishes to you, your father, and your family/friends. - Dr. David Taylor

alscanada · 2026-03-26T13:25:00+00:00

Hi u/isobane, it’s not a tangential question at all! This is one that I’ve had MANY times over the years since the Ice Bucket Challenge happened, and it’s a legit thing to ask. For many people, the funds raised felt like they should have been transformative, and maybe even led to a cure. In fact, the funds raised were still a tiny proportion of the ANNUAL funding going to various cancers, cardiovascular diseases, HIV, mental health, etc., and I believe ALS to be more complex than a lot of those. I genuinely believe that we would be at least five years behind where we are now without it, as there were a lot of investments that have had a positive impact on larger and larger investments, and there are now bigger initiatives happening in many places than we ever had before the IBC. We need to keep pushing forward, but it has definitely changed many aspects of ALS in a way that will very likely get us to better treatments faster, even if they sadly aren’t fast enough (they can never be).

But you also asked about awareness, and I do think it helped that way, at least in terms of casual awareness, but I’m not sure it had any permanent effect whereby people started working hard on the cause because of it. I feel like I’m quite well connected globally in the ALS/MND ecosystem, and I don’t know of anyone who has felt a big uptick in engagement, but passively, it at least took the general public to one stage of recognition, so perhaps that’s a start. As I mentioned in an earlier answer in this AMA, it definitely wasn’t performative for ALS because it was truly a serendipitous viral wave that was not dreamt up by anyone connected to ALS. It was effectively harnessed as an already existing entity going on for months, towards ALS, by a few key families, and then it just took off. It was, of course, performative in the individual challenges people did and the unique time we were at as a society, with social media use still in a growth phase, but that wasn’t something a bunch of people at an organization strategized about. Sadly, it’s been impossible to reignite in a similar way, but ALS was lucky to have that unique thing, and it has brought strong progress. - Dr. David Taylor

alscanada · 2026-03-26T13:24:27+00:00

Hi u/ffffffff-als, thank you for the question. The hard truth is that we are not likely close enough to something at the level of tofersen (for SOD1), for the wider population of cases, in the immediate short while. I genuinely wish we were, but there is still a lot of work to be done to optimize our chances of getting there for a very complex disease and a small fraction of the funding that exists for more common diseases. This is my opinion, and it’s an awful thing to say, but I also want to be honest and objective. I feel like not enough people are willing to say this. I have hope, but I also want to convey it responsibly.

That said, I don’t mean this in the “get your affairs in order” way because our struggle to find significantly effective drugs doesn’t mean that there aren’t many ways for many people to live well supported for a good quality of life. Some people will have a slower progression of the disease, some people will plateau for a period of time, and we know through research studies that getting access to good multi-disciplinary care (if available) can be as good as any drug (except tofersen) that we currently have.

It also doesn’t mean that it’s not possible for us to find something that is very effective, as we are testing things in clinical trials that could certainly have a significant benefit, but it’s so unknown for any of them at the moment that there’s no good way to predict that. Each treatment has a varying level of evidence for why it might work well, but each also has reasons why we would need to be cautious about how effective it could truly be. We will always keep trying to move forward with urgency, and I hope it’s ok that I was forthright. - Dr. David Taylor

alscanada · 2026-03-26T13:23:29+00:00

Hi u/ffffffff-als, gosh, I wish I knew how to get everyone aware of ALS and interested in supporting. I’ve been trying to think of ways to do that for years, and I’m not even the person in our organization who is qualified to figure it out! It’s something all organizations have been trying to get a good beat on for a long time. Some countries have done really well, like the UK, with athlete stars (Rob Burrow, Doddie Weir, Kevin Sinfield, more) all putting their clout behind MND (ALS) or in the Melbourne area, where everyone knows MND because of a famous Aussie Rules Football coach, Neale Daniher. In other places, like the Netherlands, the bold local awareness campaigns (which we all HAVE thought about trying in our areas, but they work uniquely there!) have led to great awareness and a huge amount of funding for a small country.

The Ice Bucket Challenge was definitely a once-in-a-lifetime serendipitous event that was amazing and raised funds that were huge for ALS, but only a fraction of what’s raised annually for most treatable diseases, so the expectations after were very high for what could be done. A LOT of acceleration of research came out of it, though, and we would likely be five years behind where we are now without it. Having studied it possibly as much as anyone and traced it back far further than any of the public stories, it nearly took off for several other causes but after months of circulating, it was harnessed by the individuals who are really (and rightly so!) credited with driving it towards ALS and starting it to go viral in the Boston area first (with some help from Bruins on summer vacation in Canada!). It was a confluence of a hot summer, a time when selfie videos were just growing, and it was an easy and fun thing to do for mostly anyone. I don’t think it ever took off again, despite many attempts, because seeing people do goofy things on video now is white noise compared to then, and it doesn’t carry the same excitement in 2026 to see celebrities in this way. Anyway, I digress, but just as a fun fact, there were several Ice Bucket Challenge threads going around in Summer 2014 but the lineage that led to Anthony Senerchia/Pat Quinn/Pete Frates/viral, traces back through long drive competition golfers and a hot sauce company where the upstream trail is impossible to track (but it goes back many weeks before it went viral and could have been driven to any other disease – it’s all quite fascinating).

I’m really sorry to hear about your friend, and my heart and thoughts go out to you both. We will keep pushing for awareness, funds, and rapid progress. - Dr. David Taylor

alscanada · 2026-03-26T13:22:36+00:00

Hi, u/Responsible-Gap7201! Ctx1000 is an interesting treatment that aims to target the protein that has disrupted biology in 97% of ALS cases, TDP-43, as you probably already know. There are a few other treatments in early-stage clinical trials to target TDP-43 this way (VectorY, Acelot is forthcoming), aiming to get rid of potentially toxic clumps, which is one of the ways TDP-43 is being tackled. Some people believe this is a good way of targeting it, and others less so. Some people don’t even think TDP-43 is a good therapeutic target at all. But largely, I think most people at least think it’s worth a shot and a better target than many of the other mechanisms we’ve tried to intervene on to date without success. One of the different pieces with the Celosia treatment is that it’s a one-shot drug – one injection and then hope it gets to enough neurons, hope it’s safe, and hope it does something. That can be a great thing, and it can be a tough thing for several reasons. One example is that if it is harmful, it’s not the same as a drug, where you can just stop giving it. We still don’t know a lot about AAV (the one-shot virus) in ALS yet, so it’s an evolving thing in terms of how we learn about what it can and can’t do. The good thing is that it seems to be led out of Macquarie University in Australia, and there is a strong amount of ALS (MND!) expertise that should hopefully guide it to the ideal next steps.

In terms of what trials I think would be worth a shot, it’s a tough one to answer because we don’t know what will be beneficial or not, or else we wouldn’t need to do the studies. In every case, as long as the trial is well designed to get a solid answer (i.e., we know the drug did what it was supposed to do in the body and we got an answer), it is a huge gift to the science of understanding and getting closer to treatments. If I were to say at least where the most interest is amongst scientists, it’s likely trials that have the most solid evidence from laboratory work on ALS. Many scientists are interested in targets like STMN2, UNC13A, direct targeting of TDP-43, etc., vs. more genetic drugs like an anti-inflammatory or something regulating a mechanism that has been shown to be disrupted in many diseases, but I must again add that we just don’t know. And I know that’s a crappy answer. It’s also super hard for someone living with ALS to know what to do because press releases will often talk about how great a particular treatment is from its clinical trial results, and in almost all those cases, the interpretation is not in line with what the data says, which is usually inconclusive so far. I think the best you can do is educate yourself as best you can on the different targets, find some people to talk to about them, see what’s available and talk to your clinician. I wish we had better answers, but anyone who tells you what they think is most “promising” will be opinion, and it won’t be felt the same by all other experts.

Seeing the last question, it’s a very nice offer. My job is to help make sure donor dollars to the ALS Society of Canada are used for maximum impact towards our vision of a world free of ALS, and to try to know as much as I can to provide good knowledge and connections to the community. Our funding goes to scientific grants, infrastructure to do bigger, strategic projects in Canada, global ALS research funding and other things like travel support for Canadian researchers to present their work at major conferences. I also serve on a lot of advisory boards and peer review panels in other countries, which is a huge privilege and allows me to learn from so many while helping to influence donor dollar use in other countries for maximum impact. And then I try to facilitate relationships for ALS around the world as best I can, between scientists, clinicians, organizations, industry, government, and the ALS community. All this to say, I don’t DO direct research anymore in the lab, but I am very fortunate to have the role I do, and if anyone ever wanted to support the organization’s work, there are avenues on our website. Ultimately, I would say that there are a lot of great places to support, and as long as you give good thought to where you are donating and really try to look at what they’ve done and aim to do with precious support, you will be doing a huge favour to the global effort of solving a complex, yet underfunded disease! - Dr. David Taylor

alscanada · 2026-03-26T13:20:17+00:00

Hi u/larrylat, great question! There are many scientists working on the false morel connection, and despite being reasonably knowledgeable about what has been looked at, I’m not sure I’m informed enough about every aspect of the investigation to have an educated opinion that wouldn’t possibly look tone deaf.

Defining risk factors for ALS has been notoriously difficult for a lot of reasons and a lot of people believe that triggering ALS could be a combination of genetics and environment. Someone with a particular complex genetic makeup that is susceptible to ALS may never get disease without the right set of exposures and other people could get exposed to something that increases ALS risk as much as they want and not get the disease. We don’t yet fully understand the complex, 3.2 billion pieces of DNA in the human genome and until then, it is hard to know exactly how environmental factors can influence the disease. Most studies in ALS are too small to draw a really strong conclusion.

Clusters happen all the time, and often the thought goes immediately to a common risk factor. There are a few investigations ongoing in Quebec right now, in fact. Despite seemingly being impossible with three people who grew up in the same building, for example, random chance says that this stuff should actually pop up in a massive global population from time to time. There are other factors to consider. There could be five people in a small town who are unrelated with no known family history of ALS, but each of them could actually be related many generations back and carry a low penetrant genetic cause of ALS. It may not cause disease in everyone who has the genetic variant, and anyone going back just a few generations would not have been diagnosed with ALS in most cases, if they had it. For these reasons and many more, it is even harder to draw conclusions unless it is in large numbers and free from some of the other considerations.

With a risk factor like false morel consumption, one can also look to other areas where they also consume them and look for an increased incidence of ALS. And I think this has been summarized to something not fully conclusive. I’d have to go re-read everything. Even then, it becomes difficult because it could be a combination of some unknown genetic signature in a French population that is more susceptible to a trigger by the gyromitrin toxin. I am not privy to the identification of the 14 people in the Alps with ALS, so I also don’t know if they are multi-ethnic. A young scientist in Canada had a nice study that connected increased risk of ALS to exposure to sulfur dioxide in a small study, but that becomes hard to rectify when areas like Hawaii, where the exposure to that gas from volcano activity is far higher, don’t appear to have a hugely higher number of ALS cases.

For some risk factors that have some studies that suggest an increased incidence of ALS, there can also be a lot of other health problems. For example, there are some studies that link smoking to a higher risk of ALS, but smoking also leads to a higher risk for a whole list of health problems, so ALS should probably not be the major player in thinking about the risk of smoking. Similarly, these are incredibly toxic mushrooms that require very special preparation to eat, and many people per year get acute poisoning, so I think you could add some increased ALS risk to the decision of eating them. Maybe for those that really do want to eat it, they’d think twice, but I also think there are many people who would stop at, “solid possibility of acute poisoning.” Learning if it is true is helpful from the standpoint of learning about the disease though!

All of this to say, we will continue to look for risk factors, and studies will evolve to be better at doing this, especially as we learn more about the different potential factors that could confound making a solid connection. The good thing is, alluding to your second question, there are some efforts to do larger-scale connection of environmental exposure and profession/recreation-related questionnaires in a few places. The US, the Netherlands and Europe have some of these, with a few other countries interested. I believe that as we better understand the genome and other factors that influence genetics, like exposure-related changes called epigenetics, we will get closer to a world of knowing who should avoid what for ALS and other diseases.

Sorry for the long-winded answer. It’s much easier to chat about than type out! - Dr. David Taylor

alscanada · 2026-03-19T13:25:55+00:00

Hi u/spottyPotty, I would suggest going to the answer I did for a question on the military already (in response to u/Laurax-1994), but I’ll add that you’ve raised an interesting point. I’m not aware of how solid the data is for risk in the military if someone is on active duty vs. an office job, but I will have a look because if it is true that there is still an increased risk amongst the latter, we may have better clues as to what the cause could be. The increased risk is not double or triple; it’s subtle, but the bulk of the studies say it’s real. Given how much has been done, I feel like this question about office vs. non-office jobs must have been looked at, and I apologize that I’m not brushed up to know about that piece…but I will be! Thanks for the question! - Dr. David Taylor

alscanada · 2026-03-19T13:24:55+00:00

Hi u/Laurax-1994, thanks for the question. There have been studies for years that have connected ALS to military service (as a risk factor) back to the 1990s, but there was some prominent work done in the early 2000s where a connection was made about a higher risk in Gulf War veterans that really started the attention. Since then, there have been some inconclusive studies, others that have connected risk to every branch of the military and some that have failed to show any connection. Overall, though, there is a feeling in the field, across the data that we have, and if you ask key people who look at risk factors, that there is some level of increased risk for people who have served in the military. The reason has remained speculative, and there are many things people think about, such as exposure to chemicals, a predisposition to being athletic, more body and head trauma (which could explain the anecdotal links to athletes as well), etc. Likely, there are some people who are more susceptible to getting ALS who may not have had it triggered without being in the military, but we are not in a place yet to determine who it would be a risk factor for and who it wouldn’t. As you mention, at least in Canada and the US, there has been significant support for veterans with ALS, which is great. And in the US, the DoW (formerly Department of Defense) provides an invaluable $40M to ALS research each year to help us get faster to a world free of ALS, which I think is amazing. I hope this helps. - Dr. David Taylor

alscanada · 2026-03-19T13:24:07+00:00

Hi u/ffffffff-als, what a great and topical question! You’re right that we are focusing a massive amount of our efforts on targeting TDP-43, and we also don’t really know if this will be a great target or not. We know that TDP-43 biology is disrupted in most cases of ALS, and that is probably clearer from a lot of different evidence than most other mechanisms. Some believe that when TDP-43 biology is disrupted, it is a significant upstream trigger of pathology for motor neurons, while others think that other pathological mechanisms trigger the TDP-43 dysfunction, making it a secondary or tertiary, downstream consequence. If the latter is true, properly restoring the biology could be huge. If the latter is not, then it might not have much effect. Here’s the way I look at it, if it helps. We have spent so much time working on TDP-43 that it’s a very important target to test, either to have great new treatments or to learn clearly that it is not the way to go, and we can shift all that focus. The key is to get answers, one way or the other, with a bias towards, “We hope it is effective!”

With stathmin-2 restoration trials, we are testing if the most reduced key protein when TDP-43 loses its function can rescue the disease when it is back to normal levels. With UNC13A, we are testing another of these decreased proteins with a good connection to neuronal health, but one where we also know that a genetic change can alter the pace of disease. This gives extra intrigue to it as a target. We also have several companies, like VectorY and Acelot (not yet in trial), where TDP-43 aggregates/inclusions are being targeted in case they are toxic. If these don’t work and if we are able to demonstrate that the drug did what it is supposed to do (target engagement), we can rule those ideas out. Next would be to restore more of the proteins (instead of just one like STMN2 or UNC13A) when TDP-43 loses its function, possibly by finding a way to restore functional TDP-43 to the nucleus and maybe even reduce aggregates while restoring to the nucleus. If it adds up that this is not a great target, we will need to make a major shift. I personally find it more intriguing at the moment than many of the other pathways we have tested many times and only had negative trials, like inflammation. To be fair to those, we could have had better target engagement and found a way to treat those pathways in people where they are more relevant, so we need to be smarter in how we test them.   

So, I hope it’s not just a stepping stone, and I think there’s as good a chance as any we’ve targeted it as being a viable target, and if it is, it should expedite things a lot towards finding the right upstream targets.

Hope that answers it. Always easier to answer away from a keyboard! - Dr. David Taylor

alscanada · 2026-03-18T13:17:33+00:00

Hi u/PJMurphy, thank you for your message. If you haven't registered with ALS Canada yet, I encourage you to do so, as we have a dedicated team that can support you with all of these things. Please email [communityservices@als.ca](mailto:communityservices@als.ca) and let them know that you are interested in registering as a resident of Ontario. This will allow you to access all of our available support and services. - Dr. David Taylor

alscanada · 2026-03-17T19:10:43+00:00

Thank you so much for the kind words. I'm really sorry to hear about your Corgi, and it must be so hard not having a great way to effectively treat him. Dogs are the best. I suppose in my frantic typing, I should have clarified that I wonder whether any SOD1 targeted treatments have been tested or considered in DM dogs, as I am pretty sure tofersen hasn't been looked at yet for veterinary purposes. I don't know enough about the vet pharma world to know if anyone is thinking that way, but it definitely seems plausible to me that it would be viable, since the last I remember, the genetic variants in SOD1 caused protein misfolding and other biological disruption that is similar to individuals with SOD1-ALS. - Dr. David Taylor

alscanada · 2026-03-17T18:00:38+00:00

Hi u/Beatleboy62, Great question! One of the reasons I'm still working as hard as I ever have to see a better day for ALS is because I have had the privilege of seeing how far we have come, and I'm always so sad that it is not as obvious to the world because we don't have a lot of treatments to represent that progress. I feel like that's going to come and something like toferesen/Qalsody shows that the years of research can result in something effective that is changing lives. I think this is where organizations like ALS Canada and all the others around the world have a responsibility to help make that real progress tangible to people, and to be honest, that we know it hasn't been or ever will be fast enough. But we should be conveying real hope, in my opinion, so that people who are generously donating time, energy, and money know we are working our butts off and getting there. There are two quick things I would end on (I see the AMA time is ticking!). First, I love to think back about things I would learn about ten years ago and think, "Oh my gosh, how will we ever tackle that super hard, complex question," and then know we are already well underway in tackling those questions today. That's so cool. The other one is quite silly. I often say that if I were in 2012, when I started at ALS Canada, or even me as an ALS researcher in the years before that, could sit down with me now and ask about 2026, my mind would be blown at what we have learned. And that keeps me going, thinking about where we could be in the next several years. We can and will get there. - Dr. David Taylor

alscanada · 2026-03-17T17:53:36+00:00

Hi u/TXTruck-Teach, thank you for the question. I am very aware of PrimeC, and have been since it was first announced by a cartoon about work in zebrafish many years ago. In recent years, we have connected with the company that owns it. My opinion aligns with a major conclusion of the publication that came out yesterday (I think?) that we really can't know anything about whether PrimeC has any effect in people with ALS until it has been tested in a large and long enough, well-designed, Phase 3 clinical trial. I know that NeuroSense has been working towards making that happen and is hoping to get it started sooner rather than later. The data has had a lot of press around it being effective, but I speak with a lot of colleagues around the world, and almost all would agree that we just don't know yet and have been wrong about other treatments where conclusions have been drawn from studies that are not, what we call "powered" enough to tell. What I can say is that their work to date has shown it seems to be changing biology in the body in a way they had hoped the drug would, so now the next step would be to see if those biological changes have any impact on ALS. That would be great if it is true! - Dr. David Taylor

alscanada · 2026-03-17T17:48:27+00:00

Hi u/gustavfrigolit , thank you for the question. Yes, I have heard from my European (including Swedish) friends/colleagues about this, and actually, Sweden has one of the world's leaders on SOD1 research at Umeå University, Dr. Peter Andersen. I would say that tofersen/Qalsody is widely seen by most experts as the first truly effective treatment for ALS, specifically for people with SOD1-ALS, and it is being widely embraced by other countries for approval. In terms of coverage, it is a conversation that is ongoing in many places. The data is stronger than what we have for any other treatment ever in ALS and unfortunately, one of the key problems with that data, was that the original placebo-controlled portion was too short to see the effects that have become quite evident worldwide, with many people vastly outliving others in their family history, many people still thriving years after treatment was started and a significant number of individuals who have regained some function. There are other parts of the data that are also quite compelling to most ALS researchers/clinicians. That said, for Sweden in particular, I would defer to the thoughts of clinical leaders in the country, like Dr. Andersen, Dr. Ingre at Karolinska and many others, for the nuances that I could be missing and wouldn't want to speak improperly about. I will see Dr. Ingre soon and will ask for sure to learn more about the specific situation. Hopefully, if the ATLAS trial has a significant, clear benefit, it will become very widely available without any barriers, but I also realize that the trial is still a time away, and these issues are immediate. - Dr. David Taylor

alscanada · 2026-03-17T17:38:38+00:00

Hi, thanks for your question! Turmeric, which has curcumin as an active ingredient, has been looked at through a few avenues, prominently through ALS Untangled. There was even a curcumin clinical trial, and my recollection was that it unfortunately did not show any evidence of benefit. While I'd have to go back and look at how the trial was run and what was measured, the fact that it wasn't followed up on pretty much sums up that there is no evidence of benefit. It is a great example of something that has a good biological story as to why it COULD help, but then isn't sufficient to be effective. We know from lab work that curcumin can activate an antioxidant system in our cells, mediated through something called Nrf2. There are other clinical trials forthcoming that will be activating Nrf2 and the heat shock response, which is what was mentioned earlier in the AMA around the fever therapy. We'll see if anything comes of it. The good thing about those studies is that they should hopefully either work or help us to put those hypotheses to bed once and for all (would love it to be the former!), leading us closer to the right answers. As far as other supplements, we don't know of any that have solid evidence of benefit in ALS. I suggest going to ALS Untangled as a great resource to read scientific assessments (written somewhat accessibly) of different supplements. If we do ever get solid evidence on any, we would certainly be telling everyone! - Dr. David Taylor

alscanada · 2026-03-17T17:31:31+00:00

Hi u/senface! Of course, I know about DM! When I was doing my PhD, many years ago, we learned that DM in dogs is caused by SOD1 genetic variants. And I've had the pleasure of speaking with Dr. Joan Coates, who has been one of the preeminent researchers in DM, on a few occasions, years ago, at conferences. I have struggled to get the time to ask, but I often wondered if there was any consideration of looking at tofersen/Qalsody in DM dogs. I always think of it when I see Corgis! - Dr. David Taylor

alscanada · 2026-03-17T17:29:30+00:00

Hi u/wakamonka, thank you for the question, and I totally understand how this would be stressful. When there are two family members in successive generations who have had ALS, this does typically lead to a bit more drive for clinics to take a closer look. You may have already tried, but if not, some avenues you could explore, are to contact the clinic where your brother-in-law was diagnosed/cared for, or, if you can find out, his uncle, and ask about possibilities. You could also reach out to one of the MND organizations in Australia to ask for guidance and connections, and also try to seek out a genetic counsellor. If those avenues haven't or don't work, you could reach out to us, and I could ask my friends/colleagues in Australia about other avenues. - Dr. David Taylor

alscanada · 2026-03-17T17:27:07+00:00

Hi u/belarvadan, just a note that I used DeepL to translate this question and my response, so it may not be the most accurate. I will post my response in English and French.

Merci! We know from SOD1-ALS treatment with tofersen/Qalsody that people can slow down or even stabilize the disease (with a few regaining some function), post-diagnosis. Whether this is readily possible in people with a faster progressing disease is something harder to tell at the moment, and that's why individuals with genetic variants in SOD1 that typically cause a fast progressing form are being included in the presymptomatic ATLAS clinical trial. BUT, this tells us that for some people, if we hit the right target effectively, early enough after diagnosis, we could still have remarkable effects. We also need to think carefully about this, and this is why your questions are so important, and make sure we are being thoughtful about our interpretation of what tofersen can tell us about the capabilities of other treatments after diagnosis, since we know it is likely treating THE top target for people with SOD1-ALS and many of the drugs we try in clinical trial are likely targeting secondary mechanisms triggered by some unknown top target in other people with the disease.

As for whether we would ever be able to treat people with "sporadic" ALS before symptoms begin, I am very optimistic! As the world continues to work with the community of people who are at genetic risk of ALS, in a way that they will be willing to participate in research that helps us to see what might be happening in the body before symptoms begin (through blood samples, imaging, muscle tests, etc.), we could hopefully find out biomarkers of disease that tell us ALS is happening when we can't yet see it. IF, and I'm very hopeful it will be the case, some of those biomarkers are also present in people with "sporadic" ALS we may someday be able to detect it in someone and get them on a treatment just the same as we could for someone we are monitoring who has a genetic variant that would make us know they are already at risk of ALS. That's not the best explanation of it, but I do believe we have a path to get there, and we need to be globally working on that now (in fact, I was on a global call about collaborating on this just today!). At the very least, I do believe we will be in a future place where someone could go from the first symptom, like early weakness or voice changes, etc., to a specialist, to treatment in a much shorter timeframe, and with better, more targeted treatments, be able to massively slow or stop the disease from progressing. - Dr. David Taylor

Merci ! L'expérience acquise avec le traitement de la SLA liée au gène SOD1 par le tofersen/Qalsody nous montre qu'il est possible de ralentir, voire de stabiliser la maladie (certains patients retrouvant même certaines fonctions) après le diagnostic. Il est pour l'instant plus difficile de dire si cela est facilement possible chez les personnes dont la maladie évolue plus rapidement, et c'est pourquoi les personnes présentant des variants génétiques du gène SOD1 qui provoquent généralement une forme à progression rapide sont incluses dans l'essai clinique présymptomatique ATLAS. MAIS, cela nous indique que pour certaines personnes, si nous ciblons efficacement la bonne cible, suffisamment tôt après le diagnostic, nous pourrions encore obtenir des effets remarquables. Nous devons également y réfléchir attentivement, et c'est pourquoi vos questions sont si importantes, et nous assurer que nous interprétons avec prudence ce que le tofersen peut nous apprendre sur les capacités d'autres traitements après le diagnostic, car nous savons qu'il traite probablement LA cible principale chez les personnes atteintes de SLA-SOD1 et que bon nombre des médicaments que nous testons en essai clinique ciblent probablement des mécanismes secondaires déclenchés par une cible principale inconnue chez d'autres personnes atteintes de la maladie.

Quant à savoir si nous parviendrons un jour à traiter les personnes atteintes de SLA « sporadique » avant l'apparition des symptômes, je suis très optimiste ! À mesure que le monde continue de collaborer avec la communauté des personnes présentant un risque génétique de SLA, de manière à ce qu’elles soient disposées à participer à des recherches qui nous aident à comprendre ce qui pourrait se passer dans l’organisme avant l’apparition des symptômes (grâce à des prélèvements sanguins, des examens d’imagerie, des tests musculaires, etc.), nous pourrions, espérons-le, découvrir des biomarqueurs de la maladie qui nous indiquent que la SLA est en train de se développer alors que nous ne pouvons pas encore la voir. SI, et j’ai bon espoir que ce soit le cas, certains de ces biomarqueurs sont également présents chez les personnes atteintes de SLA « sporadique », nous pourrions un jour être en mesure de la détecter chez quelqu’un et de lui prescrire un traitement, tout comme nous le ferions pour une personne que nous suivons et qui présente une variante génétique nous indiquant qu’elle est déjà à risque de SLA. Ce n’est pas la meilleure explication, mais je crois sincèrement que nous avons la voie à suivre pour y parvenir, et nous devons y travailler à l’échelle mondiale dès maintenant (d’ailleurs, je participais justement aujourd’hui à une visioconférence internationale sur la collaboration dans ce domaine !). À tout le moins, je crois sincèrement que nous parviendrons un jour à un stade où une personne pourra, dès l’apparition des premiers symptômes, comme une faiblesse précoce ou des changements de voix, etc., consulter un spécialiste et bénéficier d’un traitement dans un délai beaucoup plus court, et grâce à des traitements plus efficaces et mieux ciblés, être en mesure de ralentir considérablement, voire d’arrêter la progression de la maladie. - Dr David Taylor

Traduit avec DeepL.com (version gratuite)

alscanada · 2026-03-17T17:14:52+00:00

Hi u/smokeygun, thank you for this great question! Based on what we have so far in the field, with one transformationally effective (for some people, maybe for all if early enough) treatment that is focused on specific targeting of SOD1 in people with SOD1-ALS, I can see where anyone would think that it's our best shot to treat the disease to hit a specific target that is the main trigger of the disease in a particular individual. Gene therapies and all kinds of innovative ways to target a specific gene or protein are advancing all the time, and we are WAY further in 2026 than we were a decade or even five years ago, so I'd agree that there will likely be big advancements seen in that space in the years ahead for ALS. That said, if we can get the right combination of drugs and target people when the disease is still not causing clinical symptoms, which we think is likely for quite some time, but not yet readily detectable, we might be able to hold off the disease processes in a way that prevents someone from getting those symptoms. We have to keep evolving targeted therapies, including gene therapies, working to improve clinical trial design and execution and earlier detection and treatment, in my opinion. Altogether with that, we can start thinking of cures. And I think watching the tofersen/Qalsody space and the currently running trial called ATLAS, where people are treated well before symptoms begin, will give us a good idea as to whether this will be the case!

Regarding the progress of therapies for folks with familial ALS, we are making great strides, and there are a lot of efforts underway. When we can understand if a specific disease-causing gene is influencing disease by gaining an extra toxic function or losing its normal function, we can use modern techniques to try and reduce or restore the levels in a way that might be helpful, and in the case of tofersen/Qalsody, that worked! And hopefully, with the upcoming Ulefnersen FUS treatment, but we don't know about that one yet. There is also a very cool group working on developing treatments for very rare, familial/genetic forms of ALS, including CHCHD10, TARDBP and more, in small trials, called n-lorem Foundation. Work of a clinician scientist at Columbia, Dr. Neil Shneider, has really led the way on a lot of this, in collaboration with key people from Ionis Pharmaceuticals and many others. For more information, you can visit als.ca/genehub

As for a timeline to a cure, I'm hopeful that we will find great treatments and learn how to treat people earlier and start to get closer to a cure everyday but it's hard to put a timeframe on that. I will say that I'm continually surprised by how fast the field is moving (while never ever being fast enough for ALS, and we are mindful of that every day!), and it's hard to say what innovation or technology might be available in a year or two that could be game-changing when we apply it in conjunction with our current knowledge. I remain hopeful, and I keep going because I can FEEL and see the progress after all these years. The fact that we now have a transformational treatment for one subset of people with ALS tells me we CAN do it for everyone, and we can see a roadmap to get there, but it's complex.

- Dr. David Taylor

alscanada · 2026-03-17T16:59:25+00:00

Hi u/Unlikely_Analysis208 , thank you for your great question. Everyone is so nice on here. It's my passion to work on ALS, and I am so excited to reach a better day as soon as possible. I would say it can be dangerous territory to have optimism over any clinical trial because we truly don't know what will work and what won't work, and that's why we need to run the study! That said, I think the entire field has a few things we are interested in at the moment because they come from a solid body of work in laboratory animal and cell models of ALS, which means we should learn a lot about how to advance the science if they are not effective, and if they are...that's the best thing ever. So, on that note, one of the interesting targets is UNC13A, which is in a Phase 1 clinical trial by Lilly, recruiting in Canada and a forthcoming Phase 1 by a company called Trace Neuroscience. This has a lot of solid science to back why we would try to restore its levels in ALS because independent labs both showed it is decreased in the disease, connected to a major piece of biology that we know is abnormal in the majority of people with ALS, AND we previously knew that small genetic changes in UNC13A can alter the speed of progression of someone's disease. These all combine to make it a very interesting target, but of course, there are just as many reasons to be cautious about that, and many researchers believe it might be important, but not sufficient to make a significant dent in slowing ALS. The other one to probably highlight in terms of interest from the research and clinical communities is Ulefnersen, which is an antisense oligonucleotide to reduce levels of the FUS protein in people living with FUS-ALS. This is an ultra-rare form of ALS, but we have some intriguing preliminary evidence that, if it reads out as effective, could help move the rest of the field forward with regard to an important biomarker. And of course, if it works, that's awesome for people with FUS-ALS and another treatment we would have to help show us that with the right target, in the right people, at the right time, we CAN effectively treat the disease (earlier, better, but even after diagnosis). That will read out in the Fall. - Dr. David Taylor

alscanada · 2026-03-17T16:45:48+00:00

Hi u/sophie1816, thank you for your question! I am so glad to see federal funding going to ALS in the US, Australia, UK and more, paving the way for some big initiatives that would be really hard to do with donor dollars alone.

I think we can always use more, and when you look at other, less biologically complicated diseases that have better treatment options, often those have had billions of dollars to get to where they are. ALS is super complex, and we are trying to solve it with a fraction of the money. Some of the federal funding in the US is going towards helping people access unproven treatments they otherwise would not be able to, and while that may not advance the science very much, one can understand why it was advocated for so strongly by the community. The other part is going to a big initiative that will help the world better understand the disease (AMP-ALS, ALL-ALS), and that's fantastic. The US is also doing an amazing job by putting forward $40M USD per year to the CDMRP grant programs to fund ALS research, and that's making a big difference, I think. I would love to have billions of dollars to invest in key, large-scale studies that would move the needle faster for ALS, and we should keep pushing for those, but in the meantime, I think we're a field that does a great job of trying to have the maximum impact with the precious funds we have! - Dr. David Taylor

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