All right. Welcome to the AdaptX podcast where we have conversations with individuals who are building accessible businesses, advocating for inclusion or excelling in adaptive sports.
Our intention is never to speak on behalf of those with disabilities, but give them a platform to amplify their voice and share insights and information that can make your world more accessible.
Today we are joined by Tom Otis. He is a researcher, academic and author.
He's the chief scientific officer at Lario Therapeutics and is a professor of neuroscience at the University College of London, where he also serves as the chief scientific officer at the Sainsbury Welcome Center for Neural Circuits and Behavior.
His background spans 30 plus years of experience in both academia and industry. Prior to his university position, he led a team of 45 scientists conducting early stage drug development and neurodevelopmental disorders and psychiatry at Roche Pharma R&D in Basel, Switzerland.
I already forgot what you mentioned. Before Roche, he served as the Edith Agnes Plum Chair of the Department of Neurobiology at UCLA.
Tom received his bachelor's and master's degrees in biological sciences and his PhD degree in neuroscience from Stanford University.
His research is focused on cellular and circuit function of the cerebellum and hippocampus, motor systems function and motor learning and preclinical models of epilepsies, spinal cerebral ataxia and a myotrophic lateral sclerosis, better known as ALS.
Probably the most impressive and lengthy intro I've had so far and I only butchered a few words, so I'll call that a win. Tom, thanks for joining us today.
It's my pleasure.
My pleasure. All right, let's dive in. I'll do my best to keep up. So for our listeners who might not be familiar with SEA, so spinal cerebral ataxia or ALS, can you maybe provide an overview of what they are, maybe any intersections or individualizations?
Yeah, so I'll start with spinal cerebellar ataxia. These are diseases of uncoordination and they're neurodegenerative, so parts of the nervous system, the neurons die and this causes the symptoms and these neurons are mainly in a structure called the cerebellum,
which is critically important for coordination, coordinated eye movements, balance, and motor learning. So in sport, this is a part of the brain that's really important.
And these diseases, the other thing that kind of sets spinal cerebellar ataxia as a part, see, even I can't say it, is that they are predominantly genetic. So there are genes that cause what we call a gain of negative function, just means that the gene is doing something bad,
and it's doing something bad that affects, in particular, these neurons in the cerebellum. And so, hence the disease. In ALS, ALS is a disease of motor neurons. So these are, it principally strikes the motor neurons in the spinal cord and in the brain stem.
And these neurons, it's also degenerative. And so these neurons die and people gradually become unable to move. So they become gradually paralyzed. In ALS, it's quite interesting and similar to some of the other major neurological disorders in that we know many genes now that can cause ALS.
So, about something like 15, 20% of ALS cases are caused by known genes, single mutations. And then the remainder of ALS cases are complicated. They're unknown origin. They might be many genes that are kind of together, not failing to cause the disease.
The introduction of CRISPR allowed you to more accurately assess the genome. Has the nature of your research changed a lot since that was introduced?
It has in the sense that it's a tool for not only potentially, you know, maybe not quite yet, but potentially for transformative medicine to edit genes. That promise is there and there are a lot of people working on this. A lot of companies as well.
But it's a tool that's important for research. So it enables you really to go in and with precision rewrite a genome, either a part of a gene and correct, for example, a mutation, or to remove a gene, or to alter it in a certain way.
So, in, you know, in exploring these things, the biology of these things, it's a huge and important tool. You know, similar to many, many people remember the PCR technique, which heralded an explosion and forensics and study of the human genome where you could really amplify small parts of DNA.
Human origins, right? Fossils and Neanderthals and all that PCR about 25 years ago, I would put CRISPR in as a similar transformative advance.
What influenced you to kind of delve into like the field of neurodegenerative diseases? Was there any personal experiences that influenced that career path?
You know, when I was making the kind of the real early career path decisions when I was studying at university, neuroscience was fascinating. So I was first hooked on neuroscience and actually that happened or key events when I when I was an undergraduate, I actually was really captivated by Jacques Cousteau.
I wanted to be a marine biologist, and Stanford has a marine station and a beautiful part of the California coast in Monterey. And I studied there. I went and studied there. And part of the the lab work was with sea slugs and squid and things like that.
And these were at the time. This was in the mid 80s. These were classic preparations where you can study neurons and neural function. And so I, you know, I kind of became fascinated with how neurons can can work and signal and they form the basis of not only movement and all action that
we take, but all the cognitive stuff and memory and all of that.
And so I went to graduate school and I learned because it was, you know, a lot inter interspersed with the medical students. I learned a lot about diseases in the nervous system and and there of course they're devastating and we, we, it really, it's really a mystery even still.
Many of these diseases. We don't have a good understanding of what's what's gone wrong.
And so I've had people I have, you know, I've had relatives who've had certainly age related dementia and and other other sort of insults to the nervous system.
The biggest challenges I know there's a lot of unknowns and this might be too vague of a question, but what are the biggest challenges in kind of identifying some of the epidemiology and the genetic causes of these conditions? Yeah.
Well, I'll talk first on a positive note. There's a lot of, you know, there's a lot of unknown and I'll get to that. But on a positive note, the advances in in genetics, the human starting with the human genome and the in the early mid to late nineties, advances in human
genetics have really been have been incredibly advancing for medicine for our understanding of disease designing treatments for disease. I mean, really now we're in an age where we can we can have quite precise therapies and really effective therapies and specific
diagnoses, right, not catch all diagnoses. So an example of that really great example of that is in cancer therapy. I mean, 1020 years ago, cancer was really a disease where patients had, you know, radiological therapy, they had surgeries, they were really kind of
go and get the tumor or try to kill it with either a chemical poison or radio, you know, a radiological poison and hope you don't kill good tissue and bad. And now with an understanding at a genetic level of cancers.
There are many cancers now where we have precision medicines or cell based medicines that are much, much more effective. Jimmy Carter, you know, president who died recently, he would not he would have been he would have died 20 years ago without these advances in therapy, as an example.
So coming back to your, you know, what don't we know and what are the challenges well in in the nervous system in the brain all this is harder because you know it's inside your head, you have a barrier from the blood so getting drugs into the brain is harder.
Obviously, if you want, if there were a tumor like a glioblastoma terrible tumor, and that's in your brain. It's much harder than if the tumor is in your liver, where you can do a biopsy or on your skin, where you could do a biopsy in an outpatient office, and that biopsy could tell you about the genes that would then allow you to pick medicines off the shelf in the best case in the brain, much harder.
Right. So these are big challenges, but I do think, you know, things that we learn about biology elsewhere in the body can also really lead the way in the brain and oncology is a good example. I mean, I think, glial blastoma treatment will certainly has and will certainly benefit from from, for example, oncology of solid tumors in the body.
There's a couple FDA approved treatments for ALS, but I guess treatment. They're not treatments, but they slow down the progression of the disease. So, if there's nothing that can reverse it, but there are some options that slow it down. What's being done for earlier detection of ALS?
Yeah, I mean, these are, this is, I think, a very fair assessment. It's not what we have in terms of therapeutics is just the beginning, and they're clearly not good enough. And what I would say is that, you know, this is a very active space, ALS drug development, things that your audience might want to keep their eyes on.
There are, as I mentioned, there are genetic forms of ALS. So there are, let's say, you know, half a dozen to a dozen genes, where mutations in these genes will cause ALS or are very likely to cause ALS.
And these genes are being several of them are being very actively explored as targets for therapies. So one of the recently approved drugs is against a gene called SOD1. And this is a program that Biogen led Biogen and Ionis, I think.
And the SOD1 gene has a so called gain of negative function. So the gene and people who get SOD1 related ALS, the gene causes bad, it has a mutation that causes bad things unrelated to its normal function.
And the therapy is simply to prevent that bad gene from being expressed as a protein. Okay, so it's a it's a it blocks the effect of that gene and that that therapy was approved by the FDA.
And it's interesting it was such a transformative therapy that it was approved, even though the clinical benefit is probably not great yet in terms of outcomes. But the fact that they could show they could remove this, this gene, they could target it, and they could do what they needed to do molecularly was enough.
And I mentioned that as a story because that shows you that the field you know the field is on the march. And for many of these genes.
I think there will be some success in mitigating the terrible outcome of ALS. And it probably will, you know, it'll take some time and you see this with Alzheimer's disease as well. You know the first therapies that didn't really work.
They were controversial. Now it seems like they're starting to work. And so that I expect that momentum to continue. It's a natural question to think, okay, if you develop a therapy for a genetic subset of ALS patients, is it only going to work for those patients?
And those are things we have to learn. I mean, it you could argue this both ways. It might be that some of these targets will be effective for a larger fraction of the patient population.
It's not just those who, who have the bad genetic form, but that has to be established. So I think there's, you know, there's real cause for hope.
And there's a lot of really specific and I think very well precise incisive paths that are being explored.
You mentioned, obviously there's a genetic component, but also a variety of other factors that are somewhat unknown. Maybe some are known. Are you familiar with a study from a few years ago that looked at the association between like NFL players and ALS diagnosis?
Yeah.
Yeah. So saying something along the lines of people are four times more likely to develop ALS if they played football. And I think there was also a correlation between the length of career and the severity of ALS.
So is repeated head trauma one of those confounding variables? And if so, between the research that's been produced on CTE and stuff like ALS, do you think the public is too concerned about that?
And stuff like ALS, do you think the public is taking that seriously enough?
No, I mean, I think it's been, you know, I think anyone would have to say that this has been shocking and that the alarm, if anything, the alarm has mounted. I mean, I'm a sports fan.
I, you know, I like to watch the NFL's, you know, but I, but I, I will say that it's it is extremely alarming that and it's extremely clear that repeated repeated and strong force, you know, applied to the head like you have.
And certainly in in in pro football and in boxing and some other sports, it's we have to really think about what we can do to limit that because it's it is very dangerous.
And there's a lot of overlap, interestingly, between these kinds of chronic chronic traumatic encephalopathy mechanisms and what we would call there there are diseases that neurodegenerative diseases that are often called misfolded protein diseases.
And these diseases include ALS Parkinson's disease, Alzheimer's disease and and in chronic traumatic epilepsy, chronic traumatic encephalopathy, you see similar neuropathology to some of these other diseases.
And the neurons get they look in histopathology like some of these other diseases and we don't understand exactly why, but probably at the cellular and molecular level, there are similar things happening.
Are you collaborating then with people who are researching Parkinson's people who are researching Alzheimer's is there overlap in your research.
There's definitely overlap in Parkinson's disease.
And I, I mean, I have many close colleagues and I pay fairly close attention to the Alzheimer's disease literature, particularly, I mean, and you could probably sense this I'm, I'm, I, I personally particularly think that genetic clue clues in terms of genes that
are implicated strongly in in rare forms of these diseases, and I was just going to make the point that the genetics, the human genetics, even in rare and small subsets of Parkinson's disease.
AOS Alzheimer's disease, that these rare genetics are really important for drilling down into a mechanism and identifying possible therapeutics I think this is a really exciting area of modern medicine.
And it's not just me that thinks this.
Because, when you you know for example, in some of these genes.
Scientists have discovered not only versions of the gene that will cause the disease, where if you have a genotype of someone when they're 30 years old, you know they're going to get the disease when they're 55 or 60 years old.
Okay, so it's very powerful, you know, very predictive and a classical genetic way.
So that tells you the gene could contribute to a disease process.
And in many cases, there are also versions of those same genes that protect individuals against the disease. So if you look population wise, there are other mutations in the same gene.
And in some cases, people will on a population wide level.
They'll be protected against a disease, even a kind of non genetic form of the disease right so those two things together tell you that gene deserves attention. Right, and maybe a therapy to make, for example, to make the bad version of the gene, the
bad protein into something like the good version right that's a natural logical thing to do.
We've talked about post polio syndrome and MS on the podcast as well.
My father was diagnosed with MS when I was in kindergarten, and through therapeutics has the progression of his condition hasn't worsened drastically or as drastically as some other individuals I know with MS but
the complexity of these like neuro degenerative diseases.
How much like it's interdisciplinary like work is done, and maybe like what breakthroughs are you most interested in or kind of looking at.
Yeah, I mean I think in MS MS is a disease as you as you, I'm sure you know that is really a disease of the nervous system. So, nerves are attacked, but they're attacked by the immune system, so it's both the neurology and an immunology disease.
And it's the. It's an autoimmune disease right so the immune system antibodies are attacking the peripheral nerves, these cells that are glial cells that myelinate nerves and they're also centrally damaging nerves.
And, you know, I think it's good to hear that that the therapy, you know, at least some of the therapies for your dad have worked. They tend to be right now.
And they're good. I mean essentially most of them you could classify as immunosuppressant therapies, and those come with, with liabilities because you need your immune system, so immunosuppression is not, you know, can can be dangerous and needs to be managed.
So when I was at Roche they developed a drug called a crevice, which was an antibody that actually helped reduce B cells. And that seems to be a very effective drug and it's one of the leading drugs now for MS but the real, you know, I think the real
challenge in MS now is there are therapies that can halt or slow the disease and many patients.
It depends on the stage at which they begin their treatment. If the MS is too advanced, it can be much less affected these therapies so they talk about a relapsing remitting phase where the MS symptoms, you know, come and go.
And then there's a phase where the MS system, the MS symptoms are kind of persistent and they, you don't get, you know, near perfectly better. And I think we need therapies, obviously, to allow the nervous system and myelin, these myelinating cells to repair themselves,
so that those who suffer from MS and are at a plateau, they can come back and regain function. And a lot of companies working on this but yeah yeah I know some of our clients with MS at the gym have tried the same medication that my dad has taken and it hasn't been
effective for them so it seems like it's a very individualized thing but maybe on the topic of like pharma Do you think the last few years has made just like disseminating information and selling treatments has it hasn't made it harder with the whole
landscape of coven and maybe some distrust that people have just is is the prevalence of of these messages making it harder to to develop drugs and disseminate material.
Yeah, I mean and I think it's it's reflective of the larger world you know we're in a really fractured informational environment, it's easy for people to race ahead and to go and find what they consider to be relevant information.
But it's a complicated world, you know if I, if I said to you, okay, you know you're going to take a trip somewhere, and you're going to go by airplane.
And you're going to go to the internet and learn how to fly a plane and just see if I can do it.
And I think that's the reason why I'm flying that plane that, you know, there's a reason why why experts and institutions and so on, why we rely on them, and it's really good reason and it's the same reason why you rely on someone who's, who's trained
as a pilot to fly.
And you don't sit in the front seat and try it yourself, even if you might think I can do it. Right.
So, but you know coming back to farm, you know, the, I mean look pharma and biotech.
It's, it's, it's a wonderful thing but it's a it's a system that is capitalistic.
It's expensive to develop drugs, they are too expensive. There's no question about that.
The fact that they're too expensive means that there's, there's problems with access there are heartbreaking decisions in different countries deal with this in different ways.
The US simply pay it pays the highest bill by the way, I could say is that as an American living in London in London they have a whole system where they consider which drugs are value for money, and they negotiate at a national level with former
and they get much lower prices for the same drugs. Sometimes they get them, six months later, but if they're really important drugs they get them.
So, you know it's, I mean these are what I'll tell you what the CEO of Roche when I was there I'll tell you what he said and I think, you know, they're going to be differences of opinions and perhaps some of your audience will groan when they hear me say this
but he would make the point that when there is a transformative drug.
You know, like Roche's new new drug for ms which was a real step forward.
There are some drugs for really devastating childhood diseases that have been, you know, close to what you might call cures oncology drugs you know there are drugs in this class.
Once, once these drugs.
Run their patent life.
They are then in a way, a kind of a kind of.
There's a legacy left for humanity.
Okay, and there are drugs that were developed and, you know, before the turn of the century, that are still really important drugs. There are drugs for example immunosuppressant drugs neuro steroids, etc.
And then there are also material drugs epilepsy drugs.
And those drugs have a, you know, a high price. And then when they go off patent, there are many companies that can make them.
And then we have them forever.
And so, you know, there's the ethical and moral quandary of, well, look, if my drug is $200,000 a year.
You know, do I lose my house to, to be to be well and to avoid death. That's a big problem.
But it is in the long run, I think.
And I think that's the kind of thing that has that has a happier ending. Then we sometimes think, yeah, it just takes long to develop.
I guess everyone may be familiar with, well, ALS as more public facing for sure. What role do you think like the public awareness that's been generated from athletes like Pete Freights and Steve Gleason kind of has done for research like does it trickle down to you.
You know, you know, you have to benefit the patients, although your work benefits the patients. But I guess what role does public advocacy and awareness play in studying a rare disease or condition like ALS.
I mean, I think it's, it's pivotal patient groups can really be involved, not only having a front row seat to the development of medicines, but speaking both the scientists and to pharma and biotech companies.
I mean, I see this very much with the company that I work with now in the rare disease space where patient groups are are are absolutely essential and their voice is a really important part of the hopefully the march towards a therapy.
Also regulatory agencies, the, the Food and Drug Administration, the FDA would definitely listens to patient groups. So there's political pressure. There's guidance that can be given to regulators about what aspects of diseases are most burdensome or where there is the most need for therapies.
And, you know, and I think on the on the general patient awareness front, I'll just give an example. We we're working doing some work on Parkinson's disease and Michael J Fox's foundation is a major is really a pillar of Parkinson's therapy development and research.
They've given out billions of dollars in grant funds.
They are, you know, they really drive the field and they do it not only at the, the early kind of research stage preclinical research stage, but also with with promising companies to make sure that it's a really vibrant ecosystem.
So, yeah, so I would say to those inclined, you can really make an impact, you know, and it's not just the money. It's the voice. Yeah, I like that is the is the work that you do patient facing at all are predominantly academic and research based.
It's kind of somewhere in between. So I, with the, with this company, we are developing and hope that within and it's the website if you want to go to the website is Lario TX dot com.
The company is, we hope a year and a half or so about six months from declaring what we call a clinical candidate. And then about a year from from possibly going into clinical trials.
So we're kind of, you know, we're in, we're advanced in some senses, but still, you know, there's lots of work to do. And in that role, I go, I go to scientific meetings, and I meet with patient advocates, I meet with parents at these meetings.
So I go at conferences, you, you see, and hear from people who are who are affected by the disease in this case, the disease is so debilitating that the patients themselves are have have profound intellectual disabilities.
So it's a little harder to interact with the, with the patients, but I certainly hear about them and about their lives and what what is important to them.
What have you learned about communicating with individuals who have terminal illness.
I mean, I think you, one needs to listen. So I try hard for me but I try to keep my tongue.
Because every moment. I mean one, you know, one.
You know where all of the challenges are, and where some of the joy is if there is any joy. And I think it's so important to to hear that firsthand because not only, you know, as scientists we think I have a theory of what what causes the disease, or what might mitigate the disease.
But hearing what really matters to people.
What their challenges are what they miss what they'd like, if they had only a partial therapy. What would it do for them.
That's really important, because it can orient you to think about those things. Yeah, that the field of medical humanities is really interesting to me and just the research on how outcomes can be improved by the way you communicate and the way that
individuals communicate with their patients is is a really interesting idea to study for sure.
Absolutely, but it's kind of goes like in our, in the course that we teach the fitness professionals we talked about the social model versus the medical model of disability and obviously the medical model is essential for the work that you do.
And I think that's grounded in medicine but that there's also that social piece, where sometimes a disability is just the product of either people not understanding or inaccessible societies so it's cool to kind of have both things at play and having medical professionals
that understand that the therapeutics and the medicine is essential but that there is that patient advocacy and understanding what they want to get out of therapy that is that is important.
And I think that's a great reflection of those two.
And there's no question that therapy. I mean so many therapies and this is particularly true of neurological disorders, having the right neuro rehabilitation, or having the right, you know tandem psychiatric treatment, along with, for example, a, you know, a pharmacological
treatment, those two in conjunction are much more powerful indeed some drugs just won't work without having the second component.
So that's a key, you know, there's a whole areas research as I'm sure you know about.
How do you have the right rehabilitation component or. Yeah, absolutely. Maybe on the topic of SEA.
Can you explain to the audience kind of what a tax is, and how it's being treated and how it kind of manifests on a day to day basis for individuals.
Yeah, so a taxi is an SCA is would be genetic forms of a taxi there are are are other ways that a taxi can result. And in fact there's one that probably many people have the most direct experience with which is that alcohol causes a taxi.
The taxi is just a medical term that means uncoordinated movement.
And it, it most.
It can be maybe most apparent in someone's gate, the way that they walk.
But it can also be apparent from the smoothness and the coordination of their movements.
So, in a neurological exam, a neurologist might ask someone to walk down a hallway and back, and the patient that suffers from a taxi I might have a wider stance, and they might, you know, have trouble with balance.
During walking they might even need assistance with balance so balance is a key part of this.
Other features that a neurologist might look at our eye movements. So they might ask, you know, put their finger up and ask you to look to follow their finger with your eyes and they're looking to see can you do that smoothly.
And particularly when you get to the edge of your gaze is the gaze fixed, or do the eyes beat, you know, you can't hold a gaze and that's called the stagmas that's a classic and taxia sign.
Alternating movements the neurologist might ask you know, someone to do this repeatedly or to touch their nose and the finger of the neurologist and a taxi of patients will pass point.
And they might have a tremor when they're moving, so they might you know not be able to hit their nose.
So all of these things and then I mentioned motor learning earlier.
Any kind of coordination coordinated movement, like in sport, or in music, where someone through practice will learn to make more precise movements that is degraded in a patient with a taxia.
We see a taxic CP as one classification of cerebral palsy as well that we will sometimes observe in clients. But what is I guess what is the current treatment for taxia is a different between and other forms is their genetic component.
Is there a nurture component?
Yeah, I mean most a taxia, so a taxia. The spinal cerebellar a taxia is and also the what would call idiopathic a taxi is cerebral palsy a taxi as a nervous system insult from early life.
There are chemical sort of permanent forms of a taxi.
There are autoimmune forms of a taxi.
In all of these cases, the treatment right now is unfortunately largely symptomatic.
So neurologists can prescribe medicines to make these things better to reduce tremor a bit to, you know, to reduce other symptoms of a taxia.
But particularly in the area of the genetic a taxi is there are many, many programs now where the genes are being directly targeted, and they are gain of negative function.
So there, you know, a gene that's doing something untoward. And so blocking this gene is technically fairly straightforward, I'd say now.
And the only challenge is, can you develop a therapeutic that's safe? And obviously that's effective that blocks the gene effectively doesn't block it too much in some cases.
And there are many clinical trials now.
Proceeding so I'm hopeful, you know, I am.
Very hopeful that a lot of this stuff will within the next five years will.
We'll see some some drugs approved and hopefully they'll be.
They'll be they'll have really high effectiveness, not just a little bit.
Yeah, for individuals that might be interested in pursuing a career in researching like neurodegenerative diseases.
What would you recommend or what is your advice?
Well, and I'm not just saying this because I grew up there and you live near there, but you could go to Boston Boston. There's some good places to stay. Boston certainly.
You know, so I think there there are so many ways to make an impact.
And those can be, of course, to study a research area like neuroscience or to study medicine, medical aspects of neuroscience that might be a neurology or psychiatry.
So, those, you know, those would be traditional ways, but I think.
Patient advocacy, patient care aspects, nursing rehabilitative care. I mean, these are all areas where a huge impact could be made.
And, you know, so, so I think there's there's plenty there's clearly plenty of work to do.
What brought you to London? If there's so many good opportunities here in Massachusetts.
This is like, this is like what my relatives and but it is a it is a fair question.
I, you know, it was it was a meandering path. So I was I had a faculty position after I finished my Ph.D. and did a little bit of extra study.
I had a faculty position in Los Angeles. So I worked at UCLA for many years.
And and then, you know, really, really jobs and challenging jobs that I thought would be good for me.
Drew me first to Switzerland to Basel. So I I went from academia and I went to work at this drug company Roche, which was really thrilling.
It was exciting to see how how medicines get made at scale in a big company like that.
And then I had had an opportunity to come to London, which is back a bit more in academics, but also with the freedom to do to work to develop this company.
And London's been great. I mean, I it's nice to live in different places. You know, I think I can't relate to that as someone who really leaves Massachusetts.
I'm not sure I've left Lancaster in a couple of years, but no, that's that's awesome.
We a lot of our audience is in the in the health and fitness space.
Do you do you see any overlap in terms of what you do and maybe what someone can do to improve, I guess, their their health and fitness and just in terms of like recreation?
Yeah, well, I mean, it it is an established fact, and I'm sure most of your audience probably knows this and feels this that physical fitness throughout life is is the single most important thing you can do to stave off disease.
And that's true of neurological disease. And it's certainly true of cardiovascular disease, you know, other big areas and metabolic diseases.
But in the neurological space area, you know, in terms of dementia, age related dementia, if someone's active, it's a major factor in the plot and the plus column in terms of staving off cognitive decline.
So absolutely keeping fit. And then there's the mental aspect of it. You know, for most people who are physically fit, they and I would, you know, I would I don't know if I'm physically fit, but I would certainly say about myself that physical activity.
And even being, you know, walking around being whatever your your choice of physical activity is, but it can be more strenuous or less strenuous. It had it bears mental, mental dividends, mental health dividends where you're you're clear.
You're able to deal with stress in a better way. And those things obviously also are really crucial for health.
With ALS being a decline of physical function, is there are you familiar with anything that correlates activity levels and the progression of the disease not to imply that you can reverse it in any way just by being more active after the diagnosis.
But has that been shown to prolong it or I was even like I didn't have a thorough conversation about it, but I remember talking to a muscular dystrophy researcher a couple of years back and he said in some cases they advise against exercise because it almost expedites the decline of motor ability.
So are you familiar with any research kind of correlating physical activity and the progression of the disease. I mean, I don't I don't I'm not an expert in that area of of ALS field and muscular dystrophy is a very specific disease.
So I think there's probably specific aspects. I think in general, you know, within reason and both for mental and physical benefits, having some activity that is where there's, you know, there's there's a.
Maybe there's got in the case of a severe disease, there's guidance from a rehabilitative therapy specialist. This this is a positive thing in most circumstances and.
But, of course, for a very severe and rapidly.
Progressing they use the word progressing for these diseases, which always sounds wrong headed to me. But anyway, they call it rapidly progressing diseases.
They're not going to be, you know, they're not necessarily going to slow the disease.
And that, you know, and I think that that also that's one of the many tragedies of the disease and that.
Many of these neurodegenerative diseases and diseases of later life.
The loss of mobility is is really a very negative aspect of the disease, and it can make it so that it's harder to to to stay healthy and other and other aspects.
That's the loss of independence is I would imagine incredibly frustrating. What are you most excited to work on over the next maybe 3 or 5 years?
Well, you know, the current project on genetic pediatric epilepsy is is really invigorating.
So, I'm hoping that we can make real progress and bring something into the clinic that has the potential to be a medicine.
And it's, you know, I think our ideas, they're, they're pretty bold. So I, I'm excited about that.
I'm excited as a, as a kind of bystander, a well, educated bystander to see some of these other programs and a last and spinal cerebellar ataxia, Alzheimer's disease.
These therapy, these therapy developments for these truly terrible.
Neurological diseases there.
They're advancing and I'm, you know, I'm really hopeful that.
We might have an inflection point where there's a new therapy and it's really.
Clearly a winning drug.
It would be so satisfying for science and for the patients and every everything to see that.
Absolutely. Yeah, that that's a good, hopeful kind of way to maybe wrap up some of this and in a topic that is incredibly challenging and can be disheartening.
I would imagine working with patients that have to deal with these conditions.
Hopefully, there are a lot of.
Progress that's made over the next few years in how we treat them.
So, Tom, thank you for sharing your expertise and doing my best to keep up with with the topics that you're covering.
But if anyone is interested in kind of learning more about the work that you do, is there a specific place that they can find you or.
Resources that you would direct them to. Yeah, I mean, I'm I, my home is, as you said, at the University College in London.
And so you can find me, you know, you can find me on the web. My email address is t otis at UCL dot.
You see, dot a, I'm sorry, dot a, c dot UK, a, c academic dot UK, UK.
And yeah, I, I mean, who knows? Maybe we'll see each other at.
A conference or some other events or in Massachusetts. Absolutely. Next time the next time you come back up to mass, if you've been a visit, Dennis, or anyone, you'll have to stop by the gym and see what he's working on with us.
But we can put that stuff in the in the show notes here, your email, and then the companies you're working with. So, Tom, thanks again. I really enjoyed.
A conversation and hope that the audience finds value in it as well.
Thanks so much. It was really a pleasure from my end as well.
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