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SciPodChat is an engaging podcast led by experienced Oncology scientist Dr Biswajit Podder that aims to uncover the mysteries of science in a digestible way for all ages, making complicated ideas friendly and pleasant. Listeners are taken on an enlightening journey exploring the wonders of the universe, the intricacies of the human body, and the cutting-edge technologies shaping our future through weekly episodes featuring conversations with experts from diverse fields, all while fostering a community of curious minds eager to explore the boundless realm of science together.
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S01-E03: Unveiling the Mysteries of Motor Neuron Disease, a Rare Disease
In this episode, Dr. Doaa Taha, an expert in motor neuron disease (MND), shares her insights into this devastating condition, English theoretical physicist Stephen Hawking was diagnosed with MND . She explains how MND disrupts communication between neurons and muscles, leading to muscle wasting and loss of function. Dr. Taha highlights the importance of early detection, innovative stem cell research, and the potential of patient-derived stem cells in understanding MND's molecular triggers. She also discusses the role of astrocytes in brain function and MND progression, emphasizing the need for advanced therapies and patient quality of life improvements. Her call to action encourages listener involvement in MND research.
Disclaimer: This podcast is for informational purposes only, and SciPodChat is not intended to replace professional advice. Please note that the views, information, or opinions expressed during SciPodChat are solely those of the individuals involved, not any professional organization in which they are involved.
We Talk Science
Hello Science Lovers. This is Saipur Chet, a podcast where we explain science puzzles in a way everybody understands. This podcast is brought to you by Stemduadu. The goal of Stemduadu is to make learning fun and interesting for kids. The games and exercise on Stemduadu are fun and help kids learn math and science at the same time. I am your host, dr Bishit Prudhar, a scientist with more than 12 years of research experience in cancer disease. Today we are joined by Dr Duhetaha, a neuroscientist who has travelled to Italy and then to London to study brain cells. Now she is working at the Francis Creek Institute working on a brain condition called motor neuron disease. She is also a TED Talk speaker. Let's hear from Dr Duhetaha about her exciting work. Without further ado, let's dive into the episode. Welcome to my podcast. How are you?
Speaker 2:I am good, thank you. How are you, bishu?
Speaker 1:I am good, I am happy that you are here today to discuss about your research and talking about science. So, as I mentioned in the beginning, that we are going to talk about today motor neuron disease, is it?
Speaker 2:Yes, okay, good.
Speaker 1:Can you tell me about what is actually motor neuron disease?
Speaker 2:Yeah, that's a very good question. So, to start with, motor neuron disease falls under the umbrella of more bigger term, which we call neurodegenerative diseases. The neurodegenerative disease means is the death of a subpopulation of neurons and, as you know, and the listeners also know, that each subgroup of neurons in our brain are responsible for a specific function.
Speaker 1:Right, so I just stop you in here. Can you mention what is neuron actually? Probably some audience that would not know what is neuron.
Speaker 2:Oh yeah, so neuron is the. So in our brain we've got millions of neurons that what they basically do is that you're responsible for sending the orders for our body to function.
Speaker 1:Right.
Speaker 2:So you can think about everything that we do, even blinking, even in our sleep, the brain doesn't sleep.
Speaker 1:Right, basically, neuron. You are mentioning that neuron is communicating in our body to different organs, exactly.
Speaker 2:So it's the maestro of the whole body. It's the one that controls everything that goes on in the body Right, and it sends the orders to harmonize the functions between the different organs in our body.
Speaker 1:Right, okay, so as you're mentioning about the motor neuron disease, so can I go and do more details? Yes, yeah.
Speaker 2:So the thing with motor neuron disease, motor neurons the word motor comes from movement, it's like explained like it's like a motorway, for example. So when we talk about motor neurons, these are the subgroup of neurons that are responsible for any type of movement in the body and in order to send, they are connected to the muscles and the muscles in our body. Any muscle in our body, its function will be movement contraction and relaxation.
Speaker 2:So these neurons are connected to those muscles and they send orders to these muscles to contract and relax, and then that will perform a function, a specific function, whether this function is walking, talking, reading, eating all of that requires an action of muscles to be able to perform this function.
Speaker 1:Yeah, you, basically any kind of activities in human life.
Speaker 2:Exactly. This is all controlled by the motor neurons in the brain and in the spinal cord.
Speaker 1:So my next question lead to that how common motor neuron disease in human population?
Speaker 2:It's a rare disease. So in the UK right now there is 5000 people with motor neuron disease. The chances in a lifetime is one in 300 or 400 to get the disease and the prevalence is one people in 100,000. So it's quite rare but the problem with it, it's a quite a devastating disease.
Speaker 2:So to explain what happens with in a motor neuron disease is that, as I said, the connection between the motor neurons and the muscles are vital for the function of our body. So what happens in that disease is this connection, basically, so the neurons are no longer attached to the muscles.
Speaker 1:So meaning that cannot communicate.
Speaker 2:They cannot communicate.
Speaker 1:Right.
Speaker 2:And then the muscles. When they don't receive any signals from the neurons, what they happen is they start to waste. It starts with stiffness and weakness, but after a while the function because they're not receiving, they don't know what to do they start, this function starts to go away. So, and why is it that there is no connection anymore between the neurons and the muscles? Because the neuron starts to die.
Speaker 1:Oh, okay, so why they start to die?
Speaker 2:That's a very good question. And this is exactly what we're trying to understand in with the research that we do. We know that there are genetic factors that contribute to the onset of a motor neuron disease, but we know that there is, like common cellular who mark. What I mean is that when we look under the microscope at a very, very tiny level, look at the single cell or the neuron itself, we do see that there are proteins that are not where they supposed to be.
Speaker 1:You mean that they are dislocated, exactly.
Speaker 2:Exactly so. You know, in a cell you do have a nucleus and that nucleus is like the vault it's like what contains the DNA and it contains the most precious thing for the cell. It contains the codes that give the cell orders to do everything that we know how a cell function. So then there are some proteins that are normally should be localizing in the nucleus.
Speaker 2:But, what we find is that or they shuttle between the nucleus and the cytoplasm, so they go outside the nucleus, but then they come back In motor neuron disease. What we often find, or something that we call a hallmark hallmark is like a very evident phenotype or that we observe in majority of cases. It's in 97% of the cases of ALS.
Speaker 1:And.
Speaker 2:I'm going to call it motor neuron disease, but I'm also going to refer to it as ALS and use them interchangeably. These two terms. What we often observe is that this protein, particular proteins, are mislocalized, so they go to the cytoplasm where there are the organelles.
Speaker 1:I have questions. Is there any specific proteins, or a group of proteins, or one single protein?
Speaker 2:Yeah, that's a good question. So so far we know that there are new protein. The main one that has been described a lot in the literature is an RNA binding protein. So, it's a protein that its function is to bind the RNA. It also has a function in binding to DNA, but mainly RNA. This protein is called TDP43. And we found, or the scientists found, that this protein is, rather than doing its normal function of shuttling from the nucleus to the cytoplasm, it goes to the cytoplasm and stays there which makes it alarms the cell.
Speaker 1:So it is supposed to be like moving, or it shouldn't be in the cytoplasm stuck right Exactly.
Speaker 2:Exactly Because it takes the RNA out of the nucleus to the cytoplasm and then goes back to get more RNA out to the cytoplasm. It's like a bus.
Speaker 1:Okay, this meaning that like, like, the protein is not working anymore? She just like stopped something happening in the engine of the bus, exactly.
Speaker 2:And not just that, this is actually a very scientific term that we use which is loss of function. Yes, Because then if you have a bus that moves from its first stop to the second stop but doesn't go to the first stop to pick people, then you lost the function of the bus, but not just that. Okay, you filled the space for the second bus that was coming to the second station, right? So then it's crowding the bus. Stop the second bus stop, because it's not going anywhere.
Speaker 2:So it's already disorganized things, exactly, okay, it's alarming the cytoplasm that this protein has been stuck here. And then a lot of proteins come together and they make this aggregate, and the cytoplasm doesn't like aggregates.
Speaker 1:Yeah right, Completely chaos.
Speaker 2:Yeah, exactly so you don't only just have a loss of function from the nucleus, but these aggregates starts to overload the cell because the cell want to get rid of them right of this waste that is there and that makes a lot of pressure on the cell itself. And these aggregates as well start to become toxic to the cell.
Speaker 1:Oh, it's toxic for one. So it released different kind of toxic products or metabolites.
Speaker 2:It also that's, it doesn't. It doesn't do that, but it also attract, like it grabs, other RNA that could be, in the cytoplasm. So it disrupts their function. Okay, it overloads the machineries in the cells that are responsible for getting rid of proteins that accumulate for a long time. All of that makes it a bit of a toxic environment, right? So you don't only have a loss of the proteins function from the nucleus, but you also have these aggregates that now have a gain of toxic function.
Speaker 1:I see in the cytoplasm Right. So yeah, it's kind of misregulation of those proteins. Exactly, and then it makes kewas. Yeah, right, okay. So thank you so much for explaining what is actually motor neuron disease. So my next question is so why is happening? So what's the reason? Is there any genetic factors and governmental factors or any mechanical factors? So what's the reason? Basically to cat motor neuron disease, yeah, so we know that it's.
Speaker 2:The main factor of this disease is aging, so we do observe it in starting from 50 onward that being said, there has been reports of quite younger cases of. Als we can. Some of it can be accounted for by genetic mutations. So basically the DNA that I was talking about, this code. If there is anything wrong with that code, it won't work properly.
Speaker 2:And it wouldn't generate the right proteins. Yeah, so in that case there is around 10% of the cases of ALS that could be explained by genetic mutations, but the others 90% of the cases cannot be explained by genetic mutation, merely because when we say genetic mutation or we call it familial, it means that we know that someone's that in the patient history family history there's someone in their family that had ALS, but sporadic, which is 90% of the cases.
Speaker 2:Someone might be diagnosed with ALS, but no member of their family had ALS before, because we know that anything in the genes can be passed down.
Speaker 1:Definitely.
Speaker 2:But sporadic. Some people can have the disease, but we don't know, but without any family history. But now we know that some of the genes that we discovered in familial cases are actually also mutated in sporadic cases as well.
Speaker 1:Okay, yes, I see. So you mean that, like anyhow, even though they don't have the family history, but the gene can be muted.
Speaker 2:Exactly.
Speaker 1:In sporadic conditions. Interesting, yeah. So my next question is so how frequently people are diagnosed with mutton-neuron disease? So people I don't see many people that know about the mutton-neuron disease, probably many of my audience in here. They don't have any idea about mutton-neuron disease. So how common that people are Error about the modern European disease. Do you have any ideas?
Speaker 2:Yeah, because it's a rare disease.
Speaker 1:Yeah.
Speaker 2:I don't think many people know about it, although we do know of a lot of famous few famous people that actually are like, got diagnosed with modern European disease.
Speaker 1:Okay, can I name them?
Speaker 2:Like Stephen Hawking's oh yeah famous scientist who actually got diagnosed quite early on in his life with modern European disease. Right Louis Garrick, the famous baseball player which actually disease is named after him.
Speaker 1:Okay.
Speaker 2:And, as I'm sure people also know, george Wilson, dodie Weir, the famous Scottish rugby player, would also diagnosed with modern European disease. So there are. It is there just because it's rare. People might know about it, but it's quite a devastating disease that I think it's important to increase awareness about it because it really not only affect the patient life by slowly losing control and losing movement and losing breathing and sleeping and all of that, but it's also affect the carers around the patients.
Speaker 1:Okay, so thank you. So what is typically the disease progress in a patient. So let's say they're diagnosed in early stage, and then what could be the consequence in the later stage of the disease?
Speaker 2:So usually patients would go to the clinic with having problems like just stiffness of muscles, maybe they start tripping, maybe things start to fall off their hands more often. So they go to the clinic with these symptoms. But it usually takes quite a long time to get diagnosed with a form of modern European disease, because there are different forms and the diagnosis can take around a year and from that actually once you get the diagnosis, the disease is quite progressed, like it progressed quite rapidly.
Speaker 2:So, within the span of three to five years, the patient lose the ability to breathe.
Speaker 1:Wow, yes, so it's really surprised me like within three to five years, Three to five years. Wow, okay, interesting. So as you are working on modern European disease right now, right?
Speaker 2:Yes.
Speaker 1:Okay, what are some of the most promising areas of research in MND currently and what you're doing? Can you explain?
Speaker 2:for our audience. So I work in and Ricky Petani's lab and in our lab we model modern European disease. So we're trying to understand the disease using human stem cells.
Speaker 1:All right.
Speaker 2:These stem cells, we get them from patients.
Speaker 1:Okay, can you tell me what is stem cells? So?
Speaker 2:stem cells are very amazing cells in our body. They have the ability to become. Their potential is the sky. Basically, they can become any cell in our body.
Speaker 1:Okay.
Speaker 2:And this was actually a discovery by China Yamanaka, actually, that he got the Nobel Prize for it. So essentially he found a way that we can just take skin cells from patients and from healthy donors and then they can be reprogrammed into these stem cells, meaning the skin cells or any cell in the body, at an adult, in an adult, at that stage the cells know what they're doing. A skin cell know its function, a liver cell know its function, a neuron know its function, and there's no turning back from that. What happened is that if you turned on four genes in those cells, they go back to a stage in which they can, they have the potential, they have the capacity, they have the plasticity to become again any type of cell in the body.
Speaker 1:Wow, amazing.
Speaker 2:Which is amazing Because it allows us not to just we then take these cells and then we take them down the path. So we took a skin cell we turned it into a stem cell and then we start to give it small molecules to direct it toward the path of making neurons and this would allow us to study the disease with the genetic background of the patient in a very non-invasive way to the patient. So in our lab we take these cells, we culture them in our dishes and we're able to reproduce the phenotypes that are found in the patient.
Speaker 1:You take newton stem cells. We take just the stem cell. Yeah, okay.
Speaker 2:After it's been reprogrammed from a skin cell and then we put small molecules to. The final destination is that these cells become neurons.
Speaker 1:Oh, I see, Wow, so you're taking skin cells and converting into newton.
Speaker 2:Yes.
Speaker 1:Wow, okay, cool. And then what do you do with this model?
Speaker 2:It's a model that would allow you to look inside each cell. For us, the main goal is to find exactly what's going on or what's going wrong in these cells at a very cellular and molecular level.
Speaker 1:Right.
Speaker 2:And see if there's any proteins or any RNA or anything that changes between a patient's neurons and a healthy neuron, so that we can use them as a target for therapy.
Speaker 1:Right. That's the final goal that we want to achieve. So, basically, what you are doing in the lab, as I understand, if I'm wrong please correct me. So you are making a model, so you just try to mimic a human kind of model. So and then you want to check what's going wrong and you try to find out. New therapy probably can be used for motor neuron disease.
Speaker 2:Exactly.
Speaker 1:So you just. It's a kind of tool to study motor neuron disease.
Speaker 2:Right, and it's a tool to study also.
Speaker 1:the main thing is to study early events in motor neuron disease.
Speaker 2:Because that would help immensely with early detection and early diagnosis, because that's what we really need.
Speaker 1:Yeah, definitely. Otherwise, as we mentioned, the disease progression is quite fast, in three to five years. So the loss completely the movement of any kind of functions. What is the complexity and challenges in motor neuron disease?
Speaker 2:The complexity and challenges is exactly the I would say multiple events Like at the cellular level. There is a lot that is happening.
Speaker 1:Yeah.
Speaker 2:You've got a lot of stress in the cell. Right, you've got oxidative stress. You've got the powerhouse of the cell, which is called the mitochondria. There is a dysfunction within the function of this organelle. So there are so many things, so many organelles that are suffering, yeah, and there is misregulation, or this regulation of the RNA shuttling, as I mentioned earlier. So the problem with what makes it quite complicated disease is try to really understand what is the primary event and what happens. What actually triggers all these cascade of events?
Speaker 1:Yeah, that's the fundamental question.
Speaker 2:Yes, Because if you can find that, if you can stop it, you can stop all the downstream effect.
Speaker 1:Right.
Speaker 2:And this is what we're trying to really understand like what triggers?
Speaker 1:this disease.
Speaker 2:We know you have the mutation.
Speaker 1:Right.
Speaker 2:You know it can affect the proteins, but there is, like we know, a and we know Z Right, but all the steps in between we're still trying to understand.
Speaker 1:Right, okay, so you are trying to understand what are the main culprit to induce these modern urinary disease. So you're studying mostly protein, or also you're studying the genetic level.
Speaker 2:We're studying the messengers of the genes. So basically we're studying. We know that the genes have a mutation. They get transcribed into a smaller code of what we call it an mRNA Right. Mrna is what makes the protein, and we usually study the interaction between the mRNA and the protein and how this interaction can exacerbate, or the disease itself.
Speaker 1:Right, so I was listening to your TED talk. You are heavily mentioned about astrocytes.
Speaker 2:Yes.
Speaker 1:So I'm really interested to know more about astrocytes. So yeah, can you tell me more about it?
Speaker 2:Astrocytes have been the focus of my research for quite some time now, and basically I've been actually talking about neurons this whole time.
Speaker 1:Yeah.
Speaker 2:And because we know that they're the one, that they're connected to the muscles and connected to the movement of the body. But then there are so many other cell types in the brain, it's not just neurons in the brain, okay. There's a lot of supporting cells in the brain.
Speaker 1:Okay, I'm learning new science.
Speaker 2:Back in the days they used to call them glial cells, because they thought that the function is just merely like a glue.
Speaker 1:Okay.
Speaker 2:Like making the neurons connected to each other. And that's it, just a glue.
Speaker 1:Wow.
Speaker 2:But actually they have more of a function than just being a glue, and there are so many of them.
Speaker 1:What are they?
Speaker 2:So we've got astrocytes. There is oligodendryl-sized, so that's it, a lot more than just one cell type.
Speaker 1:It's a kind of complex environment in our brain.
Speaker 2:It's a very complex environment and actually the ratio to the neurons and astrocytes in evolution. The more you have astrocytes, the neurons, that's actually a sign of evolution, yes. So they are very important, not just as a glue but to everything for emotions, for perception, for sleep. For the neurons to do their proper function, you need those supporting cells. So what is an astrocyte? Basically, we call it an astro. Astro means star sight means a cell, so it's a star-shaped cell.
Speaker 1:Okay.
Speaker 2:And it's always found in a close proximity to the neurons.
Speaker 1:Because they are helping to neurons Exactly.
Speaker 2:They make sure that neurons can do their proper functioning. They knew the neurons have a big, big responsibility. But you have to like, we have to understand that without the proper functioning of the supporting cells this neurons won't be able to function as well. So they provide them with nutrients. They take the nutrients from the blood vessels, they give it to the neurons. They recycle some of the small molecules or some of the small messages between the neurons and each other. They help maintain a proper micro environment for the neurons to function.
Speaker 1:Right, so you're meaning that, like, let's say, astrocyte is not working properly, so also neurons will not work accordingly, right? Yes, exactly. Yeah, so you mentioned in here astrocyte is a very important cells to support neurons work.
Speaker 2:Yes.
Speaker 1:Okay, and so what happened like in case of motor neurone disease? So how is related to motor neurone disease and astrocyte?
Speaker 2:Yeah, so very good question. So we know, in motor neurone disease what happened is. We have two things actually. So the first thing, because astrocytes have also an immune role. They fight any inflammation that is in the brain. So when there is a lot of stress in this environment, what happened is two things. The first thing is then astrocytes stop providing support for neurons All right.
Speaker 2:So they stop the recycling function, they stop taking up the excess messages from between the neurons. So there is an accumulation of these messages between the neurons which make the neurons constantly feel that they need to keep their function and keep firing Right, something that we call the excited toxicity, because the neurons, as long as the messages, these messages, are there, they will keep on firing and they will keep on doing the function, so they don't get to rest at all which affect them badly.
Speaker 2:This is one thing. The second thing is astrocytes. They are very supportive, but they have a very dark side as well.
Speaker 1:Like what.
Speaker 2:So basically, in ALS, in motor neurone disease, we know that they become toxic. So not only they would draw their support, but they themselves start to be toxic to neurons. So they start to secrete cytokines and chemokines, inflammatory signals to neurons, which does not help at all. If anything, it exacerbates the progression of the disease. So that's the problem we're having is that the supporting cells start not to be supporting anymore. They even become toxic to the neurons as well.
Speaker 2:So this is something that is very important to research, because we need to know what is the switch. Why did the astrocyte decided to switch sides?
Speaker 1:in that way.
Speaker 2:And how can we take it back to being the nice supporting cells to the neurons?
Speaker 1:Yes.
Speaker 2:Because even if you try to cure the neurons, as long as it's getting this toxic signal from the astrocyte we're not going to get anywhere?
Speaker 1:Yeah Right, good. So as I understand that, like astrocyte, is also playing a key role in motor neurone disease, what do you think in that research arena is going to happen in the next probably few years, or maybe a decade?
Speaker 2:I think there is a lot of potential. Do you mean for astrocytes in particular, or for the research of mutinural disease?
Speaker 1:So I mean role of astrocyte in mutinural disease.
Speaker 2:I think now there are a lot more people interested in studying astrocytes and understanding their contribution to the disease. People are now also interested to finding, as I said, like targets in astrocytes, that we can then manipulate or restore their function in some way so that we can get them to the good side rather than the dark side.
Speaker 2:I think it goes hand in hand. Like, as we're researching neurons and trying to understand what is going on with the proteins, with the signals, with the RNA not being in its correct place and all of these things, we need to also think about the supporting cells and how we can make them function properly Together. I think that would help us massively in finding a proper drug for ALS and other neurodegenerative diseases as well.
Speaker 1:Okay, as you mentioned about proper drugs, so what kind of treatment would be suitable for for modern iron disease, like it could be, like, as you mentioned, as a protein. So do you think that would be a individual kind of thing that you can block that some function or connective at the protein structure? So what kind of drugs could be? I'm just, it's a hypothetical question, so what do you think?
Speaker 2:I think it's a very, very good question. I can tell you from what is around now. We've got one drug that inhibits, like it inhibits the function of a receptor on the neurons.
Speaker 1:As.
Speaker 2:I said the neurons. When the astrocytes stop clearing up the small messages between the neurons, there is a buildup of these messages. We call it a neurotransmitters and the neurons keeps on thinking oh, I need to keep working. So it's like they work nonstop, to the point that they get a burnout. So then you need to block the receptors that receive those messages, so that you can understand, or the signal exactly, so they understand.
Speaker 2:Oh, now we can switch off. So this is one of the drugs that is available and have been used since the 1993.
Speaker 1:Already it's FDA approved.
Speaker 2:Yes, this one is the one of the drugs that is FDA approved to, so that's an. We call it an inhibitor because it inhibits the function of the receptor. Basically, it occupies the space through which the signal should have been sitting on the receptor Rather, we fill that space with this drug. This is one of them. There is another, actually very interesting area of research now, which is anti-sense oligunucleotides. Okay what is that? Basically, it's a small strands of letters that have the same letters as the letters in the DNA.
Speaker 1:Exactly Just like a code.
Speaker 2:Like a code. It's a small sequence of a code and, if you remember, we were talking about proteins not working properly, proteins misfolding or aggregating. Not just TDP43 that aggregates, there are other proteins that aggregates.
Speaker 2:One of them is SOD1, which is one of the genes. We know that it accounts for around 20% of familial cases of ALS, but it's also been reported as sporadic ALS as well, and so essentially what happens is that if you have a mutation in that gene, the product of that gene, which is the protein, will not be working properly and it will have more propensity and tendency to aggregate and we know aggregates in the cell is not good, not good yeah.
Speaker 2:So what do we need to do is that we need to stop this gene from making those aggregated proteins. So then, when you have the DNA, when there is a small copy of it, which is the RNA, this antisense oligonucleotide or ASO bind to the small RNA and degrade that small RNA, so you no longer get the misfolded protein or the aggregates and in that way you remove the stress of the cell of having to deal with a form of aggregates in the cell and this actually now is being used in clinical trials.
Speaker 2:It's called TOFISERN and this is one of the, I think, promising how hopeful you are. For honesty, especially like I think we need to start having more like precision medicines. So it will be targeted toward the mutations that we characterize.
Speaker 1:Right.
Speaker 2:And we make drugs or therapies that are directed toward each specific mutation or misfolding or a problem that is happening in the cell. So that's why it's very important to understand exactly what is going on wrong in these cells at a very cellular, molecular level to be able to come up with these sort of therapies.
Speaker 1:Right, it's very interesting, as we talked about therapies. So my next question is that how manageable the motor neuron disease for a patient's perspective? What do you think? I know of us? You are not a medical doctor but, like I just want to know your opinion, what do you think is?
Speaker 2:I think they are one of the most courageous people you will ever meet in your life and it's really an honor to be working with them to trying to find a drug for this disease. It's not easy.
Speaker 1:Yeah.
Speaker 2:To, within a very short span of time, to be losing function, normal things that we do like when you don't think about, like waking up, going for a walk.
Speaker 1:Yeah, I can think about it, yeah.
Speaker 2:Like it's just things that we do without thinking, but that would require a lot of work from someone with a different kind of setup for them to be able to have some fresh air or go on about their days or be around their loved ones. So it's really, I think it's a very, very, very, very tough disease. And I really hope we can find a solution, probably drug to it very, very soon, because that will help a lot of people. Yeah.
Speaker 1:And it will improve the quality of life of the people who are affected? Yeah, definitely it's a rare disease and probably not so many people probably affected by this disease, but still I feel it's really highly important task to find a treatment for motor neuron disease 100% yeah 100%. Okay, cool, I learned a lot about motor neuron disease. Hopefully my audience also learned a lot of things from you. Thank you. Before wrapping up, do you have anything you want to share to my audience about motor neuron disease?
Speaker 2:I would just ask people, whenever they can, if you found surveys online, because sometimes we need data, not just from patient. We also need data. As I said, we need to have a comparison.
Speaker 1:Right.
Speaker 2:So that comparison is always against healthy people. So if you found survey that asking you about like certain questions or lifestyle things, please take part in these surveys.
Speaker 1:Very important to get the information and to get the right approach to treat a disease. Yeah, the disease Right.
Speaker 2:This is how we can all, we all making our very, very tiny contributions and this could be one of those things which is actually a very big contribution.
Speaker 1:Yeah, but you know what, Like, we receive a lot of survey email and we often ignore those emails. So I'm telling to my audience if you say any kind of survey email, please try to respond, try to spend some time to read and probably to contribute for that research If you see this kind of email, especially motor neuron disease, yeah, exactly yeah. Thank you, dway, for your insightful conversation to our listeners and to be honest.
Speaker 1:I didn't have any idea about motor neuron disease, so I learned a lot from you. Thank you so much. Thank you for listening to Cybert Chat. Thank you all the people who is listening. Cybert Chat. We talk science and let's know science together. Until next time, stay curious, stay inspired and stay tuned for more exciting conversation right here on your favorite Cybert Chat. Thank you, bye.