#46. Why we need to research Parkinson’s Disease - Bethany Facer

Bethany Facer, PhD student at University of Liverpool and Science Communicator explains the intricacies of Parkinson's Disease. We discuss Beth’s Neuroimaging research into the neurodegenerative condition as she goes over some of the key biological mechanisms, clinical manifestations and current treatments which together highlight the need to better understand this multifaceted disorder. Later, co-host Pollyanna Ward and Beth discuss the importance of science communication in current times and how researchers can improve our communication skills

https://www.liverpool.ac.uk/systems-molecular-and-integrative-biology/research/groups/brain-imaging/

Chapters

• 0:00 Beth's Journey into Neuroscience
• 8:38 Understanding Parkinson's Disease
• 17:10 The Role of Dopamine in Parkinson's
• 21:18 Current Treatments for Parkinson's Disease
• 27:26 Genetic Factors and Future Therapies in Parkinson's
• 31:25 Parkinson's Disease: A multifaceted condition
• 37:27 The Role of Neuroimaging and Diagnosis of Parkinson's
• 43:19 The future of MRI scanning and ethics
• 49:47 A Participant's Journey in Parkinson's Research
• 59:18 The Role of Science Communication
• 1:08:54 Changing the Narrative: Misinformation and Science

Transcript

0:04

Welcome back everyone to the Smooth Brain Society. Today our topic of discussion is going to be Parkinson's disease but also we're going to be talking about potential career and science communications. For that I have Bethany Facer. Wait I should have asked you, is Facer the correct spelling or pronunciation? Facer, spot on yeah Bethany Facer. Okay cool cool. You got it right. got Beth Niefacer on who I did a, I did master's with in King's College London. Now she's doing a PhD at the University of Liverpool and is also a science communicator herself. She does way cooler stuff because she does public presentations, unlike me who hides behind a mic and prerecorded settings. But she's on to talk about her work and then we'll talk a little bit about her work in science communication later. So welcome on Beth. Thank you for having me, Sahir. And as you guys know, the concept of the podcast, just for anybody who's new, we get a co-host on who has no idea about the topic. Today, I'll let her introduce herself. We've got Polyana on, who is a marketing person and has worked in the science, not science communication, communications and podcast space for a while. So she's probably critiquing how I run this podcast at the moment, but welcome on. Thank you for having me, Sahir. Definitely not critiquing. Hi, everyone. I'm Pollyanna Ward. And yeah, as Sahir said, I've worked in marketing for the last 10 years. So I'm hoping that I can sort of be a bit of a naive voice in the room for this episode. And hopefully it will come away knowing exactly what Beth actually does. So thank you. All right. So... I guess before we start with what Beth actually does, we should start with how you got here. So could you give us a little background Beth into why do a PhD, why get into the work you're doing and take it away. Yeah, of course. So I mean, it's going to be a bit boring to say I just loved the brain when I was about 16, 17. It was just cool. We didn't know what was going on. So I thought, oh, you know, I'm not quite sure what I want to do. Classic 17 year old. I went to university to do neuroscience with psychology. And it was very, it went to Kiel University, lovely little university that gave me loads of opportunities to study abroad. And it also gave me an opportunity to study in or to be a research assistant in Poland for a year, where I was able to actually I was incredibly lucky. I was able to work with mice looking at so my cat's going to be in and out. So this is moose. looking at mice and schizophrenia, looking at something called MMP9. Don't need to go into details about what it is, but they thought that it might cause some of the symptoms such as hyperm... lots of movement and specific fear responses. But it's very interesting. Got to work with animals. I don't think I... I think after doing that I was like, I don't know if I want to work with animals again. It's quite an intense, so when you're studying it. But it was a very cool year. After that, finished, came back, finished my university degree. I was one of these people who kind of had classic imposter syndrome. So I decided to take two or three years out and I worked as a wedding supervisor, which I'm actually so happy I did because my organization skills are now absolutely second to none. I could plan an event like no tomorrow. So it's very enjoyable, but I miss neuroscience so much that I went back to, and went back to university to do my masters at King's College, London in clinical neuroscience. I admit I had been out for two or three years, so I was quite fearful. I wasn't going to be able to get back into it, but I honestly think it was the best year of my life, living in London, learning all about. you know, the clinical aspects of neuroscience, which I really enjoyed. And then I started getting into neuroimaging a little bit more and working with a group who specialised in movement disorders. And when I say movement disorders, it means that they have problems with their movement, but specifically Parkinson's disease, which is the second most common neurodegenerative disease, second to Alzheimer's disease. And I was learning a little bit more about computational skills and about how we can look at the brain using MRI scanners, which I could talk a little bit more about later, and how it's a non-invasive, very cool way for us to take snapshots of the brain. I was just absolutely sold. And so then I was a little bit of research assistant after that for a little while, kind of gaining a little bit of experience, trying to find the PhD. And then I met my very lovely. lab and supervisor, Professor Simon Keller at Liverpool, who I actually applied for a slightly different PhD in infectious diseases and neuroimaging, something called neurocystic psychosis, which is basically little worms in your brain, which was wild. My friend Corey is working on that. But after speaking to him, he decided, well, he was like Beth. I can tell how much you really enjoy Parkinson's disease. It's, I can see the passion, I can see the love. And he put in an application and when he awarded it, he gave it to me and that's how I got here today. Awesome. Fantastic. I think I had just a couple of questions. One is, what is the difference between clinical neuroscience and neuroscience first? Yep. No, no, and a little bit more in the clinics. When you kind of do pure neuroscience, it can still be clinical, but it might be more cellular or molecular and a little bit maybe further removed from that. So you're kind of looking right down to the cells and the molecules, or usually not always, it can be a little bit more wet lab. And when I say wet lab, it means you're doing experimentations with pipettes and you're the usual scientist you see in the lab coats, you know, working away in the lab. But you can still, it's basically kind of caused just a little bit more applicable to humans. Closer. I don't know if you can see it. So here, if you have anything more to say about that, that's an accurate description. Yeah, that's about right. I am, what do you say? Cause I'm the non-clinical neuroscientist. And I, so I work with rats. I work with those little cells and pipettes and moving liquids from little tubes, just little low tubes. And like a real scientist. Sure. I feel clinical neuroscientists get paid more. So I don't know. I think there's a lot more, no actually I'd have to say like a lot more clinicians do clinical neuroscience because it's a lot more people focused. But that's probably as fair. Yeah. So I think naturally they've probably got about five or six years on us. So they probably demand a higher wage. I can just sneak in there and pretend that I'm part of that gang. And I imagine that working on humans are a lot less wriggly than working on animals. Well, that depends. It really depends. They definitely complain a little bit more. No, I joke. It's actually, I guess that you can get consent from a human, which I quite enjoy. Now, I've worked with humans as well and yeah, it's a lot harder. work with humans, I'd say they talk back. It's a big problem. They don't follow rules. Oh my god, rule following is so terrible in human words. Yeah, I mean, and part of my study, I'm doing some cognitive tests as well. So it's, you know, running through making sure they fill out the forms accurately, but also it lands on me a little bit as well, because if I don't explain it very well, then... other people will struggle and because I've done it so many times it's having to each time come back and be like okay what was the first time you saw it and kind of try to regularly practice on people to make sure I'm still explaining it well enough. Okay, because you said you were going to explain a little bit about Parkinson's. Let's go with that. So could you tell us a bit more about Parkinson's apart from it just being the second most common degenerative disease? Yeah, of course. So as Paulina said, it affects part of the brain called the basal ganglia. I won't go into the tens of sections within the basal ganglia, but I'll... you one area within the basal ganglia called the substantia nigra that it affects and it affects these dopamine producing neurons. Now dopamine is a neurotransmitter and a neurotransmitter is basically how the brain talks to each other and in this case with those loss of dopamine cells it causes a loss of movement in the long run and because it's degenerative that means that it gets continue to get worse and worse with this buildup, with this loss of neurons and this buildup of something called alpha-synuclein. And what's alpha-synuclein? It's basically these little protein aggregates. And when I say an aggregate, basically it's just a mass that is insoluble. It doesn't go away. It attaches to the cells and it doesn't leave and it causes problems because specifically for this substantia nigra area that I said, it causes this loss of dopamine cells. but it spreads throughout the brain. But this area, substantia nigra or basal ganglia, is particularly susceptible to the self-destructing nucleium. So that's maybe the biology behind it. Do you have any questions about the biology, Pollyanna? I could move on to the clinical, or the how it presents a little bit more. My question is, is there anyone famous that has Parkinson's disease? Yes, yes. And yes, I think it is relatively common. And you've got Michael J Fox who had quite, he was very young, he was 29 when he was diagnosed, so it's quite relatively rare to get it that young, usually affects people over the age of 55. So Ozzy Osbourne has it as well at the moment. Yeah he does, yeah. So there's, yeah. So yeah, affects everyone. I'm pretty sure Mama Deli had it, right? That's what he had. Yeah, absolutely. Muhammad Ali. Yeah, yeah. And it was that was really interesting because I can talk onto that a little bit more. But there was questions. If Muhammad Ali had it because it seems to be an increased amount of boxes and fighters seem to have Parkinson's disease and they're wondering if it's some insults to brain injury that causes Parkinson's disease. I think Michael Parkinson of the TV show from years ago was also diagnosed that now you've prompted a thought. Yeah. But no, it wasn't a, I think I maybe did see the Ozzy Osbourne had it, which is, and you mentioned there that Michael J. Fox was super young, 29. When might you start seeing it like more gently? What is the average? Average, probably it gets more common as you get older. So you will see it, the older the people are, the more likely they are to have it. I believe people over the age of 65, one in 100 people will have Parkinson's disease. I believe it goes to... about five in every hundred or one in every 20 by the time you reach 80 or 85. So it continuously increases. And yeah, some scary figures, for example, they're expecting in the next 30 years, that one in 37 people will be diagnosed with Parkinson's disease. As we've got an ageing population. Yeah, it's a high figure. So I'll put it this way, people who are alive today, there is a one in 37 chance that they will get Parkinson's disease. So it's coming in hot and fast. So it's important why we research it. So is that purely because of just the population aging or is that also for other environmental reasons? Just the population aging. Yeah, so it's because we've got an aging population. It's nothing to be that sounds scary. It's not a good thing, but it's the fact that we are living longer, cancers are being cured. And the next one that's gonna be coming in is neurodegenerative diseases, because that is the population. In fact, there's older people, so it's really important that we come up with treatments and possibly cures. I think the ones, I mean, you mentioned it earlier. And I think when I've seen people, for example, on social media, like raising money, they're running a marathon, they've got someone very close to them that's possibly been diagnosed with Parkinson's disease. but then they are then if you'd like to help donate, I'm raising money for Alzheimer's UK or the Alzheimer's Society, I follow the name. And I'm just wondering, is there a difference between Parkinson's and Alzheimer's or are they intertwined or I think you get a lot of, I mean, there's a bit of people kind of, I don't know whether it's confusion or are they the same? You know, that's a really good question. They're not the same. Alzheimer's disease is a dementia. So it affects your memory. Well, the most, so Alzheimer's is the most common that affects your memory. Other versions of dementias are something like Picks' disease that affects your frontal temporal lobe and gives you personality changes, but it's still a form of dementia. You've got things like Broca's aphasia, which I believe Bruce Willis has, where you start to not be unable to speak. It's just a different type of, I guess, loss of cells. But no, Alzheimer's and Parkinson's disease are different. But that doesn't, so when you have Parkinson's disease, there's also a bit of an increase of possibly getting dementia. But specifically Alzheimer's delight, delight dementia, so cognitive decline. Which I think possibly for some people, when I've been talking to people, that is the scariest thing. The movement is really unpleasant, but losing your movement and then also having dementia is almost like a double whammy. So I think for a lot of people who are viewing it, the movement maybe is bad, but then on top of that, the family members are losing themselves almost. So it's possible that people think, okay, I want to help with the Alzheimer's and also help with the Parkinson's, but there can be some crossover. Absolutely, yeah. How common is the crossover in that sense? Oh, I don't know. specifically Alzheimer's disease and Parkinson's disease. But within Parkinson's disease, I believe it's higher than, it's higher, I can't remember the exact numbers that might come back to me later on in the podcast, but it's definitely higher. So for example, I'm doing a study looking at cognitive decline. Yeah. And so you can't, I think my next question was really just going to be, you know, you mentioned there's cures for cancer. Is there a cure for Parkinson's disease then? There's not no. Currently, there's nothing that stops it. There's, I mean, this past year, there's been some very early clinical trials. It's called UB312. And it's a vaccine. which is meant to basically cause an immune response. So almost similar, you know, but in the brain, but imagine if you have a cold, for example, you know, you run well, your body creates that immune response to kill and get rid of that cold and create antibodies. And antibodies are the thing that comes and fights and gets rid of that virus or whatever it may be. But in the brain, if they're hoping for this vaccine, that it will fight these ace nuclein aggregates or little clumps of proteins I spoke about before that spread throughout the brain and cause problems in the basal ganglia. It's very early so they're still kind of working on it but it's on its way to hopefully helping. I wanted to ask a question sort of going back to the biology of it because we spoke about it's a reduction in the dopamine to an extent. And that's associated with, initially with movement problems. Could you, when we think about dopamine, generally, we think about it as, you know, along with serotonin as like the pleasure drug or, Yeah. also the pleasure neurotransmitter or things like that. It's not really associated with movement. Could you like explain, does dopamine have multiple roles? Yes. This Does Parkinson's also show like mood problems or like mood disorders because of the reduced dopamine? How does that sort of get together? That's a great question. And then from that question, I can move into the clinical actually a little bit more. So no, it doesn't just, you're absolutely right. Most people do think, I mean, I think a drug that we know kind of affects those systems is cocaine. It targets the pleasure center. So the substan-shnigra creates this dopamine, which feeds into the movement area. but there were other parts of the brain that also produced dopamine. So with that area that's involved in the pleasure centers, it's called the ventral tegmental area. I'll call it VTA, don't have to remember it, but it's there if you want to look a little bit more into it. And that does affect the pleasure centers. But also when people are first diagnosed with Parkinson's disease, they tend to show tremor and the three symptoms of bradykinesia, which is slowness of movement. rigidity, which is, you know, like kind of rigid movement and tremor, which is tremor. And the first port of call when somebody's diagnosed with Parkinson's disease, they're given something called L-Dopa. And this increases, there's different ways that you can give dopamine and it's affecting the neurotransmitter. Now the neurotransmitter is where the neurotransmitters is is what's called the dopamine and the synapse is where that is released and it affects the synapse. So, you know, one great way is like thinking like the synapse is the bus terminal and the buses is the dopamine and I imagine just that there's a reduction in buses but the terminal is still there. So what you try and do is you try and send in either you can block the part of the synapse so that the buses can't go back to the synapse. So they keep, keep re-triggering and doing their job over and over and over again. Or you can just send in more dopamine. So you're just sending in lots more buses is one way. But, and that will help them with some of the symptoms such as tremor and bradykinesia. So, so it's a movement. But what we also find sometimes when we give people L-Dopa is... their moods increase. Sometimes rarely they can get also hallucinations can be an effect of that. And that's because one theory of schizophrenia, for example, is an increase in dopamine. So when you increase dopamine, you can get hallucinations. You can also get impulse control disorders. And that means these people who are perfectly, you know, normal citizens go and become gamblers, sex addicts. And it's almost like that because that increase of dopamine is causing that. These are very rare, but they are sometimes caused by the cell doper. But because of that lack of dopamine, you're right. So here sometimes there is depression is really common as well. So within my studies, I'm also looking at mood, so anxiety and depression. And I'm purposefully doing it before I've given them drugs to see, so the drugs won't have affected, won't have affected their dopamine at all. So I will be looking at their mood and seeing if this dopamine loss is affecting their mood as well. So I guess because there's no cures for Parkinson's, maybe this is coming onto your PhD now. So then, what are you trying to do, I suppose, in your research? So I think just going on a little bit, there are no cures at the moment, but there are a few more treatments, I think one of the most common ones, one of very briefly discussed as I've spoken, you know, a little bit about L-Dopa, but there's actually something called deep brain stimulation that I think a lot of people are interested by. It's these videos that you see people with quite advanced Parkinson's disease, you know, really have quite a pronounced tremor and suddenly something switched and it just completely stops. And that's when you can go for brain surgery and it's later on in the disease when it starts to get quite unmanageable, some of the symptoms and the L-Dopa will at some points not work as well. When, you know, the... those neurons are completely depleted and there's basically nothing yet. Even if the dopamine was there, there's nothing it can connect to work. So basically it's putting some little electrodes into the basal ganglia and giving it small amounts of current. And this stops the tremor basically. So that's another one that's really important. And that shows us that there are treatments that are still, you know, incredibly helpful and can help, you know. years after diagnosis. In terms of with my PhD, I think it's just two kind of things I kind of want to learn a little bit more about. The first one is understanding the biologically what is happening a little bit more. So half of my study, I would say, is I'm using neuroimaging, which I'll talk about in a bit. a little bit more after this, but basically I want to look at the so grey matter and white matter in the brain. So within the brain, you've got grey and white matter. The grey matter is the grey part on the, if you were to cut it open, you'd see it kind of like around the outside and a little bit in the centre as well. And this is basically... What brains with pink? This is where all the thought is happening, all of the cell bodies are in there. And when I say cell bodies, that's where all the action is happening. And then the white matter is how those parts of the grey matter, all those cell bodies communicate with each other. So the brain needs to connect up because the brain has different parts which is needed for everyday goings on. For example, I'm moving my hand, if I say hi to somebody, I'm moving my hand, so the initiation is the basal ganglia, but then it needs to go up to the motor cortex so that I know to move my right hand and wave. And then also I need the frontal lobe to make the decision to wave and memory to see that that's my friend over there who I am waving at, which is the temporal lobe's a little bit lower. So it needs to be able to connect up with each other. which is really important. So there's lots been done on the gray matter areas because that's, you know, the hub of it. That's where it all happens. I want to look a little bit more about the white matter. So a great analogy that I'm sure Sahir will have, will know it's about train tracks and train stations. So the white matter is the tracks and how it all connects up. And some of those tracks maybe haven't been looked after properly or a little bit damaged, or they might be running extra time. So they're a little bit larger or they're compensating. for something that's happening upstream. So I'm understanding what's happening within the white matter, within people with very early Parkinson's disease, so very early in the disease course. Now for me, I think if we look at very early in the disease course, that's a time when we can really help people. The symptoms aren't so awful that they're affecting, it's, you know, there might be a little bit of tremor, there might be a little bit of rigidity, a little bit unstable on their feet, but it's still early enough that they can still enjoy their lives. So if I understand what's going on at that very, very early stage, I think that's a time when we can really still help people. So at that point, with the basal ganglia, that cell loss, we're looking at around 50% to 60% cell loss. So that means there's still some cells in there. But two things, and then for the second part that I want to kind of understand a little bit more. So the first part is understand what's happening in that white matter and very, very early on, and possibly if we can figure that out, how can that lead to treatments? and just tells us biological mechanisms. But on top of that, if we're not seeing changes until 50 to 60% of that cell loss, why is that? You would think, you know, 10% cell loss, we'd see some kind of changes in movement, we don't. So what's happening in the brain? So the brain is really resilient and it's smart. So when you have something going wrong, the brain will compensate, it will find another way to do it. and it will only really start to show the clinical changes, so the tremor or the bradykinesia, when it absolutely can't compensate or do anything more. So I'm trying to look at what possible areas of the brain could be helping with movement because the basal ganglia is struggling. Does that make sense? No, it makes sense. I mean, you keep referring to sort of like the movement side of things, but then it's a neurodegenerative disease. So is it neurodegenerative because the problem with movement is starting in the brain? Oh, so it's neurodegenerative. So when I say neurodegenerative, what I mean is, so this is the difference between Parkinsonism and Parkinson's disease. When you have a Parkinsonism, that doesn't necessarily mean it's neurodegenerative, and what that means is it's not going to get worse over time. If you have Parkinson's disease, that cell loss is only going to get worse and worse and worse over time, similar with Alzheimer's disease. And this might be a stupid question, but could they not just, like, pump loads of new cells into you? Unfortunately, not. No. They have actually tried some stem cell research where they... But there's two things of that. It's very... difficult to create stem cells that you can insert in your brain and will stay. Because your brain, if it notices anything is in there that it shouldn't be, you'll get an inflammation and that will basically destroy your brain. It'll absolutely attack your brain. So your brain attacks itself because it says this thing shouldn't be here and it's dangerous and it's just very hard to make those cells as well. You have to. I won't go into too much detail on this, but within stem cells, they're some of the earliest forms of cells that you get, you know, when you're when you when you're a fetus, basically. So we don't we don't produce those. Yeah, I always just think of you know, how they've like grown ears. Yeah, so that is that is part of the reason that is there was lots of research into it. And it's important research because that's absolutely that's why it's a good question, Pollyanna, because yeah, people are looking at that. It's just it's fiddly, shall we say. I can imagine. There's another one which on the same lines is gene therapy. So I assume because everybody doesn't get Parkinson's, like you said, potentially one in 37, that's still one in 37. That means there's a genetic sort of element to it, right? Not everybody gets it. So can't you sort of turn off those genes? So I can give you some good examples for this actually. So yeah, and they, well, so far, of Parkinson's disease is genetic that they can say this is genetic and they know the genetic gene that is kind of causing that. So for example, there's two of the most common genetic causes, something called GBA and LERK2, but they are two different genetic mutations, but they cause Parkinson's disease in different ways. Just to give you a very quick example, because I think this is quite an understandable example. With GBA, basically, it no longer creates a protein called GBA. And you need that protein and two other proteins to combine together to eradicate all of it. If you don't have this third protein, this GBA protein, you have these two. proteins that just kind of can't, can no longer be dissolved. So this is what causes problems. And then, such as the alpha-synuclein that builds up, becomes insoluble because you don't have something that is called catalyzing the reaction and dissolving it. So we know that causes that, which is, of course, a problem. But because we've got things like LIC2, SNCA, it's another one. they all cause Parkinson's disease in different ways. And it's usually, yeah, like it affects the mitochondria, for example, but because it's not one exact way that these genetic mutations are causing Parkinson's disease, they still can't pinpoint idiopathic. Idiopathic means that just an unknown cause causes it. So that's, yeah, but it's a very good question. Like you'd think that we should know by now. And we do use these genetic mutations as a as example, just differences, and as to kind of study a little bit further and see if we can find drugs that target these areas, but they don't always work. And there's not been too there's not been very much luck with them yet. So I think that's why now they're trying to target just alpha-synuclein because they know that's the issue. And yeah, with the vaccine. You're kind of saying Parkinson's disease is not like one disease with the exact same thing. It's like the symptoms are the same, but the underlying causes are potentially very different each time. And therefore the treatments very different each time. I think that's so actually just to give a little more actually with Parkinson's disease, although I've mentioned, yeah, it's a movement disorder. No two cases the same. It's incredibly heterogeneous. So very different cases all throughout. It always has to have movement disorders. But I could list off about another 10. symptoms that go along with it, I will even listen off now. So autonomic dysfunction, that's problems with your urinary tract or constipation. Autonomic dysfunction can also be problems with your sleep. So you can get something called RBD, which is rapid eye movement, behavioural disorder. And basically that's when you dream, you don't have something stopping you from almost living out your dreams. So people are all out, you know, they're moving their hands, they're walking, they're almost like sleepwalking. then you can also have depression, anxiety, psychosis. There is so many extra symptoms that a lot of people don't realize. Cognitive decline is one that I'm currently looking at. It's so multifaceted. and that could be the fact that it's, and that's another part of my research is where I'm trying to group certain people with certain symptoms a little bit better to understand the biology behind that a bit better because there's a big people, well, it's been going on for a while now, people think, can you just look at Parkinson's disease because no two cases are the same? We probably have to look a little bit better and look at something called personalized medicine a little bit more. That's where... no two cases the same, we have to take this person, their symptoms and treat them specifically to help them. How do you, you know, I think when it comes to something like cancer, everyone is very aware of it. Anyway, it's one of those things where the more people are aware of it. You kind of get, for example, in people that are perhaps slightly more pre- predisposed to sort of anxiety, etc. or have anxiety conditions, you know, because there's so there's a lot of awareness of cancer, and there's a sort of awareness and knowledge that Oh, if this is hurting, it must be cancer, you know, it's that classic thing, if you Google your symptoms, and it tells you have cancer, what is, is there a fear that you know, you talk about cancer, there's cures coming for that. And so the next second biggest one is then Parkinson's disease, then how do you avoid a moral panic where if someone essentially has a UTI, a urinary tract infection, how do you stop them from assuming the worst and that they've got Parkinson's? Like, is that going to happen? Yeah, that's a good question. So things like UTI and constipation are just something that a minority have, or not that many people have. And it's not, it wouldn't be the only symptom, it would be like an extra. So we've got something what you call prodromal Parkinson's disease. That means that it's before you can see the movement changes, so it's called prodromal. But if you were to scan these people using something called a DAT scan, you could see that there was starting to be some loss of dopamine, but it hadn't yet affected their movement. And there's probably... The most common risk factor and the most common symptom that I've just briefly discussed was the rapid eye movement behavioral disorder, we'll call it RBD, which is... that if you have that, then that's, it doesn't mean you're going to get Parkinson's disease, but it's common enough that you want to get yourself to the doctors and monitor it. You know, there's been a couple of people that I've scanned recently who started with RBD and they then went on to get Parkinson's disease. So, I guess what's the symptom then that people, you know, is it people waking up one day and suddenly they've got tremors and then they get diagnosed or is it, you know, you wake you know, a bit of a twitchy eye, and then it takes six months before it's like, Oh, no, you know, and your doctor dismisses you the first time because it's like, Oh, you probably just slept on it funny. I mean, I'm not a clinician, but I think from what I can tell, well, but when it is, but it's, it's insidious. It actually the tremor isn't always straight away. It's slow. It's very slow. And then it's just been like, yeah, six months or a year. And they're like, that tremor has not gone away. And then it's really getting worse and worse. There was a woman who came in who you know, said like she hadn't really noticed anything, but she was painting. And when she painted, she noticed that there was the tremor there when she was trying to paint and she said, that wasn't there before. And it was there for about six months. So that's, that's what, you know, it was doing everyday activities where I think people start to realize, and it's not always you that realizes because, you know, because it's insidious and it's happening slowly, you just think it's the norm. It's actually usually relatives that start to notice some of the movements, the movement issues. Yeah, that's probably but the RBD, if you were to get things at RBD and sometimes something called anosmia, which means you lose your sense of smell a little bit. There's also another one that kind of is a little bit of a prodrama one but you know, that's can also be quite common for other reasons such as COVID-19. Great names, you know, anosmia. For the nose. And anosmia just can't smell. I suppose I mean, it goes into an entirely different topic and probably a whole other podcast episode, but then I imagine with a loneliness epidemic that we are seeing, you're going to get less cases being known because like you say, if people rely on others to point it out, you might just end up with people not even realising. And I think the other thing as well then, so when you go to the doctors and you're like, right, I've got this tremor, do you have to go for an MRI? Can they do a blood test? Like, how do you get diagnosed? Yeah, that's a great question. So it's actually a clinical diagnosis. And so that means the clinician will diagnose it. And they have either, they will, some clinicians who I know who are just so, they've seen so many cases, it's almost like they just go up, ask a couple of questions and they ask them to do a couple of tasks and they just know that you do have Parkinson's disease. But then there's something called the Unified Parkinson's Disease Rating Scale, UPDRS. that can tell you a little bit more about those symptoms and the extent of them. But saying that Parkinson's disease is not the only movement disorder. So there's some other rarer ones, they're called Parkinson's plus syndromes. An example of that is something called PSP or multi-systems atrophy that look very similar to Parkinson's disease. They're a lot more, usually a lot more aggressive. So if you have one of those, the survival rate is, or the quality of life isn't as great and survival rate isn't as long, but they can prevent it very similar and if they think that they might have one of those diseases, absolutely. That's when you'd use something called, you'd look at, you'd probably want something called a DAT scan that can show you that there is one-sided loss of the dopamine neurons, which is what Parkinson's disease, how you can identify Parkinson's disease a little bit better, or if you're unsure. These stat scans are expensive. They're very expensive, so they won't always put people in for a scan because it's just too expensive and if it can be diagnosed with a clinician, then that's what they'll do. Because you said you work with neuroimaging and you and we're talking about this sort of slow change which I guess family members notice over time and things like that. Do you, can you see these changes in neuroimaging? So have I do not know exactly what you do, but if you've had patients come in multiple times can you kind of see progression? Yeah. Yeah, that's a great contrast here. And there's different types of imaging. And I'll just give you a quick whistle stop tour of a few of them that might be important for this. Sure. Yeah. Yes. So something called PET scans, which is positron emission tomography. Tomography. And, and this is basically where, now these are probably, they've been around for absolutely tens of years. And basically it's where you can tag the neurotransmitters with. with basically radioactively. It's minimal, so it doesn't affect the page. It doesn't, you know, it's not gonna cause any kind of radiation poisoning, but it tags it. Then you put them in the scanner, and the scanner can pick up on that radiation. So it shows like the clumps of the neurotransmitter dopamine in this. You can look at many others. Just to briefly say as well, dopamine is not the only neurotransmitter that is affected in Parkinson's disease. I'm just focusing on it for this, because it's... Otherwise it'll start to get a lot more complicated. So you can tag the dopamine and then it will come up with this very colorful brain. And if it's red, that means there's lots of dopamine there. But if it's a smaller pockets of it, it means that you can see that there's a reduction in that neurotransmitter. Really important, because I could just tell you about the transmitter, and that absolutely can tell you, it can tell you how advanced the disease stage is in Parkinson's disease. But you will probably see that after 50 to 60%, that also does mimic their symptoms. So if you've got less of that, less of the dopamine after about 56% loss, as that kind of gets less and less and less, the symptoms will get worse and worse and worse. The one that I use, but just say that one's very expensive and on top of that, although it's... you know, radioactive materials can cause cancer. You know, it's fine to have a few scans of that, but that you can't have many more than, I believe, maybe one or two a year really. So you can't really use that. So scans that I use are called MRI. And this basically just looks at the structure of the brain. It's like taking a picture of the brain. So we're just looking at the structure. So these are only kind of like big changes in the brain. But we've got technology now, which if I put it through a computer, it can... sometimes detect very small changes. And I can look at different groups and see if there are any changes. Within that, you don't tend to see a lot of changes until the disease is quite advanced. Although the research that I've just done recently, I did find some differences in the cerebellum and healthy controls. The cerebellum is an area that's for coordination and therefore for movement. So that's using structure. You can also use, when I talked about the white matter pathways, that mainly looks at gray matter. the T1s. And then the other one is diffusion, just what you need to know is called DTI. It looks at the water molecule composition. And that looks at the white matter tracks. And yeah, we do tend to see some changes in the white matter tracks because it's a little bit more pulling it apart a little bit further, especially in one called the cortico-spina track. And especially early in the disease is interesting. But that just tells us information about what's happening in the brain. wouldn't necessarily use that for diagnosis that just tells us biological mechanisms. So the PET scan is the only one that's used for really clinical diagnosis. We're not quite there yet with the other ones. And my question now is, so Kim Kardashian used Pranovo in the US, which is a company that is basically it's MRI scans for the public. You pay two and a half grand to go and have an MRI. When that then comes and grows and, you know, as a business, I think they've gone through several rounds of venture capital funding. When it, you know, at some point in society becomes a place where those with the money are able to go and just pay for their own MRI, is that helpful or is that a hindrance to the work that say you're doing? Like, is it useful to go and have everyone go and pay for an MRI or is that just gonna cause a moral panic? So yeah, it's a... That is a really good question and it's a debate to be had. I think, as an example, you can have changes in your brain that don't necessarily present clinically and might never mean anything. Sometimes when you see things on scan, for example, some little white matter hyperintensities, which can be linked to multiple sclerosis. doesn't mean they're causing clinical problems, they're just there. It's just, it hasn't affected you in any way. Sometimes we can have little micro strokes, doesn't affect us, but they're there, just like little white matter hyperintensities. Are we scaring people by doing these brain scans? But at the same time, you're right, is it good to check and stop before, before it causes, you know, We're brought up in, this is definitely a UK thing. I don't know whether it's the same in other countries, but we are a very reactive health society. So we react the minute something, you know, we don't wanna trouble the doctor. We don't wanna trouble, you know, fill up a hospital bed, like unless you're on death's door. And I think we're sort of told about that from a very early age. And now we're kind of in this interesting space where you're now looking at preventative care and how can we... you know, stop filling up the hospitals with things that maybe could have been prevented in the past. And so, yeah, I suppose it's just quite an interesting piece that maybe there's sort of two sides to my question. It's almost on the one hand, is it good that anyone can in the future will be able to just go and get an MRI? But then on the flip side, it's like, is there a point where you get people coming to you who are part of your research, who have been diagnosed, who could have been diagnosed six years earlier, but they just didn't want to bother anybody? I guess there's two things here. I guess almost on a moral grounds as well. How expensive are these scans? They're not cheap Who's gonna be able to afford them? I guess Sorry, I guess the would you say them the free markets? whatever argument for that would be that if enough people start doing it the prices will go down because More companies would also want to do it. But then we're getting into this very sketchy area of like sort of public, like privacy issues of like your health data? Because at the moment, if you do scans, scans are done by like the NHS, or if they're done for research, then they kept under lock and key, nobody else has them. But if you start giving it to private companies, what will they do with the data and information? What are they telling you? Because do they have clinicians who are going to... meet the person and tell them that, okay, this is nothing to worry about. Like Beth said, you could have like mini strokes and things which mean nothing really. So it's two sides to it, which everybody sort of needs to be able to deal with at some point. We haven't dealt with AI. We haven't dealt with the internet really. So I don't know how we would deal with just everybody having everyone's brain scans and health data. I mean, some would argue that the biobank has thousands of brain scans. I think they're very much so on, you know, yeah, we just scan everybody and we, yeah. But there was a little bit of a flaw with that recently, I believe. But people who run the biobank, they are very conscious and they're, as far as where they don't sell the data to big companies. But yeah, I think it's always a fear. It's like 23 and me, isn't it? you found out you've got some kind of genetic link to hunting tunds, for example. You don't really want people to find out about that. It was 23andMe selling their data. It's a moral problem. Did that go deep? Yeah, very deep. any excuse to bring up Kim Kardashian in an episode? I knew it. Fair enough. It's also scary. I don't know how keen I am on people having Instagram stories of their brain scans. Might be a funny thing to like, or dislike or point out. I guess, personally, I don't want to, I don't think I want to see what is on my brain because I don't know, what if I had something just slightly, you know, that we wasn't expecting? Would I want to know? Would I not want to know? What if it was just a difference compared to anybody else's brain but didn't really mean anything? Yeah, I think it can cause fear. Especially because, like you said, the brain is very flexible in terms of like we were talking about in Parkinson's. 50% of the matter has around 50-60% of the matter goes before you start showing symptoms. That means that just because of brain image... looks one way, doesn't mean that the brain isn't functioning well, it's compensating best it can. Yeah, like there's a case of somebody who was only born with half the hemisphere, so one half of their brain, and they were functioning perfectly fine, but because they were a child, something called plasticity, and they were fine. Awesome. Shall we? I had a few more questions about your research, actually. Yeah, of course. So... So could you run me through one of your participants if they have to come into your experiment? What does it look like? Because you did say that you do some cognitive stuff. You did say you put them through an MRI if you could take me through the journey of a participant. Yeah, yeah, yeah. I'll take you through the whole thing. So first of all, I'll call them up. They've been already recommended by the consultant I'm working with. And then she will say they're happy to be approached about this. I'll approach them. send them all the documentation about what we're going to do. And then they'll say yes or no. Then I do a quick little check to make sure there's nothing, they've got no pacemakers or tattoo or piercings, so they definitely couldn't have a scan. Can you not have a scan if you have a tattoo? So very old tattoos, no. Why? They come from, there was a pigment, I think it's the user pigment that is, it's got, no, you're fine. I think it's pre-1975. So it's old and they're usually almost always fine, but still need access things. And then I will book them in. They will come in. First thing I'll do is say hello. I will then take them through the consent forms and then the radiographer will come out and take them through some more consent forms to make sure they're definitely okay to go in the scanner. Because the MRI scanner, if anything's in there, which is... metal, it will absolutely fly towards machine because it's a big magnet. So it has to be very careful with what we take in there. Yeah, then they'll come through. The radiographer will give them a gown, they'll get changed into a gown, and then they will go into the scanner. Now the radiographer is very good because if some people haven't had this before, it can be quite claustrophobic and scary. So we'll talk them through it. And so it's going to be about 50 minutes. And what's nice with the one that I do, there's a little eight to nine minute video at the end so people know right at the end that that's when it's going to be almost finished. So then we put them in the scanner, make sure they're all okay, then we go to the little room in the back and we run them in the scanner. They just have to, they just lie there and it can be quite loud, so they're given earplugs as well. They can just relax for 50 minutes, they don't really have to do anything. Then once they've done that, we'll take them out, one of the side rooms and first of all I will give them a, it's called a hospital anxiety and depression scale. So it's a question that they can fill out themselves just on their current mood. It takes about five minutes just, and it just shares some very, just a quick overview of their anxiety and depression. And then the next one I do is a looking at their cognition. This one takes a bit longer, it's about 20, 25 minutes and it looks at lots of different areas from their cognition, so for example. language, memory, visual, spatial, so how they kind of view the world, their fluency, yeah, and then we'll take them through that. And then at the end, I was asking, do you have any questions? And that is it done. It takes about an hour and a half to two hours to do that per subject, per person. I've been in an MRI scanner before, it's not fun. That experience. Yeah, I think, sorry, see you. No, I was just saying that they, I remember them giving me a buzzer to say if I was uncomfortable. And I thought I'd been in there for 15 minutes and I was pressing it and they said you've been here for a minute and a half. It's not been that long, calm down. If you were to invent the perfect MRI machine then, what would it look like? I mean, if we're not going to... So do you know what's really at King's? I don't know if when we were at King's they were actually coming up with a machine that basically was making it quieter. So it was a quieter MRI machine. And I remember when I was first watching, I was like, oh, it doesn't seem like that much. And then when I started working with the MRI scanners, I'm like, that is genius because especially for children, it's scary and sort of very claustrophobic. So I'd wanted to be quieter and I'd want it to be larger as well. It is really quite, it can be really quite claustrophobic. But the people that have had to come in so far, especially the people who have Parkinson's disease are really keen to get involved. So even when they are a little bit scared, they're like, nope. There was one story in particular that really does stay with me. There was a woman, she was quite claustrophobic, but she's like, I want to do this and I will do this. She was so determined. And I think sometimes this is the phrase that kind of keeps me going, was that my interactions with her, she's a very lovely woman. She had quite pronounced symptoms, but was still quite early. And I asked her, do you have any questions or anything, last things you want to say, or if you want just... welcome to email me. And she just looked at me, grabbed my hand and started tearing up, crying and saying like, please, if you can just help one person with this scan, please, I will do a million scans for you because it's just the worst thing ever. And it was just, she was in her, she was the same age as my mum. It was just heartbreaking. And I think seeing that really gives you motivation to kind of carry on with these things that we help with this because it's gonna affect so many people. that is really affects the quality of life. Yeah, I can't even imagine. Oh gee. So then, like, like she said, if you could help one person, what, what are you hoping for the outcomes of your current studies of your PhD? And how do you think that will go in helping? Yeah. I think there's two kind of ones I'm kind of like interested in the moment, all the ones that I'm kind of working on currently. The first one is stuff with the cerebellum. It's interesting because if basically it looks like there might be an increase of the cerebellum, just say this is not yet been peer reviewed at all. But there's other studies that also backs up a little bit as well. So it's not just me. It's a really great study called by Kara Estes. If people want to read it, that's a peer reviewed article. and they found increases in certain areas of the cerebellum in the earliest stages of Parkinson's disease. So it's possible that we're... Sorry, by increases, do you mean like inflammation? Oh, sorry. Like it gets bigger or... No, we don't think inflammation. We actually think that it's almost working harder is in there's increased cells there. And this is supported by other research has looked at functionality between... the basal ganglia and so, oh sorry, we've just looked at the functionally, there's an increase functionally as well, which is suggesting that it's working harder. Working harder to help with those, keep those motor symptoms kind of, you know, as best as they possibly can be, considering the basal ganglia is degenerating. So if we can possibly target cerebellum in the future, I mean, this is way, way thinking, but for example, we've got deep brain stimulation in the basal ganglia. There's another possible target area, the cerebellum. I wouldn't personally be working with that, but is there possible treatment opportunities that come from this? I think second of all, because I'm within, so with using neuroimaging, I'm using particular imaging, which creates really high quality white matter images. So like, When I say high quality, it's almost like, you know, you're with pixels when you take a picture. It's, you know, like, it's very crisp images. It means that we can see more and we can understand more. So I want to look at those white matter pathways in excruciating detail, basically, and understand what is happening within this, like, entire space between the areas that are being affected. And if I can kind of figure that out, then I might be able to further to elucidate this idea that yes, there is increased communication possibly between the basal ganglia and the cerebellum and is that because it's needing the cerebellum to pick up on the slack, for example. So it's understanding which pathways are first being affected and why is that when we might see it in the white matter pathways first, maybe we can target these areas. Just understand how we can move. and compensate for so long. It's really interesting. I find it fascinating, but I'm biased. But also links to symptoms as well. Seeing what areas links to specific symptoms is probably... I was going to put it like in one sentence, I want to look at the white matter pathways and the link to symptoms. And if we can see that link, so maybe we can target those white matter pathways for those specific symptoms, as I said earlier, personalised medicine. So I would call it a decline. Nice. I think that's a good sort of statement to end your research stuff on. Yeah. I didn't want to spend the last five, 10 minutes talking about your science communication work. Yeah. Because I came across a few talks you gave on YouTube. I've seen that recently you ran a neuroscience conference in Liverpool. So could you talk to... tell people a little bit about how you got into, yeah, in your science communication journey a little bit, and then also considering you're a student, like what sort of drives you and how do you find time to do this? Yeah, nope, I can end, I'll start. I think probably quite a nice one to start on is a little story that I think Pollyanna was here for about why I think it's so important to do science communications, especially with the public. And... patience and everybody and getting the word out a little bit more understanding. So about five years ago me and Pollyanna were, well I was on a EuroStar coming back from Paris and there was a woman who was very scared. She was, it probably looked like a panic attack but she was having a full psychotic break. She was probably about my age. She was terrified, she was shaking, she was scared and people were laughing at her. and they were being nasty. She was terrified. And I just, you know, I was like, I was like, you okay? She was like, and she was just, you know, absolutely like, they're looking at me, they're all looking at me. I was like, no one's looking at you. Let's, let's, and so, you know, somebody did help out, but then, you know, they got her somewhere else to sit, you know, where she could be alone. She was very scared. Yeah, again, my, you know, mid-twenties probably. And then when she left, there were just people being like, oh, I was about to kick her off this train. Like, talking about, you know, physically hurting her and being just incredibly. you know, unkind. And I think that's when I kind of realized we need better perception from these diseases. Now that was probably psychosis, but I was like, it goes across all these diseases that, you know, we really do need better awareness. So I think it starts as far back as that, to be honest, when I was like, right, we need to do better on this. And then when I started my PhD, I was like, science communication is vital. I want to be involved in the committees. I want to be involved in the, you know, if there's any possibility of talks talking to patients I want to be there because it is so important that people are made aware and that you know just the public are aware but also the patients are aware what we're doing and you know how this can help them and how they're feeling getting their kind of feedback. So I think with the FameLab I'd never really full-on put myself out to do a full-on talk but I really enjoy talking very much so and enjoy talking about science. It's probably my favourite thing to do. I mean this is just solidified that but this this Fame Lab, which is the world's largest science communication competition basically. So I put in an application, it's basically where you have to, for three minutes, you have to talk. You can basically talk about anything, but I choose to talk about our research, we have to make it engaging, so it has to be charismatic, it has to have good content, and it has to have good clarity. So I put in first a video entry, that got accepted, then I got through to the Northwest Finals in Liverpool, that's between Liverpool, Manchester, and North Wales. which is great, I won that and then I went to the final. That was, you know, I mean, it was absolutely fantastic. You know, it was my favorite thing. I was able to talk about Parkinson's disease. I was able to use neuroimaging to take people through the lifespan of somebody with Parkinson's disease and try to explain that, you know, it happens a lot earlier. You know, these changes happen, you know, 20 years before you might even see symptoms, but we just don't see it. And this is how neuroimaging, as you said previously, looking at these longitudinal changes. But... explaining it in a way that people can understand why, why would you do this? So, you know, when I did that kind of final fame lab, I spoke a little bit about Michael J. Fox and those changes, because it's important that they understand why are we doing this research? Why would they even care about what we're doing? And why is it important to be aware that, you know, these people, you know, people with Parkinson's disease are going through this and just to understand a little bit more science around it, why would you not want to, you know, know a bit more about that? Fantastic experience. I mean, I think. over 400 people applied and there was eight of us at the end. So it was very enjoyable. It's very enjoyable. It's very important that we keep, you know, that people get excited about science. And I think that to me is just what science is about. Let's get people excited. Let's chat about it. Let's, you know, tell me if it's too complicated. Tell me if, you know, it's, you know, it's some things, you know, too complicated. You know, it just is not making sense. You know, there was no blonde questions. I think somebody said this to me, and they're like, I'm sorry, if it's a blonde question, like, there was no such thing. There was no such thing as a stupid question, please. If I'm not, if you're not understanding it, it's on me. It's not on you. I think sometimes people feel so stupid, you know, coming to the science community when it should not be the way. So that's what kind of got me into it a little bit there with the science communications. And how do you stop the... I guess because we've never had more information than at our fingertips than ever before. If I want to go and find something out, I can go on. Google, TikTok, Perflexity, ChatGPT, Pinterest, do you know what I mean? So, and then that's not even counting like the TV programs, the podcasts, the whatnot. How do you, or how can people be sort of empowered to go to the right sources and understand that they get, like, so we're not spreading misinformation basically? Yeah, that's a really good question, Pauline. I think misinformation is like, with the internet is such a problem. I think... this is the exact reason why science has to be more accessible. Um, because otherwise we just, you know, we will read what is on the internet and just be like, oh, well, there's no scientists, you know, they, they use all these big words that we won't understand, but no, it's this and rather than, I think sometimes, I mean, for me personally, an approach is you don't just, you know, bam, saying like, no, you're wrong. It's all about understanding. So being diplomatic, I say, why do you think that? No, it's, I'm not saying it's, it's never about outright saying you're wrong. Cause it's If you tell someone you're wrong, it's combative. You know, it's like, why do you think that? You know, let's talk through it. I can tell you why it's right. You know, let's set up these lines of communication about, you know, that piece of information that seems very plausible is wrong and dangerous. And let's, you know, discuss also your point of view and why you think that. And that doesn't mean even as wild as it can be, there's not, how have you got that information? And I'm sure there will be a little nugget that has gone, you know, further and further back. that is fueling that line of thinking. So it's just discussing it a bit further. So do Pint of Science as well is another great one where we can get scientists involved. So it's like FameLab, but on a smaller scale where around the city, we set up these talks with people on their research. But again, it's quite nice because it means that local people can come and listen to scientists around their area, talk about their research that they're doing. Yeah, so I helped organize that as well. And that's another really fantastic way to share all this information. And we've got the British Neuroscience Association Festival that's coming up to Liverpool next year, which is really exciting. I hope I'm going to see you there, Sahir. And that, you know, I'm working with Everton and the community to try and work with those communities from the football club, you know, they, they have groups of people with Parkinson's disease, work a lot with them. neurodivergent people who are neurodivergent. There's all sorts of these groups that we need to work better with and we're very keen to bring that into the festival as well. It's just about learning, but it's not just that. I think with science sometimes we need to listen. If we're just speaking and speaking and speaking, and I think it's quite easy as a scientist to, you know, you have to defend your work so that it's so important that we just sit back and listen and be like, okay, I'm gonna listen to what you're gonna say even though, you know, I've been told I have to be right. I'm not always right, but I'm happy to listen to what you have to say. And then I can talk you through my line of thinking, but it's just about listening and learning, but a bit of backwards and forwards, I think. Yeah, it's very important. Do you think science needs to sort of change the way we disseminate information? Because I personally have found it takes a long time and there's good reason for it as well just to defend how research works. The whole making sure everything's peer reviewed, making sure everything is as tight as can be. You don't have any sort of... There's no sort of like data manipulation. There isn't all that kind of nonsense going on. It requires quite a bit of time. But misinformation spreads a lot faster. And then also, I guess, the way scientific journals are or where a lot of science is published is in places which people cannot actually access and read them, which does not help countering any narratives which are formed. So in your opinion, do you think we researchers need to change their approach and also as a science communicator, how do you think you would do this? If Beth was in charge of disseminating all the sciences, how would it work? I think we do relatively well. I think we have things like science festivals, Chelten Science Festival, but I think, and there are a lot of science museums that do it beautifully, but I think sometimes, you know, with the bigger research, you know, you write like the peer reviewing, the scientific papers, I even struggle to understand them sometimes. It's making sure we disseminate those, you know, in a clear fashion and, you know, how does it affect people? I think we're getting there with it. And I do think, you know, there is a lot of, you know, where people are very keen to, well, not actually I say this, you know, I say it because I'm very keen, you know, to teach people. I think sometimes there's this whole idea of, you know, I think this is gone now though, you know, like everyone looks, you know, like Einstein who does science, you know, they're all, everyone's like in their 50s and, you know, in their kind of stuffy offices. But I think there is like, there was definitely a change with like younger communicators coming out and, you know, wanting to change it. You know, there's, I think what's really interesting is recently I was looking at possibly going to Green Man Festival and they've got a whole tent that is science related. science-related talks but I think it's actually I think it should almost be mandatory that every single PhD student has to give a public lecture somewhere and whether that's to you know 10 people or 20 people 500 people I think that will really help them kind of you know not dumb it down I think that's why but even if or even you know as a present you know part of part of their PhD has to be that they can deliver this information to people who are not scientists or even patient groups. So you know, because then you can kind of understand the nuances of it, of you know, how you speak to people from that, you know, from there, you know, possibly with that disease. I mean I'm talking about it because I work with people with diseases, but it then can, you know, I think it's a skill that's really important. So then when we're at parties, we're not just talking about, you know. the in-depth scary, you know, like the Substantia Niagara Pals Compactor and the subthalamic nucleus and the thalamus and its disinhibition and it's, you know, it's all a little bit much. So the more we practice, I think the more it will get better. Well we should ask the marketing person here, Pollyanna, what do you think? No, I think, I know that Beth and I, we have spoken about this before. You know, I think it even comes down to our brains process visuals a lot easier than they do, like audio, for example. And then most people, again, you know, pictures are louder than words. And I think if I then apply that to how I see the academic and science community, I don't know who is reading 25 page long or 50,000 words, journals and papers, no one, apart from it's just, it's like a bit of a self-fulfilling prophecy of just scientists reading scientists' work. Sorry, Polly, can I just confirm, you're saying nobody's going to read my thesis, my 100-page thesis when it's completed? No, there's not going to be tens of people, hundreds of people reading that? No, not unless, you know, but having said all of that. Just before you continue, I remember reading somewhere that on average four people read your read a journal article you publish. Wow. That's scary. But I think that doesn't negate doing the research. I mean, there's two different sides here. There's a need to do the research, but then it's how do you then communicate it? And for me, the medium is the message, right? If you see something and it's put out on TikTok, the contextual environment and the mood you're in and, you know, everything kind of plays into it. So if you see, I mean, I'll talk about it from my world, right? If I, if a luxury brand puts an advert on the back of a toilet door, that's terrible, right? Because it suddenly degrades the brand. And you think of it as cheap, smelly, whatever else. However, a luxury brand going and doing a huge runway show in the biggest cities in the world with, you know, everyone getting given free goodies, et cetera, suddenly you think really positively. If I apply that same logic to research and science and communication, it's if you want everybody to really care about your work, and we think that the medium is the message, And so that basically where you show up is how people are going to take it in. I think there's, that's why science communication in places like the Cheltenham science festival or the BBC breakfast red sofa in the morning or. Yeah. The person on Tik TOK. And I think that's why do the research, but then I don't expect scientists to then also be great. I don't think you need to be a great marketer to be a great scientist or a great communicator. but working with people who are passionate about communications to go, Hi, please help me turn the complex into the simple, you know, complete, how do we, and I think that's where things like AI are actually going to be really helpful. Because if you can upload your PhD into an advanced chat GPT and say, Hey, give me the five key takeouts. Amazing. Incredible. That's your five. TikToks gone, done. So. And I don't think I say this in a very simplistic and very reductive way. I don't believe it's that's the whole truth of it. But for the purpose of this, I think there's, there's ways to communicate. And coming back to that sort of self-fulfilling prophecy, the, the other thing as well is that, you know, every industry needs diversity of thought. So if you're only bringing in people that understand science into science, who then care about science, who that, you know, you're never going to get. anyone else interested who maybe didn't even think that science was for them, who might have a completely different approach to research or a different approach to, yeah, bringing in, you know, bringing in patients, recruiting patients. So yeah, I think for me, do more things like I've seen Beth talk at FameLab, amazing, incredible, who doesn't want to be in a pub and listen to a story that actually has a really important message underneath it. I hope everybody was taking notes. But I think there's an overarching point there, isn't it? Because there's going to be loads of people who will, what's it called? Is it the Donning-Kruger effect? You find out a little bit of knowledge and then you end up that you think you're an expert. You're going to get, you'll have a lot of people who probably read one thing about Parkinson's because that was the one thing that got picked up and then they'll go on. TikTok and they'll wax lyrical with cool emojis and gifts and things flying all over the screen. And then you're suddenly you've got a million people going, oh, my god, if I eat broccoli, I'm going to get Parkinson's. Just to clarify, broccoli will not cause Parkinson's disease and it's definitely not been proven to do so. Awful example. Awful example and definitely not. But you see, so that's why I think it's super, that's why I think science communication and the sort of the the skill of science communication is incredibly important because I think when I've sat and watched or Beth shared with me like, Oh, look at this Instagram or look at this person's TikTok and it's someone who's an expert and is great at communication. It's like, that's a unicorn that needs to be catapulted into the world. Yeah, no, I agree. Yeah, you get you get some really good sort of, especially YouTubers now, like doctors and stuff who explain things pretty well and are really engaging. these days. So yeah, I agree with both of you that we are getting better at it and just need just need more people. I think you need to hire a Gen Z to be honest. And they'll tell you how to make Parkinson's wrap. I wish I could afford hiring a Gen Z. I feel I feel they'd be expensive at this point in time. But yeah, thank you so much guys for coming on. No, thank you so much for having us here, it's been very lovely. I had a great time. Thank you Pauliana. Thank you Beth. The last thing which we ask our guests, I bet this is for you. If you had one piece of advice to give to all our listeners, what would it be? Oh, can I give two very quickly? Sure. Yeah, okay. So first we'll... When you're starting out, say yes to almost everything that you get offered. If you think it sounds interesting or a bit scary, just do it because you're trying to figure out what you enjoy. You can say no later down the line, but just say yes. The amount of things I've put forward, Fame Lab is a great example. Just put it last minute, put something together. I was terrified, did it. Amazing. Second of all is, this is... maybe, so that's maybe for other kind of students kind of coming up. Second is for just everybody is please get involved in research. And I know it can be scary, especially in terms of MRI imaging, but these studies are not possible if people don't get involved in it. It's so appreciated when you do. And, you know, you are helping, you know, future treatments, cures, and finding out more about these diseases and about any, anything in the world. Awesome. very good pieces of it was. And of course we'll put the BET study or like BETH Labs contacts up on the show notes so that if anybody is interested in the Liverpool area and wants to participate in research in neuroimaging research then they could probably find you that way. Yeah yeah I'm looking for people between the age of 55 and 80 but I have friends. I do not know if that's my target. demographic. So please listeners show this podcast to your grandparents, parents. Yeah. But yeah, thank you everybody for listening. Thank you again, Beth and Pauliana for coming on. Yeah, until next time. Take care. Thank you. Thanks everyone. Bye.