Podcasts

Podcast – Researching Sanfilippo syndrome

Hosted by Dr Anna Volkmer & Dr Kamar Ameen-Ali

Reading Time: 24 minutes

In this weeks Dementia Researcher Podcast, we hear from Dr Karissa Barthelson, one of the latest Race Against Dementia Research Fellows from Flinders University – discussing her research, and specifically an introduction to Sanfilippo syndrome, a rare form of childhood dementia, and her research on this disease.

Regular Dementia Researcher Bloggers Dr Anna Volkmer & Dr Kamar Ameen-Ali lead the interview, helping us to understand Karissa’s work and exploring the science.

All types of neurodegenerative diseases share common molecular mechanisms responsible for disease etiology and progression. Karissa, is interested in understanding these shared mechanisms, as targeting the common problems could lead to new therapeutics to benefit more individuals who live with these diseases. To understand the shared molecular mechanisms, Karissa utilises zebra fish, as a model organism. Introducing mutations into zebrafish, equivalent to those which cause neurodegenerative diseases in humans (e.g., Alzheimer’s disease, Sanfilippo syndrome childhood dementia), then analysing their brains with very high molecular detail.

For more information about Sanfilippo syndrome visit – https://en.wikipedia.org/wiki/Sanfilippo_syndrome

For more information on Race Against Dementia visit – https://www.raceagainstdementia.com

If you’re interested in becoming a Race Against Dementia Fellow join our webinar at 4pm BST on the 20th July – watch live / set a reminder


Click here to read a full transcript of this podcast

Voice Over:

Welcome to the NIHR Dementia Researcher Podcast, brought to you by dementiaresearcher.nihr.ac.uk, in association with Alzheimer’s Research UK and Alzheimer’s Society, supporting early career dementia researchers across the world.

Dr Anna Volkmer:

So welcome to the Dementia Researcher Podcast, bringing together early career researchers and leaders within the field, to discuss their research and share career tips. I’m Dr. Anna Volkmer, and co-hosting with me today from the other side of the world, because I’m in Australia today, is Dr. Kamar Ameen-Ali. Hi Kam, why don’t you tell our listeners what we are discussing today?

Dr Kamar Ameen-Ali:

Hello Anna. Today we’re joined by special guest, Dr Karissa Batherlson, to discuss her research on a rare form of dementia that many of our listeners may not have heard of, called Sanfilippo syndrome. Hi Karissa.

Dr Karissa Batherlson:

Hello.

Dr Kamar Ameen-Ali:

Could you introduce yourself and can you also allow me to congratulate you as the newest Race Against Dementia Fellow? Congratulations.

Dr Karissa Batherlson:

Thank you so much. Yeah, so I’m about to start the Race Against Dementia, Dementia Australia Fellowship. So I’m based at Flinders University, in Adelaide, in South Australia. So yeah, I haven’t actually started yet, that should be happening in the next couple of weeks and I’m really keen to get into it.

Dr Anna Volkmer:

Do you know what? I did my master’s at Flinders University.

Dr Karissa Batherlson:

Oh, did you really? Oh, fantastic.

Dr Anna Volkmer:

I did.

Dr Karissa Batherlson:

It’s a lot. So my PhD was at the University of Adelaide, which is about half an hour down the road. So it’s a whole other world up there, up on a hill. But it seems a really beautiful campus. Can’t wait to.

Dr Anna Volkmer:

Yeah.

Dr Karissa Batherlson:

Can’t wait to get started.

Dr Anna Volkmer:

I only ever went there for my graduation, and what I realized is, when I went, because it was remote, they do remote study so beautifully, don’t they, in Australia. And when I went to the campus, I realized how beautiful it is, and additionally, how many lovely wineries there are around the campus.

Dr Karissa Batherlson:

Yes.

Dr Anna Volkmer:

Take note.

Dr Karissa Batherlson:

Yes.

Dr Anna Volkmer:

As our regular listeners will know, however, I am a clinician. So I did that master’s, was a Master’s of Clinical Rehab and then I went more into research, and did more research in the area of dementia, but Kam is a fundamental scientist. So we are going to come at this from two different ways, different angles. It feels a bit like Mastermind really, doesn’t it?

Dr Karissa Batherlson:

Hopefully.

Dr Anna Volkmer:

And so let’s set the scene. Are you ready to tell us everything you know?

Dr Karissa Batherlson:

All right, let’s do it. Let’s do it.

Dr Anna Volkmer:

So yeah, as Kam mentioned at the start, lots of our listeners don’t know what this syndrome is, and I thought it would be really helpful for you to tell us a bit more about Sanfilippo syndrome. When are people diagnosed? What causes it? Can you tell us a bit about that?

Dr Karissa Batherlson:

Yeah, of course. So Sanfilippo is a genetic condition and it causes childhood dementia. So it’s a really rare disease. So about one in 100,000 children will inherit it. And it’s a recessive genetic disorder, so it means that for a child to inherit Sanfilippo, they have to inherit the faulty gene from each of their parents. And the genes in this disease are responsible for breaking down a complex sugar molecule called heparan sulfate. So when a child inherits these faulty genes, they can’t break down this complex sugar molecule anymore. So it starts progressively building up and clogs up the brain cells. So this causes a cascade of really detrimental events in the brain and eventually is going to lead to dementia and loss of life, typically before they reach 20 years old.

Dr Anna Volkmer:

Okay. Wow, so has a really significant effect. So does it also affect cognitive domains, like memory, speech and language, in the same way some other dementia types do?

Dr Karissa Batherlson:

Yeah, so these kids, they generally develop pretty normally until they’re about two or three years old. And so about the time they start learning simple sentences, everything’s going normally. But then it’s after that’s when the cognitive things start to occur. And this is where the commonalities with the adult onset dementia seem to start appearing. So these kids will start showing problems with attention, memory loss, confusion, aggression, irritability, problems with sleep. Then they start to lose their newly learned language skills. So yeah, there’s a lot of going on and I could go on for ages. But yeah, these are really highly reminiscent of what happens in adult onset dementia like Alzheimer’s.

Dr Anna Volkmer:

Okay, that’s really helpful. Thank you. So you’re talking about the genetic component. It must be really devastating to families who do actually find out their child has this diagnosis. Does it have, I mean, it sounds like it does, it must have implications for other family members?

Dr Karissa Batherlson:

Oh yeah, devastating doesn’t even begin to describe it. It’s really, really difficult for the whole family. So I have been fortunate enough to interact with a few families who have kids with Sanfilippo. And the parents have to deal with so many things, and it puts them under a lot of pressure. They can’t communicate as clearly with their child as one normally would, so that makes them feel really helpless when they can’t understand what their child wants. So yeah, this pressure [inaudible 00:05:33] is quite unimaginable really. They also have to be really vigilant, they need to be constantly watching their child, for their wellbeing as well as the safety of others. So there’s a few stories, playground stories that I’ve been told.

Dr Karissa Batherlson:

So one child who had Sanfilippo, she just didn’t have any sense of safety. So she jumped off a playground structure onto a concrete floor and actually ended up in the emergency room. And the mom was just devastated, as she just felt like a really awful parent, even though it’s not really her fault. And yeah, there’s another story I’ve heard when there was another child, who, he was really excited to go down one of the slides, and in then his excitement, he actually shoved another kid down the slide, and he ended up getting reported. But he didn’t push the kid because he was angry, he pushed him because he was excited. So yeah, these behavioral problems, which happen because of Sanfilippo has really big impacts, not only on the child, their parents, but also other people.

Dr Anna Volkmer:

Yeah. Yeah, I can see that their social circles. Being a parent, I know how complicated that can be, negotiating those social circles. And then if your child has got this diagnosis, it must be, yeah, even more difficult. Goodness.

Dr Karissa Batherlson:

Yeah. Yeah, it’s pretty full on. And I also feel for the siblings, the unaffected siblings, who, of kids who have Sanfilippo and it’s like they may not always get the attention that they need or deserve. And actually, the whole family gets affected as there’s a lot of sleep problems in Sanfilippo, so that kind of keeps the whole household up. So yeah, there’s a lot of things that the parents need to deal with. And yeah, the stress and heartbreak when there’s no cure for this disease really extends out quite widely in their circles.

Dr Anna Volkmer:

Yeah. I hear you. I’ve personally met somebody with Niemann-Pick type C, which I think is one of the other main types of childhood or early adult onset dementia. And I’ve certainly seen and observed that in their family dynamic. It’s just such a difficult thing, almost unimaginable thing to live with. But I wondered, with that in mind, are these two syndromes similar, so Niemann-Pick type C and Sanfilippo. So would your research therefore have relevance to this other type of childhood dementia syndrome?

Dr Karissa Batherlson:

Yeah, yeah, definitely. There’s definitely some similarities between Sanfilippo and Niemann-Pick type C. So a lot of the childhood dementias are what’s known as lysosomal storage disorders. So there’s about 70 different types of lysosomal storage disorders, and they’re all because someone has been born without a functioning copy of a particular lysosomal enzyme. So when you don’t have the functioning copies of the enzymes, they can’t break down the specific molecule they’re supposed to. And it means that that particular molecule starts building up within the lysosome, and so it’s kind of referred to as their inappropriately stored in the lysosome, therefore, lysosomal storage disorder. So in Sanfilippo, the molecule that builds up is the complex sugar molecule, heparan sulfate. But in Niemann-Pick, the molecules that build up are cholesterols and fats.

Dr Karissa Batherlson:

So between at least those two disorders, while the primary causes are different, I think that the secondary effects are similar, like how the cell is responding to this inappropriate buildup of the partially degraded molecules. And so these secondary effects, I think, is what we need to target for childhood dementia, as they’re all highly related disorders. So while the primary causes are different in the lysosomal storage disorders, I think that the secondary effects are similar and that’s what I want to target, because I think that this could have really widespread benefits for all types of childhood dementia. But I do want to note though, that it may not be a cure because I just want to find something that at least helps and slows down the decline, as this could be so important to the families, giving them some extra precious years with the child that they love so much.

Dr Anna Volkmer:

That makes so much sense. Thank you. I’m going to hand over to Kam now, back to the other side of the world.

Dr Kamar Ameen-Ali:

Thanks Anna. So now we know a little bit more about the disease, and its impact as well, I’ve been dying to get into more of the science of this area. So in my research, I focus a lot more on studying the pathology of different neurodegenerative diseases that lead to dementia. And we know that dementia’s something that we would typically associate with getting older, with age being the more significant risk factor for diseases like Alzheimer’s that lead to dementia. With Sanfilippo syndrome, it’s known as one of the more common forms of childhood dementia. So this might be the first time that many of our listeners have actually heard that childhood dementias exist. So what I want to ask you, Karissa, is, are there similar changes in brain pathology to what we see in adults who have dementia to the children that have Sanfilippo syndrome? So for example, do they have brain atrophy? Do they have a certain build up proteins in the brain? What is these pathology changes like with this condition?

Dr Karissa Batherlson:

Yeah, well, I think it’s a bit of a common hallmark for all neurodegenerative diseases that there’s build up of proteins. So in Alzheimer’s there’s amyloid and tau build up. Motor neuron has aggregates of SMN1. And yeah, in Sanfilippo, like I’ve said, we get accumulation of the heparan sulfate molecule. And I think that the process of proteins building up inappropriately in brain cells is, yeah, a common hallmark of all types of dementia. And these buildups are clogging up brain cells, so they can’t work properly. Brain cells now can’t get rid of waste as efficiently, and this also leads to brain cells not being able to make as much energy as they need to. And I think the energy production is probably the most important part of cell biology of dementia. As if our brain cells can’t make enough energy, this means they can’t do any of their other functions as efficiently.

Dr Karissa Batherlson:

So this will be eventually leading to the brain cells dying. And we can see this clinically as atrophy or the shrinkage of the brain. So there’s definitely some similarities between adult and childhood onset dementia. And yeah, like I mentioned earlier, the primary causes may be different, but how the brain cells respond, I think, to these causes, are going to be pretty similar.

Dr Kamar Ameen-Ali:

So is the energy production the mechanistic focus of your research, that is then leading to the development of these pathologies? Is that what you are going to be focusing on, as a potential mechanistic reason for the buildup of these pathologies?

Dr Karissa Batherlson:

It’s all kind of related. So my research is going to be focusing on what’s called the endolysosomal pathway of the cell, which is the little trafficking system where cells will bring in its nutrients, get it to where it needs to go, and one of the things that this pathway is responsible for bringing in glucose into the cell to generate ATP for the cell to fuel all its other processes. So yeah, this whole network of processes is what I’m really interested in and seeing whether I can develop some therapeutics to see if I can correct any of these processes.

Dr Kamar Ameen-Ali:

That’s really interesting because often, we’ve seen the use of animal models to interrogate these mechanisms. And we’ve seen how over the years, that mouse models of disease, like Alzheimer’s, have been used to try and understand what these mechanisms are, and then develop these new therapeutics. But we know that, specifically with Alzheimer’s, these models have not been successful in then translating to treatments, that have either significantly prevented or slowed down progression of the disease. So this might be, in part, because these mouse models fail to fully replicate the disease that we see in humans, and they often only model certain aspects of the disease. So what I find really interesting about your research is that you’ve used zebrafish as a model organism. And I guess, many of our listeners, they’re probably less familiar with the zebrafish as a model organism, they’re more familiar with mouse models, for example. Can you tell us a little bit about how zebrafish might have advantages of using mouse models, which is something that have been used for many, many years?

Dr Karissa Batherlson:

Yeah, that’s a great question. Yeah, so my whole PhD was about using zebrafish as a model organism to understand the early changes which happen in the brain, which eventually would lead to Alzheimer’s many decades later. So my approach was a bit different to what’s normally done in using it the mouse models of Alzheimer’s. So the current state of play with mouse models of Alzheimer’s disease, that they’re very highly genetically modified. So I think the idea was they originally made a mouse model that had a single mutation which would cause Alzheimer’s in humans. But when they looked at this mouse model and the effects of this mutation, it didn’t really seem to be doing much, they didn’t see any brain pathologies that was consistent with the human disease and they didn’t really show many behavioral phenotypes. So the idea was that they kept adding more and more mutant genes into these mice until they showed the brain changes that happened in the human disease. And ideally, when the mice were pretty young, so that research could get done fairly quickly.

Dr Karissa Batherlson:

So I personally don’t agree with that strategy. While it may be useful for certain aspects of the disease, I don’t think it’s really replicating what’s happening in the human disease. So our approach was to go back to the start, where we introduce a single mutation that would’ve caused Alzheimer’s in humans. And we were doing it in zebrafish. So our lab made a little collection of seven different mutations which cause Alzheimer’s in humans, and we introduced them to the zebrafish. And then we analyzed the effects of these mutations in the brain, and when the fish were very young. And the idea is we were looking for what each of these different mutations did in common, and the earliest change, which eventually would lead to Alzheimer’s disease many decades later. So to cut a long story short, we found the effect in common looks like it was changes to energy production in the brain.

Dr Karissa Batherlson:

And my PhD lab’s now going to go on and find out exactly what’s going wrong in those brains. But why we use zebrafish, one of the most attractive things is that they are so much cheaper than mice to look after. So I’ll give you an example, a behavioral experiment we did in zebrafish. We raised a family of 100 sibling fish until they were six months of age. So our zebrafish facility is completely self-run, we don’t pay for tank space or anything like that. We just feed them twice a day and clean their tanks when they get dirty. So I’d estimate that would cost about less than $100 Australian dollars for a raise these fish until they were six months age. When we do a similar experiment in mice, we needed to raise that many mice until they were six months of age, and we needed to do that across multiple cages. And these mice costs about $15 a cage, a week.

Dr Karissa Batherlson:

So once we factored in that, plus all the other things we needed to pay for, it was about $16,000 for one experiment. So compared to the $100 for zebrafish, this is a huge, huge benefit. And one kind of related to that is, yeah, the fact that we can get 100 siblings quite routinely from a single pair mating event with zebrafish, and we can raise all of these siblings in the same tank. So we minimize any genetic and environmental noise. And this is something you can’t really do in mice, which only generate maybe 10 mice in a single litter. So yeah, I think that that’s the main benefit of zebrafish is their breeding capacity and how you can eliminate all other sources of noise. And you can really focus on your effective mutation.

Dr Kamar Ameen-Ali:

I feel like a lot of people that have maybe used mice in their research previously are exploring using zebrafish as a model organism, because it’s not just the financial benefits of using zebrafish, it’s also the ethical ones as well. They’ve been using developmental biology a lot, and a lot of the experiments can be done before they become legally protected. I think even if, at some point down the experimental pipeline, if mice have to be used to test a drug for regulatory reasons, at least we can eliminate a lot of the use of mice in those earlier stages with something like zebrafish or other organisms. So that’s really interesting to see how you’ve applied that in your research. So you research previously used zebrafish to understand those early cellular and molecular changes in inherited forms of Alzheimer’s disease, and now what you’re going to do, if I’m right, is to be looking at whether there is a common pathological basis between these forms of Alzheimer’s disease and Sanfilippo childhood dementia. So what can you tell us about your plans for this project over the next three years?

Dr Karissa Batherlson:

Yeah, so I think you touched on what my plan is here. So I’m going to be testing three new repurposed drugs, to see whether they have any therapeutic benefit in models of these two diseases. So my first step is going to be screening these drugs in human patient-derived cell lines. So I’m going to add the drugs to the cell lines and see whether they can rescue any of the differences that we know happens in these cell lines. But while cells in dish are pretty useful, it’s not really representative of what’s happening in a living organism. So that’s where my zebrafish are going to come in. I’m going to see whether any of these drugs can rescue any behavioral defects that the Sanfilippo model fish show. And then the best out of the three are going to be tested in the Sanfilippo mouse model, as we want to see whether the drugs are translatable to a mammalian system. Zebrafish aren’t mammals, so that’s really important to show as well.

Dr Kamar Ameen-Ali:

We know that often, research doesn’t work out as we plan, we have to change things as we go along in a project, or sometimes we find things that are really interesting and we decide to pursue those things. But if it does all work out in this project, as you’ve planned, and you do manage to find a common pathological basis between Alzheimer’s disease and Sanfilippo syndrome, and you do manage to identify these potential treatment targets, what will the next step be? Have you got a long-term plan post this fellowship of where you see your research going?

Dr Karissa Batherlson:

Yeah, definitely. So my next steps will be doing a few more animal model testing. I will only be testing it in a Sanfilippo model mouse. We need to make sure that it works on the Alzheimer’s [inaudible 00:20:37] too, in a mammalian system. And then I want to extend it out to other types of neurogenerative diseases, so including other adult and childhood onset dementias. And yeah, my grand plan is to eventually see a clinical trial with one of these therapeutics, that will have a wider patient benefit rather than just going straight for Alzheimer’s or straight for Sanfilippo. I would like to see a cohort that includes both.

Dr Kamar Ameen-Ali:

So, do you think this will have implications for sporadic forms of Alzheimer’s disease? Because obviously that’s the most common type of Alzheimer’s disease. So, do you see it kind of having applications and implications there as well?

Dr Karissa Batherlson:

It’s been something I’ve been thinking about a lot, because there isn’t really a good animal model of sporadic Alzheimer’s disease. So, I’m hoping that by the time I get to that pet stage, something’s going to be out there that I can test, preclinically, any drugs that I come up with.

Dr Kamar Ameen-Ali:

Yeah. I think that’s the challenge, isn’t it? For anyone working in preclinical research, especially in the dementia field. Thanks Karissa.

Dr Anna Volkmer:

Thank you, because actually, in that explanation, you’ve made it so clear. I think a lot of the preclinical research is really difficult to understand, for the people we work with and some clinicians. And I just really enjoyed your description of how cells work and use energy, and that consequently results in cell death. Because I think that’s one of the hardest concepts for the patients that I see to really grasp. And of course, also, this disease is so complex, it’s also hard for a lot of our funders to grasp. So, before we wrap up today, we should probably talk a little bit about your funders, Race Against Dementia. And we had a couple of questions about this, I guess. So, both Kam and myself, we’re early career researchers. So, we are probably also a bit obsessed with getting fellowships ourselves. And you are what now, two years post-PHD?

Dr Karissa Batherlson:

One year, I haven’t actually graduated yet. All the paperwork’s been signed off now, just waiting for the graduation ceremony next month.

Dr Anna Volkmer:

Oh, has it been delayed because of COVID?

Dr Karissa Batherlson:

Oh, I think just the time that I submitted. I missed last year’s graduation rounds, but that’s okay. I got the doctor title so I’m happy now.

Dr Anna Volkmer:

That’s the main thing. Yeah, yeah. And they were all delayed in the UK actually, so I just had mine two years after I [inaudible 00:23:03].

Dr Karissa Batherlson:

Oh, my goodness.

Dr Anna Volkmer:

But this award, the Race Against Dementia Award, must have come along then at the perfect time for you.

Dr Karissa Batherlson:

The stars really align with me for this fellowship. So, Race Against Dementia had a fellowship round in 2020, and I was still in the late stages of my PhD and wasn’t quite ready to apply for it yet. But as a longtime fan of Formula 1, I was really devastated that I may have missed out on applying for it back then. But then, yeah, they did the second round in 2021, so that’s the one I applied for. And I was still trying to write up my thesis at the same time as get this fellowship application in. So it was a lot of work, a lot of sleepless nights, and trying to jump between a thesis writing and trying to think about my next steps as well. It was a lot of work. I think, yeah, I was about version 10 on both sides by the time I was ready to submit both of them. So yeah, it was a crazy, crazy time in my life.

Dr Anna Volkmer:

Absolutely. And I guess in some ways, I was just thinking about writing my thesis as well. And I was thinking actually, although it sounds really intense and a lot of work, it probably complimented each other that you in that, writing can be so challenging, can’t it? Yeah, that makes so much sense. Kam, did you have a couple of questions as well around this?

Dr Kamar Ameen-Ali:

Yeah. So how much support did you have when you were writing your fellowship applications? So did you have support from your current PhD supervisor, the university more widely? How much support did you have and did you find the support really helped you?

Dr Karissa Batherlson:

I had a lot of support. So yeah, my PhD supervisor had a lot of input onto this fellowship application, and I’m so grateful to him for all the work he put in for me to move on, which, yeah, I thought it was quite selfless of him. That he went through a lot of drafts with me and helped me shape the application, even though he’s not probably going to play a big role in that, in the current work. Then I also had a lot of support from my next mentors. So I have three, I have two scientists, one that’s a world leader in Sanfilippo syndrome and then one that’s a world leader in Alzheimer’s disease. And I also have a clinician as well. Together, they have quite a broad knowledge to really help me generate the perfect application. I also had some support from the main charity in Australia that supports Sanfilippo syndrome.

Dr Karissa Batherlson:

So I reached out to them to get their advice on what would be really impactful for patients. And yeah, their thing was therapeutic, it has to be a therapeutic based application, that’s what we’re all here for at the end of the day. And so yeah, they were a massive help, and they actually helped me set up a little public advisory group with myself and three parents of kids who have Sanfilippo. So actually, part of the application process, I did a little presentation to them, explained what I was planning to do, and they helped me write some of the lay summaries and stuff within the application. So that, to me, was the biggest source of support during this application process. Having the motivation from them and doing this together with them, I think, is so important. And I guess, yeah, the last source of support was my other half. He definitely was there to help me through every step of the way. And yeah, feeding me lots of coffee and Red Bull to get through it.

Dr Kamar Ameen-Ali:

So it sounds like for a successful application, you really need that support from lots of different areas, not just…

Dr Karissa Batherlson:

Oh, you definitely do.

Dr Kamar Ameen-Ali:

From the scientific part of it, but also from, like you said, just writing the lay summaries and trying to get that right. And actually, making sure that each different aspects of the application have the same amount of attention and focus on them because I think sometimes we can easily fall into the trap of focusing too much on the scientific side of the application. And the lay summary is something that just gets written maybe at the end, as a summary of everything that we’ve written. But that is actually a really, really important part of the application. And it’s great that you sought advice on that part as well.

Dr Karissa Batherlson:

And to be honest, I think it’s the most important part of the application. At the end of the day, the funders aren’t just scientists, they’re scientists and people like the general public that need to understand what you’re doing, and understand why it’s important.

Dr Anna Volkmer:

Yeah. And I think actually, it pays off because you speak, I’m coming back to this point, I’m circling back to the way you’ve spoken about this, because obviously having spoken to so many people with it, with lived experience, the way you speak about it is so clear and accessible about this very complex tasks. And that’s going to bode well for you in terms of impacting dissemination into the future, won’t it? I was also going to make this point about your PhD supervisor spending so much time with you. And I think that gets forgotten, is this pay it forward culture. It’s so valuable. Well, I’ve realized now that I didn’t realize how important it was that people help you, you pay it forward to the people you are supporting, and that’s how the wheel can keep turning. Unless we do that, unless we’re generous with our time, I’m not sure that research develops in the right way that it needs to for people.

Dr Karissa Batherlson:

No, you’re absolutely right. That’s probably one of my favorite parts of the job, is the paying it forward aspect, when you’re helping out the students, and you sit and watch them flourish and develop. So it’s one of the most rewarding things about the job.

Dr Kamar Ameen-Ali:

Yeah, definitely. So Karissa, do you have any other tips that you might give to ECRs, who are maybe looking to apply for fellowships and they’re in the process of trying to put together an application?

Dr Karissa Batherlson:

Yeah, I guess the biggest thing I would say, and it’s a lesson that I’ve learned, is start early. If I were to do this again, I would’ve started even earlier than what I did because you’ll go through so many versions, and things start coming up, trying to get feedback from lots of different people and trying to incorporate it all, it takes a lot of time. And yeah, to try and minimize the amount of stress it gets when you get towards the deadline, start early. And the other thing I would mention, it’s got to be your own work and ideas. I’ve seen other people before, where they’ve just written a proposal that it’s been their supervisor’s idea. And if your heart’s not in it, it’s not going to come out when you’re writing it. It has to be your own ideas and you have to be excited about it, for it to really shine.

Dr Anna Volkmer:

And, and I think it really shows how passionate you are, Karissa, and that’s the key, isn’t it? You need to be passionate about it for the people, but also to keep doing the research in this field. But for more information on Karissa and her bio, and how passionate she is about this topic, as well as information on Race Against Dementia and Dementia Australia, you can have a look at their websites. You’ll find the links in our show notes. We also have interviews and webinars with some of the other RAD fellows, discussing their approach to applying for fellowships as well. And also, what makes Race Against Dementia and Sir Jackie’s mission so special. But it’s time to finish up today, sadly. It’s been so lovely talking to you all. We’ll be back again in two weeks time. So have a really great week and we’ll see you all next time. Thank you. Bye.

Dr Karissa Batherlson:

Thank you.

Dr Kamar Ameen-Ali:

Bye.

Voice Over:

Brought to you by dementiaresearcher.nihr.ac.uk, in association with Alzheimer’s Research UK and Alzheimer’s Society, supporting early career dementia researchers across the world.

END


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