Podcast – ADPD 2025 Conference Highlights – Part 1

Voice Over:

The Dementia Researcher podcast, talking careers, research, conference highlights, and so much more.

Dr Amanda Heslegrave:

Welcome to the first of our two-part special from AD/PD in Vienna. We're going to bring you some of the highlights from the 2025 conference. This is one of the world's leading events for Alzheimer's and Parkinson's disease research, and researchers from all over the world have gathered here today for this week to talk about these diseases and the research that's happening.

Hi, I'm Dr. Amanda Heslegrave, I'm principal research fellow at the University College London, and it's really good to be back to host the show, which I've done previously, and I just need to remember how.

So, over the next two episodes, we're sharing key takeaways, expert insights, and the latest breakthroughs that have been presented at this year's event in Vienna. So, we've got thousands of researchers, clinicians, and industry leaders here, coming together to talk about and be a vital hub for collaboration and progress in the neurodegenerative disease research arena. And we're excited today to give you a front row seat.

So, joining me today, I have Dr. Loukia Katsouri from UCL, Dr. Imogen Swift from Vesper Bio, but previously from UCL, and Dr. Anna Mallach from Imperial College London. So hi, everybody.

Dr Loukia Katsouri:

Hello.

Dr Anna Mallach:

Hello.

Dr Amanda Heslegrave:

So, I'm now going to let you all properly introduce yourself, starting with Loukia. So please tell me a little bit more about yourself.

Dr Loukia Katsouri:

So I'm a senior research fellow at the Sainsbury Wellcome Centre. I work with John O'Keefe, and my main research interests are behavioural characterization of different mouse models of Alzheimer's disease, as well as single cell electrophysiological recordings in these mice. We have a lot of mice in the lab that we have crossed with tau or APP, and we're also very interested in how tau propagates in these mice, and also how the neuroinflammation is affecting either tau or amyloid. Okay?

Dr Amanda Heslegrave:

Thank you very much for that. Now, Imogen, tell us a bit more about yourself.

Dr Imogen Swift:

Yes, hello. So, Amanda you know me very well from 2018 when we worked at UCL and now I've moved into industry and I'm a small Copenhagen based biotech called Vesper Bio and I'm a research scientist. So my role is basically to run lots of fun experiments and it's all related to frontotemporal dementia and Parkinson's disease. So we're a little bit left field for AD/PD, but there is some Parkinson's in there too-

Dr Amanda Heslegrave:

Oh, no, I think it fits.

Dr Imogen Swift:

Which is ... Yeah, it fits. Thankfully it fits. It's all dementia relief.

Dr Amanda Heslegrave:

Yeah.

Dr Imogen Swift:

But yeah, our focus is basically to target [inaudible 00:02:54] receptor to treat these conditions and it's really exciting times. So it's great to be here though, and see lots of familiar faces.

Dr Amanda Heslegrave:

Thank you very much. Now Anna.

Dr Anna Mallach:

Hi, it's good to be here. I am a research fellow at Imperial where I recently set up my own group where we're really looking at cell-cell interactions and how they're disrupted in Parkinson's disease and kind of what role that plays in developing dementia downstream. So it's good to be here.

Dr Amanda Heslegrave:

Okay, so that's great. So right, before we actually start to talk about some highlights, really like to know about what you've actually been doing at the conference, are you presenting yourselves? And I know you all have been. So first of all, I'll just talk a little bit about what I did yesterday. I was lucky enough to be invited to present at a product theatre for Quanterix. Now these are a company who produce technology that in our lab we utilise all the time.

And so it was really nice to be able to give a kind of ten-year perspective on what we've done with the company and where we started and where we've got to now. So that was great fun. So tell me now about what you've done or doing.

Dr Loukia Katsouri:

So I had an oral on demand, which is on the website and you can watch and also a poster that was presented yesterday and today. So this is a work that started during COVID. So it's a five-year work. We characterise two different APP mouse models at six, 12 and 22 months of age. We did this longitudinal study with independent cohorts, did some behavioural tasks about 10 for each one.

And then we applied machine learning in this mice to, A, speed-up our analysis. Secondly, to remove all of the bias that one experimenter might have against the other. And third, because we want to extract features from this analysis to be able to stratify the animals into each genotype and predict which mice will be more impaired over time or not. So this is quite a big effort from a lot of people. So I'm really happy that it was selected for here.

Dr Amanda Heslegrave:

And one thing, is these mice that might perhaps their samples come to us in our lab to do some biomarker research?

Dr Loukia Katsouri:

That's exactly what I'm going to give you as soon as I get the green light. Yes, that's exactly the one that I'm going to send you.

Dr Amanda Heslegrave:

Okay, we'll look forward to that then.

Dr Loukia Katsouri:

Yeah.

Dr Amanda Heslegrave:

Okay. So what have you presented or will you be presenting in?

Dr Imogen Swift:

Yeah. So we've got kind of two sides of it. There's the preclinical, I've learned lots of new industry words that I try and assert in sometimes. I said there's the preclinical world and then there's the clinical world and our boss, Mads Kjolby is going to be doing a talk in about an hour's time actually on the clinical side, which is very much the world I know less about, but there is biomarkers related to that. So that's exciting.

Dr Amanda Heslegrave:

We're happy.

Dr Imogen Swift:

Yeah, exactly. And then the preclinical world is where we've got some sound models and some mouse models, so very relevant discussions there. And we've got a poster for that, what she has been presenting today and yesterday. And so it's been really cool actually because it's been work that previous colleagues have been running and now we are continuing with and it's like lots of very cool assays, which I'm learning more and more about by the minute because obviously I'm from biomarkers, but we're aiming to increase programming levels in these FTD programming carriers and it seems to be very successful so far. And we're in Phase 1b/2a, so it seems exciting and I've learned what that means now, so that's always good. But yeah, so it's been really cool to be here.

Dr Amanda Heslegrave:

All right, wonderful. So Anna, what are you going to have done?

Dr Anna Mallach:

So I'm going to present my poster, so that's tomorrow and on Saturday. So I'm in the second poster session and it's kind of a continuation from my postdoc work that I've now developed further at Imperial. So during my postdoc we generated spatial transcriptomics data, which is really cool data because it allows you to query expression of genes in cells with the spatial component. So you can not just say this is a microglia and this is expression profile, but this is how it changes when it approaches pathology.

And so we published this before, but the thing that's been bugging me about generally spatial transcriptomics is that cell segmentation is really difficult. So you throw away a lot of the data you acquire because you don't really know what cell that belongs to. And so what I've been working on since summer and what I'm presenting now is a way to effectively optimise the data that we have and to be able to look at subcellular changes. So pull out the nucleus data that we already have and pseudo bulk the transcript information.

And so we can now start to look at cell states that we know are located to the kind of cell body of a cell such as specific microglia states are associated with diseases. So this kind of allows us to do some really fun analysis and also look at how cells are polarised close to pathology. So this is kind of a proof of concept for the methods and we're very excited to make sure it works, it does what it should be doing, which we're slowly confident about, and then ultimately apply downstream to other disease models.

Dr Amanda Heslegrave:

Okay. Thanks. That was all good information to have and I'll come and have a look at your poster later. Okay, so now we're moving on to the highlights so far. I mean obviously we're only halfway through the conference at the moment, so this is the first half highlights. So I'm going to go round and ask you for some insights and observations so far of what you've really enjoyed. So first we'll start with Loukia.

Dr Loukia Katsouri:

So the first session that really I really liked was one from Rudolph Tanzi. He spoke about translational drug discovery. It was the session translational drug discovery and experimental models one. So he talked a lot about drug repurposing and the reason for that is because they want to identify targets. So like the [inaudible 00:08:41] speaker said, they can't use these repurposed drugs but they're safe. They could potentially use that to make new drugs, for example. And what he was saying is that they used a lot of transcriptomics and some 3D culture model systems. I guess it's from iPSCs. That's what I understood. And you said that especially for phospho-tau, hyperphosphorylation, A-beta 42 is very important.

And is what is driving the tauopathy. So they did some pre-screening, they found ... They looked for small molecules to modulate gamma-secretase to change the ratio from 42 to 38, which is the protective one, which is really nice. And they found some that changed the ratio and decreased A-beta 42 production. They also identified some glia plasticity modulators, so that they thought were very interesting. They also used some BV-2 microglial cells and some microglial cells from iPSCs neurons. They also made some 3D models and they did some drug screen with fluticasone and mometasone to see the microglial uptake. And what they also saw, which to me was very exciting, was that [inaudible 00:09:59] increases microglial uptake.

Dr Amanda Heslegrave:

Okay. Of diabetes?

Dr Loukia Katsouri:

Of yes, which is great, but he said with 50K per year for the drug it's a bit difficult, but at least based on that they were able to screen more drugs and they found about 48 drugs that would do the same, induce microglial clearing. About 52 that changes the microglias to the [inaudible 00:10:28] and all of this. And 40 that are inhibiting TNF alpha release, which is also very important. And they found some indications that this is due to microglial senescence, mitochondrial senescence in microglial cells. So all very exciting, which-

Dr Amanda Heslegrave:

Okay. Yeah, I mean the whole drug repurposing thing at the moment is a huge thing I think because there are so many drugs. I mean actual in-person drugs that we know are safe and are tolerable, but we don't really know all of their effects, for example, the GLP-

Dr Imogen Swift:

Inhibitors.

Dr Amanda Heslegrave:

So I think that these kind of talks and this kind of work is really, really exciting.

Dr Loukia Katsouri:

Yeah.

Dr Amanda Heslegrave:

Yeah. Okay. Thank you very much for that. That's very cool. Imogen?

Dr Imogen Swift:

Yes-

Dr Amanda Heslegrave:

Anything to highlight?

Dr Imogen Swift:

Yeah. I mean I really enjoy the poster sessions because I feel like you can really get a lot of information but also the key things that you want to ask. Whereas I guess with a talk it's a slightly different dynamic and I also am very afraid to go and ask a question at the end of a talk, there's all those people, and there's a microphone, so-

Dr Amanda Heslegrave:

Just try it once.

Dr Imogen Swift:

I've literally never did it. Okay, I need to try it. This is my mission for this week. But one of the posters, it was very relevant to our work especially it was Thomas Cucar who's from Emory University in the US and he has some really cool work that's actually linking mouse models and the lysosomes and especially granulins and lysosomes. And as my PhD looked a lot into it. I was very biassed with my interest in it, but it's actually really, really cool work.

And they're basically showing that by adding this granulin-2 and granulin-4, they were able to ameliorate some of the effects of not having progranulin. And so he dived a lot into the lipidomics as well. And they showed that there were decreases in the BMP lipid and the glycosphingolipids, oh no, glycosphingolipids was increased. So it was these two kind of lipids that were big. And obviously in the world of biomarkers I was very interested in that and measuring lipids. And I know that a lot of people are looking at these lipids at the moment and seeing in Bioflow and seeing those changes.

Dr Amanda Heslegrave:

So was there any insights on the best way to measure them? Because that's not-

Dr Imogen Swift:

Good question.

Dr Amanda Heslegrave:

... something that's very easy.

Dr Imogen Swift:

No. So I think they must have done it by mass spec as in from the poster indicated. So I know other people do it from mass spec, but I don't think it's easily done.

Dr Amanda Heslegrave:

I don't know of any other way to do it.

Dr Imogen Swift:

No, I don't think there's any [inaudible 00:12:45]-

Dr Amanda Heslegrave:

I also think it's quite specialised in the field of mass spec.

Dr Imogen Swift:

Oh yeah. I think even within that, I think there's two people in the world or two groups of people that seem to be able to do it. But it was really interesting to see that the same markers do keep coming up as BMP. But it was also in the mouse model and I have seen some kind of controversy around the idea that is actually translatable into humans. So I don't know if that's ... Because I know when we measure BMP's in the lab and we measure in urine, we didn't see any difference-

Dr Amanda Heslegrave:

No, I remember you doing that actually.

Dr Imogen Swift:

Yeah, exactly. So I'm intrigued how that can translate, but also urine maybe isn't the best way to look into it. I think about lipidomics, I mean, there are so, so many different lipids and the regulation of them is so-

Dr Amanda Heslegrave:

It's so dynamic.

Dr Imogen Swift:

... complicated that there must be a reason for this.

Dr Amanda Heslegrave:

Exactly.

Dr Imogen Swift:

And people don't look at it because it's hard. And so we need to do the hard things I think.

Dr Loukia Katsouri:

But I think also it's very important to note that the cholesterol in the brain is de novo, so you never get it from the periphery.

Dr Imogen Swift:

Okay. So measuring it in urine is a bit of a waste of time is what you're saying to us.

Dr Loukia Katsouri:

Maybe it's what is degraded, so it has to come out somehow, but at deleted the production is de novo.

Dr Amanda Heslegrave:

Yeah. Sorry that was [inaudible 00:14:01].

Dr Loukia Katsouri:

Just my PhD was on ApoE, so I read a lot about cholesterol and is so, so complicated.

Dr Imogen Swift:

Yeah, I remember I did one of the diagrams training, including my thesis and the diagram went bigger and bigger and bigger and I was like, "I'm going to get squeezed." But it's very relevant and like you said, I think now we have dived into a lot of the stuff, is easy to measure or easier to measure, and the sensitive methods are getting more and more sensitive. Maybe it is the time to dive into the harder stuff, but I agree that it's still controversial and if there's only two persons in the world that do it's still hard.

Dr Amanda Heslegrave:

Yeah, exactly.

Dr Imogen Swift:

Cool nonetheless.

Dr Amanda Heslegrave:

Yeah. Okay. Well, thanks for that. So Anna, what have you seen that excites you?

Dr Anna Mallach:

What I found really interesting, I'm switching diseases at the moment from Alzheimer's ever to Parkinson's. So I've been ... I think AD/PD is the perfect conference for me at the moment because it's still like the comfort of Alzheimer's every now and again when I feel like a bit like I don't know enough what's going on, I go to an AD session like, "Ah, hello." But yeah, I've been branching out into the PD session because I really need to know what's going on. So I went to one on PD and lewy body dementias yesterday about advances in diagnosis where what [inaudible 00:15:09] from Innsbruck was giving a really interesting talk on clinic, a biologically defining Parkinson's instead of doing it clinically. So the clinical, kind of the way that Parkinson's presents is incredibly heterogeneous, a lot more so than Alzheimer's disease. You have all of these different subtypes and that makes it really difficult to study it as researchers but also to any run clinical trials.

And so there's been a push in the field quite recently to say actually we want to define it based on something that we can measure biomarker wise. So for example, with the seed amplification assays, by looking at imaging for dopamine laws and combining this with known genetic variants. And that was a really interesting shift to say this is our like biologically defined Parkinson's. Now if you have these three markers a bit to Alzheimer's, what we have already in the AD field, if you have these markers we can put you into category of Prodomal Parkinson's or then actually active Parkinson's disease.

And I thought that was really interesting to see concepts that after million that dealt before an AD being applied now to Parkinson's at the end, coming to conclusion that really what the field needs is good bio PET biomarker for office nuclear. And I was shocked that that didn't quite exist yet. Maybe I was RNA even, I was like, "This is crazy." There was another talk here at AD/PD that presented something that could be used as PET marker for alpha-syn but that's maybe my next highlight to discuss later.

Dr Amanda Heslegrave:

Yeah. And I know that alpha-synuclein is a field that there is a desperate need for some good marker that we ... I mean there are the seeding acids and that's fine, but it's not enough, there needs to be more. But also I think that when you talk about the biological definition and the clinical definition in Alzheimer's at the moment, that's causing quite a lot of controversy because in the States they will say that a biomarker positive person you can diagnose with AD even if they don't have any clinical symptoms. That's kind of-

Dr Anna Mallach:

It needs a bit of both in some way.

Dr Amanda Heslegrave:

But the European view is that you are now at risk, but in Parkinson's it's going to be even harder because of all the subtypes and all of the kind of ... I mean I don't know enough about Parkinson's about where that ... Because we know with amyloid you can have that in your brain and never actually progress. You die before. You know what I mean? You get old and die before. What about Parkinson's? Can that happen with that? Can you have alpha-synuclein aggregates in your dopaminergic neurons and not get it? I don't know.

Dr Anna Mallach:

So I think you can to some degree have some alpha-synuclein aggregates like lewy bodies. But I think in Parkinson's it's this loss of dopaminergic neurons in the substantia nigra. Right? And that's-

Dr Imogen Swift:

[inaudible 00:18:06].

Dr Anna Mallach:

Exactly. So also the way the disease presents is quite different. I think the worry you always have with Parkinson's in a way is because pathologically, it's also there's a lot of heterogeneity. You have a lot of co-pathology, which I find really interesting, this idea of you have alpha-syn aggregating, but you also have amyloids aggregating and while do we know what's happening there, is the alpha ... Is it amplifying the disease, is it driving us towards something? All still unknown. Really interesting questions.

But I do agree that there's ... I think in a way, and this is what we've seen for example with Huntington's disease and what [inaudible 00:18:49] has been doing of saying if you are at risk of developing Huntington's, if we know this, then you can classify you as Stage 1 Huntington's and then makes then clinical trials a lot easier. So part of me thinks if you-

Dr Amanda Heslegrave:

Stratifications, yeah.

Dr Anna Mallach:

Exactly, if you restratify might make life easier down the line for [inaudible 00:19:09].

Dr Amanda Heslegrave:

And actually that's a really, really good point. That was not in my consideration at all. But yeah, good point.

Dr Imogen Swift:

The benefits of genetics were in that, like the GBA mutation, I imagine it's probably easier to stratify that group for Parkinson's versus the sporadic group and you have a huge sporadic group. Yeah, exactly.

Dr Amanda Heslegrave:

And I think it's more info, more info about what the risk factors are. Okay. Loukia, so what's next?

Dr Loukia Katsouri:

So I'm going to switch gears back to mice.

Dr Amanda Heslegrave:

Okay.

Dr Loukia Katsouri:

So I watched a talk from Frank LaFerla. That he was presenting some of their model AD works. The model AD is a very ambitious NIH funded consortium of quite a few universities that they're trying to humanise a lot of the genes in the mice and then see how they behave. So what they did, they made mice that carried the H2 haplotype of MAPT, which is the protective I think, and they cross them with some amyloid mice that were floxed. So you can activate them wherever you want.

And also with the human ApoE4, which we know E4 is a risk factor for Alzheimer's disease. And they did some studies in these mice and they saw that even at young age, at four months of age, these mice have plaque formation. They did plaque-associated amyloid and oligomeric diffuse amyloid. And they saw that when you cross them with the E4, the amyloid moves from the parenchyma to the vessel. So you have a lot of CAA in these animals, which resembles a lot of what they see in the humans.

Dr Imogen Swift:

So did they have both the protective and the ApoE?

Dr Loukia Katsouri:

They had the E3, which is the canonical.

Dr Imogen Swift:

Okay. It was three different groups, not in the same MAPT?

Dr Loukia Katsouri:

Two groups, E3 versus E4.

Dr Amanda Heslegrave:

Oh, okay.

Dr Loukia Katsouri:

So to see the normal, so E3 is human E3, which is the ... It's not the productive, productive is the E2. And they didn't present any data on the E2 on this-

Dr Amanda Heslegrave:

It's so rare though, isn't it? Would it be-

Dr Loukia Katsouri:

Yeah, it's quite rare. And also you get a familiar hypercholesterolemia with E2.

Dr Amanda Heslegrave:

With E2?

Dr Loukia Katsouri:

Yeah.

Dr Amanda Heslegrave:

Okay, so it's like good, bad.

Dr Loukia Katsouri:

Exactly. Yeah, yeah. So they-

Dr Amanda Heslegrave:

[Inaudible 00:21:32].

Dr Loukia Katsouri:

Exactly. And what they saw is that there was a lot of microglia response to the dense deposits, but not to the diffuse ones. And especially they had a lot of stronger astrocytic response in this E4 mice and the astrocytes looked weird. They were more kind of less mature than the normal E3 mice. And they also saw that basically these mice develop H-related extracellular A-beta deposits and CAA in the appropriate brain regions introducing ApoE, it's promoting CAA.

Interestingly, they found phospho-tau217 by staining, accumulating in this one deadlines in the CAI and this mice and there's a limited evidence of plaque-induced in [inaudible 00:22:26] tangled pathology. I guess they're going to look at these mice at an order age. And he also presented some data from old breeders and he said that they have differences between male and female. I said the female are had worse pathology, especially this E4. But what I said to him is what I've noticed in my mice, if you compare breeders with, for example, female mice that never gave birth, the pathology is always worse than the breeders. And he said, "We're looking into this" and they're waiting for some naive virgin mice that they haven't bred to compare them, but it's also going to have a lot of repercussions in...

Dr Amanda Heslegrave:

So that's a real kind of hormone-driven, you must [inaudible 00:23:10].

Dr Loukia Katsouri:

It seems. Yeah, it seems so that it's bad news for a-

Dr Amanda Heslegrave:

And good reason not to have children?

Dr Loukia Katsouri:

Yes. I think it's protective for Alzheimer's if you have no children. But...

Dr Imogen Swift:

Yeah, I wonder in the context of humans, if it's shown that-

Dr Loukia Katsouri:

I think it's the hormonal and I think there was another study I was reading recently that the burden of pregnancy on the body lasts for years after you gave birth. So I'm not surprised that there's effect on like Alzheimer's.

Dr Amanda Heslegrave:

Well, I mean and the whole hormone effect as well. There definitely is. I mean they keep doing the studies of the people on replacement therapy and they keep coming up because it's kind of retrospective and it's not been planned. I don't think that they're coming out with concrete enough conclusions from this because they're looking at a population where they weren't really caring about their implant [inaudible 00:24:06] women. Is that controversial to say?

Dr Imogen Swift:

Yeah. No, no, it's true. It's unfortunately an under-researched work of women in medicine.

Dr Loukia Katsouri:

But I think definitely now that you have more women that by choice don't have children, would be a good time to measure the [inaudible 00:24:25].

Dr Amanda Heslegrave:

We know the birthrate because the world is-

Dr Loukia Katsouri:

Declining.

Dr Amanda Heslegrave:

So yeah.

Dr Loukia Katsouri:

So yeah.

Dr Amanda Heslegrave:

Okay. Well, thank you. That was really interesting. Imogen, what do you have?

Dr Imogen Swift:

So I am going back into the biomarker space. I have a safe space as-

Dr Amanda Heslegrave:

You like it there. It's fine. You stay there.

Dr Imogen Swift:

Yeah. But it was actually interesting. It was a talk yesterday and it's this group in Rochdam actually used to work with them a bit. So again, slightly biassed, but it's the Genfee cohort and they've done Olink on [inaudible 00:24:53]. So I'm always intrigued when people do Olink or SomaLogic or these big mass spec panels. Because there's a question of do you see the usual targets that we know, but also how similar is it? How replicable is it? And it was interesting. They did a lot of ... It was actually a lot of data. They also had a discovery cohort and a validation cohort, which I thought was pretty strong. The genetics of the validation cohort was limited by numbers for fair reasons, the genetics for ... This was in STD patients. I should have ... Well, pre-symptomatic and symptomatic, so not just patients.

And they had a few markers that flagged up and neuropentraxin seemed to be this ... I feel like they're a bit of a theme so far. I know a couple of talks have come up and one of my later highlights also references them. So watch this bit-

Dr Amanda Heslegrave:

Teaser.

Dr Imogen Swift:

Yeah, a teaser for later. But I think it's going to be really interesting using these panels in the context of studying people and introducing people to trials, but also thinking about diagnostics and things. But I do question the methods a bit if we're getting all different results from the same samples.

Dr Amanda Heslegrave:

I wonder ... So what, was it 5,400 samples?

Dr Imogen Swift:

It was 2,900. It was the one from a few years back I think. So now it's got even bigger.

Dr Amanda Heslegrave:

Well, it's got even bigger, but I feel like the more studies get done, the more they're finding that the same set of results occur. So is it necessarily better to go bigger and do thousands and thousands?

Dr Imogen Swift:

Well, exactly. There's nothing [inaudible 00:26:23].

Dr Amanda Heslegrave:

Well, actually the ones that come out are always going to be not the same. They're not exactly the same. But some of those are in the panel for ... I'm not saying no reason, but I think that there needs to be some sort of thought about what you're measuring and how useful that is.

Dr Imogen Swift:

It's the risk of the fishing trip, I guess versus the target side. I think that there's value in both, but I think if we keep repeating these and we keep getting like you say, similar results, is it just down to abundance of them and actually, and what's the meaning behind it? But I think the best thing now is to get more stratified cohorts and all these conditions to really understand what's going up and down and then we can get amino acids in measuring them better.

But it was an interesting discussion as well about referring to them as genetic or proteomic. So basically obviously they're proteins or peptides or however they're measured, but they refer to them in the genetic context with the gene names. And this caused some controversy after, because I suppose you're not really allowed to call them by the gene names because it's not on expression, it's a protein level. So that was also separate discussion, but I found that interesting. So very biassed to biomarkers obviously.

Dr Amanda Heslegrave:

Yeah.

Dr Loukia Katsouri:

Was that a European cohort or?

Dr Imogen Swift:

Yes, it's this genetic SUD cohort, but it was led by the Erasmus Centre. This Julie, I think she's led by Haro Silo, is the leader-

Dr Loukia Katsouri:

So I'm guessing it's predominantly northern Europeans?

Dr Imogen Swift:

Yeah, with some Canadian cohorts. It's a bit European with Canada.

Dr Loukia Katsouri:

Which would be interesting to expand, for example, these biomarkers to Asia or to Africa, how different it's going to be.

Dr Amanda Heslegrave:

Thinking of ... I mean India, the DRI have recently announced that they're punishing to make a brain science centre in India where they've got lots of samples. So what they need to do is start to profile these samples and then start proper studies so that we ... Because apparently I learned this morning, one in six people in the world are in India.

Dr Anna Mallach:

Wow.

Dr Imogen Swift:

Oh, wow.

Dr Amanda Heslegrave:

I know.

Dr Imogen Swift:

I know they had a big population, I didn't realise [inaudible 00:28:28] than that.

Dr Anna Mallach:

It wasn't morning meeting.

Dr Amanda Heslegrave:

It was very early, but I'm sure that's what I heard.

Dr Anna Mallach:

It makes sense, really.

Dr Imogen Swift:

Yeah. Thinking about [inaudible 00:28:39]-

Dr Amanda Heslegrave:

I think that there is such a drive at the moment to look at those...

Dr Loukia Katsouri:

For India and China.

Dr Amanda Heslegrave:

Across those populations, I mean, because there are ... I mean people have shown differences in like, was it Black Americans and non-white Hispanics? I don't know if that's right. But there are differences in the way that tau accumulates even. I don't know why that is.

Dr Anna Mallach:

Even the GWAS studies have reported very different hits across different populations.

Dr Amanda Heslegrave:

Yeah. I mean in Africans, the ApoE4 genotype is much more common, but accumulation of amyloid is much-

Dr Anna Mallach:

Yeah, it's not the strongest hit for Alzheimer's disease actually.

Dr Amanda Heslegrave:

Yeah. Exactly.

Dr Anna Mallach:

In fact, I learnt that at dinner last night.

Dr Amanda Heslegrave:

So the things that we learn that we take for true are not true.

Dr Imogen Swift:

Not for everyone. Yeah.

Dr Anna Mallach:

Yeah, exactly.

Dr Amanda Heslegrave:

If it's not me, for example.

Dr Imogen Swift:

That is a lot of the issues I guess the demographics of many of these co-authors representative.

Dr Amanda Heslegrave:

And I suppose also then the conferences like this, it's the people who can afford to come, come. And the people who come, who have the differences in biology that we need to be looking at are not here. So yeah.

Dr Imogen Swift:

Progression is needed. I agree.

Dr Amanda Heslegrave:

Yeah, yeah, definitely. Okay, Anna, what other things have hit you, hit you? Grabbed you?

Dr Anna Mallach:

I mean, it's a very intense conference. It might've fit me as well. So obviously I'm going to switch back to PD. So I went to a really interesting talk this morning from Amit Kumar from the Karolinska Institutet in Sweden where they've been trying to assess a neuroinflammation, specifically astrogliosis in Parkinson's brains using PET traces. So they used two different PET traces of very intense names that I was like ... It goes over my head, but effectively looked at how astrocytes become reactive in Parkinson's disease. Which is really interesting because up until now we haven't ... I think there's still under appreciation maybe in the field for astrogliosis in the field.

And found that astrocytes or GFAP positive cells in the brain of Parkinson's patients expressed this other protein ICAM, which is linked to ... Which said at the end we're trying to link to phagocytosis of dendrites. And so at the end they pulled out this really interesting GFAP astrocytes microglia crosstalk around dendrites in Parkinson's disease where they were starting to hypothesise whether astrocytes reacting might invite microglia to phagocytosis synapses.

And ultimately ended up with this conclusion of that there were different kind of waves of astrogliosis in Parkinson's disease. So you have this initial wave as the pathology is aggregating, but you can in post-mortem samples, you have to go quite high into the cortical areas for you to even catch this first wave and then this subsequent second wave of astrogliosis quite later.

So I thought it was quite interesting to see ... I think what I'm interested in slowly starting to become important to the field as well there glia crosstalk and how is it regulated and is it quite similar to what we see in Alzheimer's? Is it ultimately the same cells interacting with each other through known pathways just in response to slightly different pathologies?

Dr Amanda Heslegrave:

So I think that I'm seeing quite a lot of interest in astroglia or astrocytes at the moment. It goes in waves with these cells because I did my PhD on astrocytes and I was really interested in them, but no one else was. But now I see such a lot, but now I see an appreciation of all the ... I mean oligodendrocytes are going to come into their own shortly I believe.

Dr Anna Mallach:

They will. They've been dancing around the edges. I think the problem is they are really complicated in of itself.

Dr Amanda Heslegrave:

Or the harder something is to study, the less [inaudible 00:32:45]. And we know this by talking about lipids earlier, but the more tools we get and more people think thinking outside the box and what maybe is important isn't necessarily going to be very easy, but we still need to do it.

Dr Imogen Swift:

Oh, a good insight. Something that can be cultured easily, I feel like is the wrong word, because culturing cell seems impossible either way, but I know microglia and astrocytes are harder or is it astrocytes who are?

Dr Amanda Heslegrave:

I mean, astrocytes are the easiest.

Dr Imogen Swift:

Oh, is it microglia?

Dr Anna Mallach:

Microglia and neurons are harder.

Dr Imogen Swift:

Okay.

Dr Anna Mallach:

The microglia is that since they're immune cells, you can't really grow them in stuff like penicillin or streptomycin. So you grow them without any antibiotics.

Dr Imogen Swift:

And just hope for the best.

Dr Anna Mallach:

Yes, yes. Very much that's [inaudible 00:33:29].

Dr Amanda Heslegrave:

Just don't breathe on them.

Dr Anna Mallach:

Don't look and then breathe, looking at them funny like, "Oh, I've got activated," [inaudible 00:33:37], I think when it comes to oligodendrocytes, because you have myelinating oligodendrocytes and then you've got not myelinating oligodendrocytes.

Dr Imogen Swift:

Wow, there's even subtypes. Oh, okay.

Dr Anna Mallach:

Subtypes. And I think if I haven't tried it yet, but from what I've, talking to other people, I think the myelinating oligodendrocytes might just about be able to culture them. I think the non-myelinating ones are really, really, [inaudible 00:34:03]-

Dr Amanda Heslegrave:

Yeah. I was reading something about this the other day and I've got no further insights.

Dr Imogen Swift:

But it's a topic that's relevant to the field.

Dr Amanda Heslegrave:

It's a topic, yeah.

Dr Imogen Swift:

That's very cool.

Dr Amanda Heslegrave:

It's definitely a topic, so yeah. Wow, that's really interesting then. Thank you. Do we go round again?

Dr Anna Mallach:

Do you have any highlights?

Dr Imogen Swift:

Yeah.

Dr Amanda Heslegrave:

That's really-

Dr Anna Mallach:

That's really a question.

Dr Amanda Heslegrave:

I told you I didn't go [inaudible 00:34:25].

Dr Imogen Swift:

I feel like your talk yesterday about saying 10 years with Simoa that I realise that's been so long. I didn't realise.

Dr Amanda Heslegrave:

10 years since we actually got the machine and then it took another couple before we started to publish.

Dr Imogen Swift:

Yeah, so the HD1.

Dr Amanda Heslegrave:

So the HD1 was where we started.

Dr Imogen Swift:

I do feel like, I don't know if it's just me, but obviously I have a biomarker hat on, but when you go down to the exhibition hall and a lot of the main areas are like Quanterix and Alamar, it's really a bummer. And I feel like what, five years ago you would see maybe one person from Quanterix. Like it really wasn't big.

Dr Amanda Heslegrave:

Yeah, they grew a lot.

Dr Anna Mallach:

Absolutely.

Dr Amanda Heslegrave:

And the interest still, I mean the buzz around Alamar is quite something at the moment. And the fact that the CNS disease panel is coming out in mice, actually, surely.

Dr Imogen Swift:

Yeah. Well, that's what you need across the spectrum to really look into it.

Dr Amanda Heslegrave:

And there will be, I think, more exciting things from there. But at the same time, the Quanterix, the HDX, it's not going anywhere. We are still using it-

Dr Imogen Swift:

Proven to work very well.

Dr Amanda Heslegrave:

... on a daily basis.

Dr Loukia Katsouri:

So do you think that one is better than the other or do you think there's a lot of fuss about Alamar that-

Dr Amanda Heslegrave:

No, no. I think that there's different things you can do with them obviously, but you are not going to have one of them that does everything that you need.

Dr Loukia Katsouri:

Yeah.

Dr Amanda Heslegrave:

I mean the panel, targeted panels are good and we need more of them. But I think smaller panel, that's where we're going to end up. I think we're going to end up with smaller panels that we'll be able to differentiate. We'll get alpha-synuclein sorted, we'll get TDP-43 sorted, we'll be able to at least exclude some diseases with a panel or include into a further screen. And that's got to be better than where we are now. I mean it's lovely. What was I just going to say? It's lovely if you've got Alzheimer's. I was not going to say that.

What I was going to say is that if we could prescribe in the UK and you go to your doctor and he says, "Oh yeah, you've got amyloid in your brain, but you've also got..." like it's not pure Alzheimer's so you can't have that drug. I mean, there's very few people who can have the monoclonal antibodies at the moment.

Dr Imogen Swift:

[Inaudible 00:36:36].

Dr Amanda Heslegrave:

But I think most people have co-pathology and they've got some vascular involvement probably. And so it really, at the moment we're at a point where a very select few people could have this therapy and those people I think are going private right now if they can.

Dr Anna Mallach:

But I guess that's also, up until now, the way we've been studying these diseases has been in such a clean inclusion exclusion criteria like an Alzheimer's model, amyloid beta and tau maybe-

Dr Loukia Katsouri:

At best. At best.

Dr Anna Mallach:

[inaudible 00:37:13]. But also when you then go into human post-mortem brain tissue, you exclude everyone with co-pathologies or CAAs.

Dr Loukia Katsouri:

It's interesting, when I was at Imperial, I used some of their brains to test my base antibody and as it happens, I increased BACE1 at the cancer brain and I never followed that. But I remember talking with the same gentleman, he said, "Oh, this is really interesting. Nobody has really thought of looking BACE1," which is the beta secretase gene in a cancer perspective. So we don't even know what is happening with these enzymes in comorbidities. So are they going up, are they going down What they're doing?

Dr Amanda Heslegrave:

Was it the gamma-secretase?

Dr Loukia Katsouri:

The beta. Oh, yes, the gamma-

Dr Amanda Heslegrave:

[Inaudible 00:37:59] they did work on and then discovered that they were affecting so much more in the body?

Dr Loukia Katsouri:

Yes. Because-

Dr Amanda Heslegrave:

But actually you couldn't target this. They were trying to-

Dr Loukia Katsouri:

Because they're affecting all the notch pathways, so yeah.

Dr Amanda Heslegrave:

Yeah.

Dr Loukia Katsouri:

Causing cancer.

Dr Amanda Heslegrave:

So I suppose that the way that ... You have to start looking at something in isolation, otherwise where do you start? But then we need ... And I think that there will be, so the trials that have happened so far are very selective, very much homogeneous populations. But I know from talks and things that are being planned right now that there's much more of a push to get populations that are just normal populations into the trials. And so we-

Dr Loukia Katsouri:

Isn't that-

Dr Amanda Heslegrave:

... need to work towards this.

Dr Loukia Katsouri:

Isn't that one of the NHS initiatives that are following these people over years from a very young age throughout their life? I can't remember-

Dr Amanda Heslegrave:

Is this Our Future Health? No?

Dr Loukia Katsouri:

Is that it? I heard of it when I was in-

Dr Amanda Heslegrave:

It might be.

Dr Anna Mallach:

Is it the UK Biobank?

Dr Loukia Katsouri:

Maybe that they are selecting samples, and they're following them through their whole life.

Dr Imogen Swift:

Oh, you mean 1946 study?

Dr Loukia Katsouri:

No, that's the one with a cohort.

Dr Imogen Swift:

Oh, gosh.

Dr Loukia Katsouri:

No, this is one that started more recently.

Dr Amanda Heslegrave:

Maybe it's Our Future Health then. I think it might be that one.

Dr Loukia Katsouri:

Probably.

Dr Amanda Heslegrave:

But I also think that cohorts like that and UK Biobank are very self-selecting, they're people that decide I'm going to go and do this. Now I'm going to suggest that that might not be representative. [inaudible 00:39:37]. So I think that we still need new ways.

Dr Imogen Swift:

But there's also from the biomarker perspective, isn't there the big push to really cover as many people as possible for the work that John shot. And obviously with [inaudible 00:39:53].

Dr Amanda Heslegrave:

Yeah. The blood biomarker challenges. So there's the readout study and the adapt study and both of those are really trying to look at community rather than people coming into UCLH or Prince Square or somewhere like that. So yeah, there is a real push, but I mean it's never going to be perfect because we're not as a whole population all able to do these kind of things. And that's partly why, I don't know if you've seen anything, I don't know if I've seen anything presented on fingerprints today.

Dr Imogen Swift:

Oh, right, with the remote testing. I know [inaudible 00:40:30] have obviously released this new drug-

Dr Amanda Heslegrave:

Well, they released a method, a protocol for that, which is really exciting.

Dr Imogen Swift:

So is that the key Alzheimer's-

Dr Loukia Katsouri:

The one that you did at home?

Dr Amanda Heslegrave:

Yeah, I mean potentially this is done at home.

Dr Loukia Katsouri:

Drop AD.

Dr Amanda Heslegrave:

Drop AD is what? Michael Schultz.

Dr Imogen Swift:

Ah, is it Michael Schultz?

Dr Amanda Heslegrave:

It's Nick [inaudible 00:40:49] and Michael Schultz.

Dr Imogen Swift:

Yeah.

Dr Amanda Heslegrave:

Some guys.

Dr Imogen Swift:

It's really cool. But I think the drop AD is focused on what the tau and AP ... I'm not sure what their focus is. But I think-

Dr Amanda Heslegrave:

I mean, I think that what they need or what they want is neurofilament light and phosphorylated tau. Yeah. If you can get a genotype somehow, I think you can get a genotype. Actually they're moved from plasma now. I know you can do it on the LMR platform that can-

Dr Loukia Katsouri:

I mean they do the Down syndrome screening of the baby from the mom's blood that can detect the DNA of the foetus-

Dr Imogen Swift:

Really from the blood? So not without the amniocentesis?

Dr Loukia Katsouri:

Yeah, yeah.

Dr Imogen Swift:

Oh, wow.

Dr Loukia Katsouri:

So now you ask this, is a few years. Yeah, so I'm sure they can get genotype from your plasma if they can do that.

Dr Amanda Heslegrave:

But I think that, yeah, the push towards getting these remote testing things out is going to be ... Could be transformative as long as we can prove that what we're measuring is what we think we're measuring and that it's-

Dr Imogen Swift:

A golden question.

Dr Amanda Heslegrave:

... indicative of brain health. I mean, which is pretty amazing, isn't it? A little [inaudible 00:41:57]-

Dr Imogen Swift:

It is. It really is.

Dr Amanda Heslegrave:

... finger to do that. Yeah.

Dr Imogen Swift:

This actually reminds me of a discussion yesterday. It was Juan Fortier. I'm definitely not pronounced like that correctly, but he does a lot of really cool work and looking at Down syndrome and the links to AD obviously, because there's a massive link. But he was saying obviously with this, all the drugs are out in AD at the moment and the ApoE for exclusion element, he was like, "Do we want to start pushing the idea of screening people, basically everyone?" And is there an extent of how far we should go to get genetics on people so then we can advise. But also then there's the ... I don't know, people with information and who you don't want to go too crazy with it.

Dr Amanda Heslegrave:

If you screened babies for ApoE4 and you were marked with a-

Dr Imogen Swift:

That doesn't feel ethical.

Dr Anna Mallach:

You stop.

Dr Imogen Swift:

Exactly. So it was a really interesting, almost ethical debate at that point of saying, how is this going to come into it? But like you say, if we've got such clean trials and such specific cohorts, it's never going to really work.

Dr Anna Mallach:

Or in a way, like we said, we've had these clean cohorts, we've got these clean trials up until now and let's have this push towards looking at, for example, the Michael J. Fox Foundation is now kind of relaunching a new ASAP call to fund Parkinson's researchers. And one of the themes is on co-pathologies. And I was like, "This is brilliant." Like, let's pour some money, let's pour some real money into do these things we've been ignoring up until now. Which just...

Dr Imogen Swift:

I think that's been a big thing, especially in the research field. I feel like ALS and FDD is an example I had where they weren't fields that overlapped. I mean they overlap hugely biologically and with the patients and C-9 and everything, but the researchers don't overlap at all really. They don't meet at the same meetings and now they do more and more and more. And the fact this is AD/PD is a really good sign. I feel like more needs to be done.

Dr Amanda Heslegrave:

Yeah, exactly. So do we have any more highlights? Having made sure that I didn't have any?

Dr Imogen Swift:

You're leading the highlights.

Dr Amanda Heslegrave:

Oh, but I going to say-

Dr Imogen Swift:

[Inaudible 00:43:51].

Dr Amanda Heslegrave:

Oh, thank you. I was going to say one thing though about, so the recent trial where they've been using the monoclonal, I think it's to NanoMab on pre-manifest-

Dr Imogen Swift:

Oh, pre-symptomatic.

Dr Amanda Heslegrave:

... SID.

Dr Imogen Swift:

Really? Okay. That's interesting.

Dr Amanda Heslegrave:

And I feel like there was a certain amount of success with that slowing of-

Dr Imogen Swift:

Disease.

Dr Amanda Heslegrave:

... the onset.

Dr Imogen Swift:

Well, that's the ideal place to do it, right?

Dr Amanda Heslegrave:

So which gives us real confidence that they can put that into sporadic ... A normal population without any ... Well, they still need, of course, they still need to make the drugs better so that we don't get ARIA and things like that. And maybe by the brain shuttle method of giving the drugs.

Dr Loukia Katsouri:

I saw this cool talk yesterday. It was this guys that they had a bi, I don't know, bimodal antibody that it was binding to the transpharyngeal receptor and it was going into their brain and then it was targeting, I think it was TREM2, I might be wrong. But anyway, it was really nice because they tried different fragments of that antibody and then a nanobody and the nanobody wasn't as good as a huge thing, but still it had an effect. So again, I think that would be a nice way to get the mean and not having them huge because I think the nanobody was like 40 kilodaltons, so quite small was a big antibody was 240.

Dr Amanda Heslegrave:

Yeah, okay. So better methods to get the drugs in and also drugs that aren't some big, massive.

Dr Imogen Swift:

Yeah, yeah. Size obviously [inaudible 00:45:23].

Dr Amanda Heslegrave:

Yeah. Sounds good.

Dr Imogen Swift:

I think one other final thing, if you want to do a [inaudible 00:45:30] just because I teased earlier and I realised that I should probably mention it. I don't know loads on it yet because the talk is technically tomorrow, but it's on this neuropentraxin 2 as a Simoa assay. And to me I was like, "That's super exciting." Because I think so far I've only seen it in a mass spec context. I think there was an immuno assay a few years back, but I don't know if it's been replicated.

Dr Amanda Heslegrave:

I've not seen it used in ... We haven't used yet.

Dr Imogen Swift:

No. Exactly. Well, this is what I was thinking. I was like, it definitely wasn't in our spheres at least. But I think I know the person who's developing it and it seems really exciting. But also these ratios linking to neuropentraxins. So there's like tau and I think that's also being presented on Saturday. So I think it's, I don't know if it feels a little bit of a bubble of neuropentraxins right now, but I thought that was exciting.

Dr Amanda Heslegrave:

I feel like I might try to get that on demand because [inaudible 00:46:13]-

Dr Imogen Swift:

Yes, definitely.

Dr Loukia Katsouri:

I think I have one last thing from Wendy Noble.

Dr Anna Mallach:

Oh, I listened to that talk.

Dr Loukia Katsouri:

It was amazing. Right?

Dr Anna Mallach:

I was on my list and I was like, "No, I'm not going to hype about Wendy Noble because I feel like I do that way too much." Now if you're [inaudible 00:46:28] debate star for, I'm going to chime in.

Dr Loukia Katsouri:

So basically the one thing that she said, she got brains, she made iPSCs, did some proteomics I think or transcriptomics. And she found her signatures in these brains. So four brains were more like in Braak stages. They did long-read sequencing or they're planning to do. So some of the brains had more sitting of endogenous to mention that she created [inaudible 00:46:56] from these iPSCs, whereas others were more clearance of tau. And she showed different signatures between these brains and also very distinct from the control. And she kind of intrigued me as in how is this working? So I think she was spiking the media with some insoluble, sarkosyl insoluble material. So I'm guessing this is mostly tau.

Dr Anna Mallach:

Yes, I think that it is must-spec and tau was the third most abundant protein. You're like, there's a lot in the sarkosyl insoluble fractions.

Dr Loukia Katsouri:

Exactly. So I don't know how you feel. And she also showed that she can get tau when she's injecting mice peripherally. I don't know how exactly that goes into the brain. And she says a lot of pathology into hippocampus and amygdala. So it intrigued me. It's kind of like the two signatures.

Dr Anna Mallach:

Yeah. But yeah, exactly. Was this idea that if you have AD patients and you get the sarkosyl insoluble fractions, that there are still differences. There are different phosphorylation sites of the taus and that they ultimately then lead to different astrocytic responses. They had the same iPSC astrocyte lines and the same cells effectively got these different fractions and then either showed some self-seeding tau activity or not.

Dr Loukia Katsouri:

Or clearance.

Dr Anna Mallach:

Or clearance. So I think that again really makes you question how are we modelling-

Dr Loukia Katsouri:

Well, that's the thing.

Dr Anna Mallach:

... tau?

Dr Loukia Katsouri:

And Virginia mentioned in her talk yesterday that what they do, for example, when they do their seeding assays into mice, they get one brain. They characterise it really well with the seeding assays with the profile in mice. I don't know what. And then they carry the study and because you could have different responses if you use a different brain for example, which again is like, what do we even modelling when you do this tau brain extract? So very interesting. Yeah. So now she's getting more and more into this transcriptomics with long-read sequencing. She said they have an excellent facility at Exeter. So I would be really, really thrilled to see what is coming out of this.

Dr Anna Mallach:

Yeah. They also do some nice organoid [inaudible 00:49:13] and they have a new lecturer who started there a year ago who kind of cast all of the [inaudible 00:49:22]-

Dr Loukia Katsouri:

Together, yeah.

Dr Anna Mallach:

The TREM2 mutations and the TREM2 signalling pathways. And it's like Exeter is building, I think a really nice neuroscience centre at the moment.

Dr Imogen Swift:

I went to university in Exeter, this is very good to hit. I feel like there was no neuroscience when I was there.

Dr Anna Mallach:

No, but they've made a [inaudible 00:49:38]-

Dr Imogen Swift:

Really, it used to be diabetes. That was amazing.

Dr Loukia Katsouri:

No, there's also electrophysiology. They recruited Andrew Rundell from Bristol few years ago, he went there with-

Dr Imogen Swift:

Oh, really?

Dr Loukia Katsouri:

... a huge group.

Dr Anna Mallach:

And I think Katie Lennon from the same kind of sphere is talking tomorrow.

Dr Loukia Katsouri:

Yes.

Dr Anna Mallach:

I've seen her someone else like...

Dr Amanda Heslegrave:

Yeah, I've seen her.

Dr Anna Mallach:

This evening after, maybe.

Dr Imogen Swift:

Is it?

Dr Anna Mallach:

I think we've got a transcriptomic session where I was like, "I'll be there. Thank you."

Dr Imogen Swift:

[inaudible 00:50:02].

Dr Anna Mallach:

Made us for Katie speaking.

Dr Amanda Heslegrave:

And I grew up near Exeter.

Dr Imogen Swift:

Yeah, I thought there's some links.

Dr Amanda Heslegrave:

Maybe I'll go back.

Thanks so much for that. But we don't really have any more time today. If you want to see more from this event, there are lots of posts on social media. Take a look at #ADPD2025 on X and Bluesky. You can also visit the event website on kenese.com, adpd.kenes.com.

So thanks to my brilliant guests today. That was a really nice conversation. So thanks, Imogen, Loukia, and Anna, and of course the AD/PD committee for making all this possible. I'm Amanda Heslegrave and you've been listening to the Dementia Researcher podcast. So bye-bye.

Dr Anna Mallach:

Bye.

Dr Imogen Swift:

Bye.

Dr Amanda Heslegrave:

Thank you.

Dr Loukia Katsouri:

Bye-bye.

Dr Amanda Heslegrave:

Bye.

Voice Over:

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