Podcast – 50 Shades of Microglia

Voice Over:

Welcome to the Dementia Research podcast brought to you by dementiaresearcher.nihr.ac.uk a network for early career researchers.

Dr Katy Stubbs:

Hello, my name is Katy Stubbs and I’m a communications officer for Alzheimer’s Research UK. And I’m pleased to have been invited to host this podcast for the Dementia Researcher website. So today I’m up in Harrogate at the Alzheimer’s Research UK annual conference and I’m pleased to be joined by three early career researchers, some of whom are working within the UK Dementia Research Institute at the University of Edinburgh.

Dr Katy Stubbs:

And today what we’re going to talk about are microglia. So for those of you who don’t know, microglia form part of the brain’s immune system and are key players in controlling brain health by multiple mechanisms. These mechanisms include releasing cytokines, phagocytosis of debris, synaptic pruning and forming the glue of vascular unit. In neurodegenerative diseases like dementia, nearly all physiological microglial functions stray away from homeostasis and contribute to disease pathogenesis. So you can see why research in this field is important and why it’s been such a hot topic at our conference this year.

Dr Katy Stubbs:

So I’m pleased to introduce Dr Katy Askew, Dr Mike Daniels, and Dr Makis Tzioras. Did I get it right? Tzioras, there we go. So just to start off with, if we take it in turns, just introduce who you are, a little bit about yourself and why you started working in dementia.

Dr Katy Askew:

Hi, I’m Katy and I am a postdoctoral research fellow at the University of Edinburgh. I’ve just started my first postdoc, working in the Horsburgh lab and we’re really interested in the mechanisms that contribute to vascular cognitive impairment, so form of dementia that has a strong vascular component and is linked to reduced blood flow in the brain. So my background is very much in microglial biology. I did my PhD looking at microglial turnover in healthy brain and in ageing, and what we’re trying to do is figure out exactly what microglia are doing in a mouse model of vascular cognitive impairment, with a particular focus on their turnover and also phenotyping new cells to see what’s going wrong in disease.

Dr Katy Stubbs:

Cool. How about you Mike?

Dr Mike Daniels:

Great. Hi, I’m Mike. I’m a postdoc also at University of Edinburgh. I work in what’s, we’ll discuss later, which is the UK Dementia Research Institute and I work for the lab of Barry McColl and in the McColl Lab we’re really interested in microglia, as is the whole reason of this podcast and my specific interest in terms of microglia is what’s called lysosomal function. So how microglia eat stuff, how they go around the brain, they eat debris, they eat lots of things and how does that change what they do and how important is that in neurodegenerative disease? How does it go wrong? How can we fix it?

Dr Mike Daniels:

My background is probably more of a macrophage, so immune cells from outside the brain. I did my PhD at the University of Manchester where we worked on an immune complex called an inflammasome, which is something that microglia and macrophages can secrete pro-inflammatory cytokines and can be extremely damaging. And what’s interesting for me is it’s now kind of putting on another hat, working in Edinburgh because we’re interested in how microglia, really may be protective in some senses. And really the message is that they need to be retuned in some sections and we need to work out exactly how to do that.

Dr Katy Stubbs:

Cool. And Makis.

Makis Tzioras:

Hi, I’m Makis. So I’m a PhD student, so I’m not a doctor yet and I’m saying yet, because I’m hopeful to eventually pass my viva. So I am working also at the Dementia Research Institute and I’m working with Tara Spires-Jones and Barry McColl. So both of them are GPIs of the Institute. And the project is a collaboration between the two where we are trying to understand how these microglia cells, as Mike said, really like to eat things, how actually that eating can maybe go wrong in dementia like in Alzheimer’s disease and how that can lead to the loss of synapses so we know that the synapses, which are the points of connections between the different brain cells, which is effectively how cells communicate, are actually being lost in Alzheimer’s disease. And we believe that by stopping the synapse loss we can stop the progression of the disease.

Dr Katy Stubbs:

Cool. So I think you’ve already kind of touched a little bit on this, but you’re all working on slightly different aspects of that biology. And so we’re just going to probe a bit more into that now. So why are microglia so important and why has neuroinflammation as a whole, as a topic, become such a hot area of focus within the dementia research community?

Dr Katy Askew:

I think typically people used to think of microglia as just sitting quite statically in the brain, clearing debris that’s there, but not really doing a lot. And with the GWAS studies that have been published in the last decade or so, we know that there are a lot of immune related genes that are implicated in Alzheimer’s disease and other dementias. So research focus has really shift to kind of figure out, well did the microglia have a causal role? Are they shifting from, what we would consider as a neuroprotective phenotype? So, their typical housekeeping functions, in protecting your neurons from harm, keeping them signalling as they should to a phenotype where they are actually damaging the cells around them and actively contributing to that process of neurodegeneration. And I think we’ve made a lot of steps towards understanding that, but there’s still a long way to go. And I guess one of the biggest debates in the field is this neuroprotective versus damaging phenotype.

Dr Mike Daniels:

Yeah. And I think that makes it really, really exciting to be working in this field just because we’re learning so much so quickly. I think when it comes to microglial research, it’s like every time my paper alert comes out there’s another paper and someone’s redefining how we thought these cells function and that there’s so much still to understand, which is really great. It kind of makes it hard. It means that sometimes there’s controversies in the fields, there’s disagreements, there’s often two camps almost and people believing that microglia can be broadly detrimental in neurodegenerative disease. Other people thinking they can be broadly beneficial and obviously as it always is, it’s going to be a complex mixture of the two. But that’s why it’s really exciting. And another thing to touch on in terms of why microglia are so exciting and why people are so interested in that, just in the context of neuroinflammation, in addition to the GWAS hits is PET studies.

Dr Mike Daniels:

So studies showing them we can use positron emission tomography ligands and show that microglia are becoming activated and they’re becoming activated very early, earlier on than you would see any of the cognitive impairments that we see in dementia. And again, there’s more and more evidence showing that they’re playing not just a role but, but a causal role because that’s what the genome-wide association studies would suggest is, you’ve got variants in microglia, you’re changing their function that’s leading. So that really doesn’t apply. They are playing a causal role and yeah, it’s a really exciting place to be working.

Dr Katy Stubbs:

So one of the things I think always comes up when you talk about anything is, is it good, is it bad? But also is it always that way? And I think this is one of the things that I’m hearing more about, is how that role that they have within the brain, they can be both good and bad, but also that can change over time and how does your work take that into consideration in what you’re doing?

Makis Tzioras:

So for sure there’s been a big shift in the field where people used to believe that microglia were just bad and now we appreciate that they’re not just bad, they are actually really, really important for the normal function of the brain. For example, in my field, it was until very recently that we didn’t know that there’s this process called synaptic pruning where you know how kids learn really, really fast and this, because it gets so many synapses that form the developing brain, but you don’t actually need all of those synapses.

Makis Tzioras:

So for many, many years and we know that those synapses then go down, but we didn’t know how this happened and this has been now shown to happen through synaptic pruning where microglia can actually go and eat away the synapses that are not required. So this is absolutely essential for normal brain development, but then we believe the same process that was once really important is now part of how this disease progresses.

Makis Tzioras:

And this is what we are trying to understand. Why is this happening? Why is this developmental signature almost, reawakening in disease? So absolutely, you can’t say they’re only good or only bad, but they exist in a spectrum and we have to appreciate that they can be both things at the same time.

Dr Mike Daniels:

I guess the question is, I think it’s something again that I don’t think we really fully understand this. Like what are they supposed to do in health? Which is crazy because that’s something that should be so obvious. Like for most things it’s very simple. You know what it’s supposed to do in health and then you look at what it does differently in disease and then you bring it back to what it’s supposed to do in health. And it seems with microglial cells, probably not uniquely but quite different to a lot of other disease context is we really don’t know what a good microglia does. And I think that’s something that some of your PhD work and the stuff in your lab is touching on, that sort of stuff. And actually I guess stuff that you’re doing now, Katy. But yeah, that makes it even more interesting to work that out.

Dr Katy Askew:

Yeah. Yeah. I mean I think my research focus is very much, I want to know how cells are dividing, how they’re dying, just the normal turnover and how that changes in disease. So we know that microglia, they have a relatively low baseline rate of division and this is coupled with their cell deaths to make sure you have a constant population of microglia in your brain throughout your lifetime and as you age. But we also know in a number of different neurodegenerative diseases, Alzheimer’s, ALS, prion diseases, we get a huge increase in macular proliferation and there have been a lot of studies, I say a lot, a handful of studies recently. They’ve also looked at how the profile of these microglia changes in disease. So we know that they’re proliferating, but we also know that the kind of molecular identity or kind of, yeah, the molecular identity will change from what we call a homeostatic phenotype, so something that’s very associated with baseline turnover, the sensing properties of the brain to a disease associated phenotype.

Dr Katy Askew:

And I think what’s really interesting from my perspective, if you block the proliferation of cells in a disease, we seem to alleviate some of the symptoms. But what I want to know is whether it’s that disease associated phenotype, is it the proliferation of those cells that we’re blocking? Is that what’s sorting everything out or is it just generally if you change all of the microglia, is that having an effect? And I think we’ve still got a long way to go to understand what are diseases associated, populations of cells are doing, how they are different from homeostatic because we still don’t understand really what the changes in the molecular profile actually mean for the cell functioning as a whole and there’s a lot of questions that we don’t have answers to at the moment.

Dr Katy Stubbs:

Yeah. I guess that also has quite strong implications when we think about potential therapeutic strategies.

Dr Katy Askew:

Absolutely.

Dr Katy Stubbs:

As if you have this unhealthy population and a healthy population, certain functions may be up and others may be down and actually it’s this, I guess the understanding we will have that it’s not going to be one drug, one wonder drug. You’re going to have to target even one cell type in multiple different ways.

Dr Katy Askew:

Yeah. Or even you know, a subpopulation of one cell type, right? Like we need to, I suppose it would be great if you can find a drug that’s specific for your disease associated cells that might be causing all the damage. If we can just, either get rid of them or stop the transition towards that disease state, that will be fantastic. Maybe that will sort everything out. We don’t really know. But I think yes, there’s a lot of things that need to be unpicked. It’s not as simple as saying, all microglia are bad, we can target all microglia and solve the problem. That’s definitely a lot more complex than that and I think a lot of people realize that now and it’s good to be working in a field where people, I think understand the intricacies of the challenge they’re trying to address.

Dr Katy Stubbs:

So you’ve already mentioned Mike, PET scans and that’s one of the ways that people can understand microglia. But what are some of the tools and techniques that you use in your work that are helping you to unpick these questions?

Dr Mike Daniels:

So we work mainly on mouse models of what we use mouse microglia. We have some mouse models of what broadly can model the symptoms of neurodegenerative disease, I would suppose. These models can be really, really great but can’t be stretched too far in terms of what they mean. We use some models where there’s over expression of some of the key proteins like amyloid and tau, and in those models we do see responses of microglia. We don’t really know whether those responses are beneficial or detrimental.

Dr Mike Daniels:

Yet, these microglia that come out from these models that people have termed them disease associated microglia, which is one of these things where people probably knew about it for a long time, but no one really coined a fancy name for it. But the general consensus is that these are protective and the evidence for that comes from looking at some of the genes that they express and linking those genes back to, for example, the genome studies that Katy mentioned earlier, and what we see is that the genes that were important in driving these disease associated microglia, some of them are the same genes that are variant mutations and they’re non-functional in Alzheimer’s disease. So, what that basically suggests is, people who have non-functional variants in these genes can’t produce these diseases associated microglia. Those people also have dementia, therefore disease associated microglia must be protective. Probably more complicated than that but that’s the kind of general theory at the moment.

Dr Mike Daniels:

But we’re really trying to unpick how that happens. We’re really trying to unpick how these cells actually, what molecularly leads to you having a normal microglia, homeostatic microglia. It’s, you know like go around this brain and I’m doing actions here for podcast and there’s a lot of hand waving going on. I’m being a microglia and it must meet something at some point on its merry way and that changes it, to turn into this disease associated microglia and we don’t know if that’s something that it’s touching. We don’t know if it’s something that it’s eating. We don’t know if it’s another cell type in the brain. Because this is again something that I think we should in this podcast like it’s all about microglia and that is, that’s obviously for the nature of the podcast. That’s the whole point of the podcast, but we’re all fully aware of how complex it is and how things like your vascular endothelial cells, astrocytes and even infiltrating cells can be involved in all of these. But we really have no idea what’s causing these cells to turn into this phenotype.

Dr Katy Stubbs:

How about you Makis?

Makis Tzioras:

So I mean, at the end of the day we want to cure Alzheimer’s disease and all these diseases more in humans rather than in mice. So this is the problem for us and we’re very lucky in Edinburgh and with Tara to work on human post-mortem tissue. So mouse models are really, really great to try and understand the molecular pathways that lead to this because many of those can actually be conserved between mice and humans. But actually, if we see something in mice, then we cannot apply to humans, that does not really help us much. So in my project in general in the lab, we tend to use the human post-mortem tissue in order to see what’s going on in the brain. Are the data that we see in mice actually translatable? Are they translating to human research? Is there something for us to look there?

Makis Tzioras:

So this is I think something that needs to be more popular, because again, we’re very lucky to have really great donation programs in Edinburgh in the [inaudible 00:15:56] pathology team. But the more popular this becomes, in more countries, the better it’s going to be to actually make this research more applicable to treating the disorder and not just treating mice.

Dr Katy Stubbs:

Yeah, yeah indeed. So I guess you’re taking tissue from healthy controls, but are you also able to look across the different disease stages? Say if it’s like Braak stage?

Makis Tzioras:

Yeah. So we have this [inaudible 00:16:20] pathology team in Edinburgh led by Colin Smith and they do a lot of characterisation where we get the different Braak stages, different health stages, we get cause of death, a lot of other variables that may affect the tissue and things that could affect the research. And then we try and stratify, depending on what our question is, for example, I’m looking at one of the genes that are increasing the chances of getting Alzheimer’s disease. So upper level protein E4 which is the greatest genetic risk factor for late onset Alzheimer’s. So we get all of this information and that way we can actually answer these questions.

Dr Katy Stubbs:

Cool. That’s quite nice. So bringing it all together from lots of different methods to understand more. So with it being such a hot topic, where do you see the field of research moving? What are the big questions that are next to be answered?

Dr Katy Askew:

I think that’s a really good question. I mean I think it depends on what you’re interested in personally as a researcher, right? Obviously the proliferation side of things is very much my bag and I think that we have a long way to go in terms of deciding whether that’s going to be a viable therapeutic target in humans. So in mice, we know that that works. We’ve got a very well characterised predictive pathway in microglia. We can target that with small molecule inhibitors. You know, proliferation goes down, pathology goes down, fantastic. Cognitive decline not reversed, but improved. In humans, I’m possibly going to talk absolute rubbish now because I can’t remember if there has been a trial that’s failed or not, or if there’s a trial in progress, that’s coming to completion. But I think it’s the same with a lot of different things. As Mike said, because we’ve sorted things out in mice, that doesn’t necessarily mean that’s ‘going to work well in humans.

Dr Katy Askew:

I’m also really interested to see what comes out of the identification of these disease associated microglia because I think that seems to be the most feasible route to defining pathways that are actually, either causing the disease… I think I’m talking rubbish at this point. But yeah, I think identifying this phenotype associated with disease is, it’s really interesting, right? It’s going to give us more targets to investigate therapeutically. But one big caveat is that we actually don’t know the function of a lot of the genes that are associated with these disease cells, right? There’s RNA sequencing studies are fantastic, but you get thousands and thousands of genes. It’s like, “Oh, this gene isn’t annotated. We have no idea what it does.” Then you’ve got to go down, the whole route of characterising the gene, finding out what it does functionally. Then seeing if you can target it therapeutically.

Dr Katy Askew:

I think we’ve defined some great things but also there’s about a thousand other questions that have come out of all of that research. So I’d like to follow it up, not me personally. I’d like to see people following that up, find out, what these genes are doing, how that might help us in finding treatments for the dementias.

Makis Tzioras:

And that’s absolutely important because as you said, there has been so many clinical trials have failed and because they were looking generally trying to reduce inflammation and they thought of pro-inflammatory microglia as just being detrimental, really bad. But as we said, this is not the case. So those stereo-typically thought as pro-inflammatory microglia being bad is not actually the case. You need those traditionally pro-inflammatory microglia for normal functions. So many clinical trials said, well reduce the microglia or reduce inflammation, that wouldn’t help because it hasn’t done anything. But as Katy said, we need to understand what those microglia are. Which microglia? When do we intervene? Because I think we were having so many talks in [inaudible 00:20:27]UK now about this in the conference and I thought that kind of relates also to other diseases, for example, most viral infections where you get a shot and you prevent so many diseases or vaccinations. If you get a vaccination after you have the disease, it’s not going to work. So we need to understand when do we actually have to intervene.

Makis Tzioras:

And I do think that intervening specifically to microglia, is going to be the next big thing, which we haven’t been able to properly do in human clinical trials.

Dr Mike Daniels:

Yeah, I guess, I mean in terms of getting a vaccination after you had a disease, like the reason that a smallpox vaccination after you’ve had smallpox doesn’t work is because you died from smallpox. So I don’t necessarily, I think this concept of it being too late in terms of inflammation. I mean look for something like rheumatoid arthritis like that people, we don’t have to find people before they become inflammatory, give them anti-inflammatory drugs before onset of symptoms to treat them. Like the drugs for rheumatoid arthritis have been really, really good and they’re treating people that have inflammation. The question is, and this is what everyone’s really struggling with, is the brain is really weird. Like stuff is super different. I mean I think for years, no one could tell the difference between a microglia and a macrophage and yet functionally they do such different stuff.

Dr Mike Daniels:

But look, I mean people even like we’re looking just kind of like five genes basically that people can use to distinguish between these two different cells. And it’s like, well if they’re that similar, genetically, but they do such different stuff, it’s like it’s no wonder we’re struggling. So I worry when people saying, “Oh, it’s too late off the inflammation. It’s too late.” I think as conceptually targeting inflammation can work and you don’t have to do it before like really, really early. But I think because the brain is so complicated that’s making life much harder.

Dr Katy Stubbs:

Yeah, I think it’s understanding the dynamic nature of the changes that the population of cells might be going through. And then knowing that actually if you’re choosing a later stage, you’re probably more trying to prevent any collateral damage that they’re causing. Or if you’re going in an earlier stage, you’re trying to turn them off from going down that pathway and tripping off other things. So I think the dynamicness is really important cause.

Makis Tzioras:

That’s a great point because if you’ve gone to point where you’ve lost so many of these neurons, the brain is notoriously bad for not being able to repair itself. So if you lost those neurons and it’s been too long, then you can’t actually bring those neurons back. But what you can do, and this is why we’re so interested in synapses, is you can, from your synapses. See if the synapses have died, there is a way to making new synapses, but it’s really, really difficult to make new neurons. And I think that’s the whole point of trying to stop it before it gets so far down the line. So if you have some of the inflammation then great to stop it then, when you’ve lost so much of the brain. It’s really striking when you look at a human brain of Alzheimer’s because you see so much of it has gone away.

Dr Mike Daniels:

That’s one of those images that really gets you, isn’t it?

Makis Tzioras:

Yes, absolutely.

Dr Katy Askew:

I think it’s a good point because what we’ve got to think about is you’ve got a cure and then you’ve got treatments that will slow things down, right? So obviously if you’ve lost a significant number of neurons, we can’t repair that damage, but we can slow progression, we can alleviate symptoms. Like we might be able to maybe support new synapse formation or at the very least, if microglia are pruning more synapses than they should be in disease, we can slow that down. So it’s the kind of thing, at least my personal bugbear with some of discussions about treatments is people seem to be shifting towards, “We have to find a cure.” Which I do agree with. But I think it’s also important not to take light away from the fact that we need things to alleviate symptoms. We need treatments for those that we can’t cure because they already have a disease that’s progressed far enough. And I think it’s worth just bearing both of those things in mind.

Dr Katy Stubbs:

So thinking about it in another way. So like biologically there’s a lot of interest in this particular area, but here in the UK we’ve been really fortunate in the last few years to see some new programs of work and new ways of working coming on board. And so a couple of you guys work for the UK Dementia Research Institute. So, for those listeners that haven’t heard much about the UK DRI before, this was set up in the last three or four years and it’s got a hub base at UCL, but it’s also got other centres around the UK. So you’ve got Cardiff, Cambridge, and Edinburgh, and then there’s also Imperial and King’s in London as well. So you guys are based at the Edinburgh one. So as researchers, how have you seen things like this help to support these expanding areas of work?

Makis Tzioras:

It’s been really, really great because Bart De Strooper who’s the director of the UK DRI is actually comparing this to, not us being function centres but being all part of one big building, so different floors of a building and when you’re part of it you actually realise that this is really true. So in terms of things that go in collaboration, it’s really, really amazing and you can get such great feedback from other people. You can meet, for example, our first connection that we had for the DRI in September, I met a great collaborator who we are now doing this part of a project where I was telling him what I’m doing and he said, “This is exactly what I need for a new paper that I’m doing. I got back reviews this one we need.” So it’s absolutely amazing because that way you wouldn’t really be able to do that, even at another conference because you feel so close to everyone there, it’s easier to talk about it.

Dr Mike Daniels:

Yeah. I think it’s kind of leading to what Makis is saying. It’s very nice, not feeling like you’re on the same team as people in the same way. Like one of the best things about the three of us all working together in Edinburgh is we’re all on the same team. So someone’s got a reagent like did they got some spare of you, that’s what you always do within the same Institute, because you’re all on the same team. But really, I mean in a way is dementia research is where we’re all on the same team and the UK Dementia Research Institute, the UK DRI, has been really good in forcing through that feeling that even cross institutionally around the UK, we all really, really are on the same team. And there’s a lot of… They’re bringing opportunities in to fund postdocs to work across institution within the DRI.

Dr Mike Daniels:

And it’s a really, really exciting place to be working because they’re making a big point out of funding what’s potentially quite high risk, high reward projects. Which for us as researchers, that’s really exciting. That’s the most exciting project because they’re the ones where you have this crazy idea and you’re like, this might pay off. And they’re really putting a lot of faith in us to come up with these ideas and really drive them through. And it is really… We’ve got these little permission to fail cards, which is a little bit… I think I’m probably overusing my permission to fail card sometimes. But it’s part of the idea that they’re trying to push through, which is really exciting. And then the other thing which I think we’ve wanted to talk about a little bit is that, although they are forcing this kind of like you’re on the same team thing, we’re also being able to collaborate with people that aren’t technically within the DRI.

Dr Katy Stubbs:

Yeah, the doors are open.

Dr Mike Daniels:

Yeah, definitely. For example, Katy.

Dr Katy Askew:

Yes. Yeah. So the Horsburgh lab isn’t part of the DRI, we’re just downstairs on the floor below. But we work really closely with the McColl labs and with Charles Hardingham’s group who’s also in Edinburgh in the DRI. And you know, that was great for us. I mean I’ve always thought it’s hard. Science is meant to be collaborative, right? We get more done if we work together and within one kind of building that’s really easy to do. You know, people were working on similar things. We’ve got similar ideas. This is used to drive research forward, but across different institutions in one country, there are people with expertise that maybe we may not have an Edinburgh and if someone else in another DRI centre has that, we can go to them, be like, right, great. So I need to use that as Makis was saying, “This is what I need to do. Can you help me do that?” And that’s how science should be.

Dr Katy Askew:

It’s really exciting to be exposed to so many different people doing different things. And I think for them to be so welcoming be like, “Yeah, that’s great. Let’s work together. Let’s push our research forward and get where we need to be.” And I think that’s how science should be, at least in my opinion.

Makis Tzioras:

And it sounds like a no brainer, but this actually has not been the case for most of the science. So I think recently people were very, very close about their data. So they would sit on data for many, many years and just never release it until they’re absolutely ready to publish it. And now this is saying, “You know what? If we share this data with someone else, someone else can help.” And that’s a way that we can actually find cures faster. You take half the time to do something.

Dr Katy Askew:

I think the other thing is, it’s not about us as researchers. I mean obviously we love what we do, we think it’s great. We’re interested in the science, but us sitting on data for a long period of time doesn’t benefit anyone apart from ourselves. We get high impact papers, great, but what does that mean for everybody else? And if you’re pushing people to be more open about what they’re doing, it benefits the public and that’s obviously what’s more important.

Dr Katy Stubbs:

Great. So I think we’re going to start to wrap up now. It’s been really good discussion. I think we’ve heard quite a lot about microglia and the role that they’re playing in information and in the diseases that underpinning dementia and actually how it’s not going to be a really simple answer. We’ve got to understand the dynamic nature of these cells. We’ve got to understand how their role changes over time with the diseases and actually they’re providing quite a lot of hope around new treatments and the shift in focus away from protein aggregates to also how cellular function could support some of those changes. And I think it’s always been really good to hear about the UK DRI and just how this new initiative is bringing size and scale and this collaborative working on a grand scale and making sure that researchers here in the UK are supported to do amazing work. So if people wanted to find out more about your work, I think you’re all on Twitter, am I right? So do you want to share your [crosstalk 00:30:37].

Dr Katy Askew:

So my Twitter handle is just my name, Katharine Askew, but my parents decided to spell Katharine weirdly, so I think it’s going to be on the website with the podcast which is probably the easiest way to look me up, but yeah, absolutely follow me on twitter. I have two bunnies which I tweet about all the time. So if you want to hear about microglia and bunnies, I’m kind of your girl.

Dr Mike Daniels:

Yeah, I’m on Mike underscore, JD underscore Daniels and also a plug for something else that’s quite close to my heart is working on public perception of science in the news. And we set up a project a couple of years ago called Have you heard, which is haveyouhearduk.com and there we go out to groups and we talk about how research happens. We talk about the process from the lab through to press releases, through to what you read on a newspaper and just try and have an open discussion with people about whether when you read something in the news, how much credence you can take from it.

Dr Katy Stubbs:

Great.

Makis Tzioras:

And you can also find me on Twitter at Makis Tzioras, which I don’t think anyone will be able to spell. M-A-K-I-S-T-Z-I-O-R-A-S.

Dr Katy Stubbs:

Yeah. So, all the panellists’ profiles will be available for you and all their twitter details as well. If you want to follow me, most of my stuff is about public engagement, so I’m very much focused on getting incredible science these guys do out there. And I should have brought my handle list, which is terrible. It’s on the profile. You can read it thereafter. It’s been a long week, so yeah, brain’s not all there. So yeah. You can find out all the details of the panellists. And finally, I always like to say this, but please remember to subscribe, rate, and review the podcast. It helps other people find it. Tell your friends and colleagues it’s on SoundCloud and iTunes and come back in two weeks’ time for the next instalment. Thank you.

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