Podcast – AAIC 2023 – Day One

Voice Over:

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

Adam Smith:

Hello and thank you for tuning in. I’m Adam Smith, I’m the program director for Dementia Researcher, and it’s my pleasure to be hosting this show. For the next four days, we’ll be bringing you a new podcast each day to share highlights from the Alzheimer’s Association International Conference, which as you all know, is currently taking place in Amsterdam. Sadly, we’re not there in person. Well, we’re not, but some of our guests will be. However, thanks to the marvels of technology, we can enjoy most of the talks, but we will be missing getting our daily steps. But on the plus side, we can watch at home in our pajamas, which I know I did today, well until lunchtime anyway.

With over 800 orals and thousands of posters, there’s no way we’ll be covering everything in these highlight shows. But instead, what we will do is bring together three people to talk about their best bits. So, let’s meet the guests. I’m delighted to welcome Sam Keat, who, as you can see is I’m guessing, you’re outside. Oh, well you can’t see if you are listening to this, but if you’re watching on YouTube, you can. We’ve got Sam Keat who is joining us live from Amsterdam. Hello Sam.

Voice Over:

Hello.

Adam Smith:

We also have Dr. Mizuki Morisaki, who is joining us from Bristol today.

Dr Mizuki Morisaki:

Hello.

Adam Smith:

Oh, and do you know what? I’ve set myself up for failure here because I can’t quite remember. My third and final guest is Dr. Arunima Sikdar, who is in Oxford.

Dr Arunima Sikdar:

No, I am in North Carolina, USA.

Sam Keat:

You’re close.

Adam Smith:

You’re close. Not even slightly close. Somebody else is North Carolina. Well, I’m in Oxford, but I wish I were in North Carolina. I’m sure the weather is better there than it has been in Oxford today. Thank you so much for joining us today. Let’s start with some proper introductions. Arunima Sikdar, I got your location wrong. Why don’t you go first?

Dr Arunima Sikdar:

Yeah, sure. Yeah. Thank you, Adam, for such a nice introduction. Hello everyone. I’m Arunima and I’m a poster research associate working at the University of North Carolina at Chapel Hill, North Carolina, USA. And my expertise is molecular biology and biochemistry. So, my job is to design the assays and screen compounds for novel drug targets for therapeutics. And it involves different projects such as Alzheimer’s that I’m presenting in as a e-poster in this conference. And there are other projects such as antiviral projects also involved, yeah.

Adam Smith:

Brilliant. Thank you very much. I was worried that we didn’t have any fundamental scientists joining today because we’ve had a last-minute change of guests and I thought, well, it’s always bad when you turn up and you’ve missed, nobody’s there to talk about some of the biggest talks because nobody else understands them. So, I’m really pleased you managed to join us. Thank you. Mizuki, why don’t you go next?

Dr Mizuki Morisaki:

Right. Hello. I’m Mizuki, and I’m in University of Bristol working in health science, Bristol Medical School, Clinical Neuroscience, dementia research group. So, I work in a sort of medical school using the mainly postmortem brain tissue from the brain bank that is closely related to our group. And mainly I do research looking at the depression and dementia. And then now I do some in vitro work looking at the antidepressant. So that’s sort of, it’s not quite translational but not quite basic, somewhere in between.

Adam Smith:

Amazing. And I noticed that one of the hot sessions from today was new horizons on human postmortem neuropathology.

Dr Mizuki Morisaki:

Yes, I did.

Adam Smith:

Which do I assume you attended?

Dr Mizuki Morisaki:

I did watch that.

Adam Smith:

So, if Melissa Murray is listening, you’re going to get a review of your session now. And last but not least, of course, super sub-Sam Keat, who didn’t even know he was joining this podcast until about seven minutes ago, who has done amazingly well to drop in. So, Sam, no pressure. You can introduce yourself too.

Sam Keat:

No pressure. I definitely won’t be a superstar, but my name’s Sam Keat and I’m a PhD student at Cardiff University, but I’m currently halfway through my PhD project, but I’m looking at the role of complementing Alzheimer’s Disease and I’m mostly a dietician and a geneticist, and I’m very lucky to be joining you live from Amsterdam today, so [foreign language 00:04:33], I probably butchered the Dutch there, but yeah, [foreign language 00:04:38] from Amsterdam.

Adam Smith:

No, that’s brilliant. And I think you’re also tethered to your phone as well, so we apologize now if we have any signal quality issues, but it is also a hot topic for you because I see the big announcement for today was about the new CRISPR work, but maybe you’ll talk to that. If not, I’ve got notes, so don’t worry. So, thank you very much everybody for joining us. Why don’t I give you a chance to talk about any work you’ve been presenting? Sam, are you presenting this week?

Sam Keat:

Unfortunately, not. No, I’m just an attendee this week, but.

Adam Smith:

That’s okay.

Sam Keat:

Regretting it, I’d love to have presented a poster. There are so many people there to talk to and network with, so I do feel the regret of not presenting a poster here.

Adam Smith:

No, and I’m sorry for asking you first. I should have asked in advance. Mizuki, what about you? Are you presenting?

Dr Mizuki Morisaki:

No, I’m not presenting.

Adam Smith:

Okay. But do we know that Arunima is, because you already said so at the start, you tell us about your poster?

Dr Arunima Sikdar:

So, my poster number is 76479. If anyone is interested, please go ahead, and check it out. To summarize the story, I have been working with the kinase protein, and this is a kind of non-receptor kinase, and this protein is actually important for phagocytosis and the innate immune response in our body. So, this protein gets activated when it interacts with the particular motive of a receptor, immunoglobin. So, our target was to inhibit or prepare some compounds or screen some compounds, which can actually inhibit the interaction between that kinase protein and the immunoglobin, the receptor protein, to break the bridge with our compound. So, we have screened almost a thousand compounds and we have developed our own assay, TFR assay, and we have screened the compounds and we have done secondary assays such as SPR, ITC and GST pull-down assay. And we found that there are some particular thiouric acid compounds, which are interesting, and they show the inhibition of that particular kinase protein with that immunoglobin protein. So that is what I am presenting in the poster.

Adam Smith:

Brilliant. So, what are the implications for that then? What and the next steps?

Dr Arunima Sikdar:

So, the next step will be to check those compounds in the microglia cell. That will be kind of in vivo experiments to do so that we will look forward to do with our collaborators because we are not doing this in vivo experiments such as animal experiments in our facility, but our collaborator who in a different institute in US or Canada, even in UK, yeah, they can do that in future.

Adam Smith:

Brilliant. Well, I gather Cardiff’s pretty good for collaborating. You’re in the DRI, I assume Sam?

Sam Keat:

Yes, I am. Yes.

Adam Smith:

So maybe you could reach out, Sam. Thank you very much for talking about that. So do go check out, what was that poster number again?

Dr Arunima Sikdar:

76479.

Sam Keat:

76479. I’ll visit.

Adam Smith:

Brilliant. And the online, I mean that’s one thing of course to highlight to everybody is obviously the thousands of posters. I have to say, I think you have an advantage if you’ve actually watched this at home instead of in the conference whilst you might, because walking up and down the posters, I mean, given that they swap them every day as well, you don’t leave your poster up all week like you do with many conferences. You put them up, you take them down the same day, that it’s just impossible to digest that many. Whereas online I think, I know you can obviously look online even if you’re in person, but online at home you can search for the people, you can search by topic. I know that they’ve just revised how you find posters, which makes it a lot easier. And I assume you’ve then got to log in and check to see if you’ve had questions and queries from people?

Dr Arunima Sikdar:

Yeah, I have checked. Until now, I haven’t found any questions.

Adam Smith:

No. Well with 8,000 I think it was?

Dr Arunima Sikdar:

I know, chances are slim.

Adam Smith:

But no, it might also not be the day, I guess because usually they vary by theme, don’t they, each day. So, it might be your theme or later in the week. Thank you very much.

Okay, so let’s get into your highlights and to the main point, actually, do you know what I’m going to go first. I’m going to ease you all into it and give you a little break. The session I really enjoyed; Maria Carillo chaired a session on the work being done by the NIA to revise the clinical criteria for Alzheimer’s disease. This was very towards the end of the day, I think 15:15, if you’re watching on catch-up, you can go back and watch this. It included a panel discussion and a presentation from Jose Montminy from the Alzheimer’s Association and Clifford Jack from the Mayo Clinic. And there are three reasons why they’re updating this guidance. Firstly, in response to new treatments because the present guidance is really aimed towards being a framework for research where of course now with disease modifying therapies on the horizon, it’s intended to be updated for clinical use as well.

Secondly, with so many new biomarkers being validated, the guidance needs to be updated to incorporate plasma biomarkers into the new criteria. And then thirdly, I’m reading from my notes here, research studies have demonstrated that imaging fluid biomarkers within the category are not equivalent for many uses. So, they’re updating biomarker classification criteria as well. This was clearly, I mean, I don’t think I fully understood everything that was discussed, but it was clearly a hot topic. It went on for 20 minutes longer than scheduled. You could see from home there were cues of people queuing at every microphone, generally not really to ask a question, but to make a point about something they seemed to disagree on or that was slightly controversial with the guidance that had been put forward.

So obviously a hot topic, the main takeaway from that session was is that they’d love you to go away and read the draft guidance that they’ve produced, which they’ve published online, and it’s open for feedback. They’ve got a massive panel of the great and the good that have contributed to this. So, it’s a very esteemed panel of people. But if you go to aaic.als.org/nia-aa, that should take you to the guidance. We’ve also tweeted it from the Dementia Researcher account today. So, if you go to @dm_researcher, you can have a look at what they’ve published and they’re welcoming feedback on that. I don’t know, did anybody else see that session?

Sam Keat:

No, I unfortunately didn’t. I think I was at another session in person. But yeah, I certainly heard a lot about it.

Adam Smith:

Clearly. I mean, I think it’s a hot topic, isn’t it? That definition, moving away from just the biological to incorporate that for clinical with neurologists now with this, to whom do we give these new amyloid therapies? Having that guidance and that clear definition of what constitutes disease is a hot topic. So go check that out. I think it’s worth watching. Arunima, why don’t you tell us your first highlight? What have you enjoyed today?

Dr Arunima Sikdar:

Well, I enjoyed first of all the awardees because many scientists, many professors, they received the lifetime achievement award today. That was pretty much interesting, such as Anne Fagan from Washington University in St. Louis for her research. And then Professor Philip Scheltens from University Medical Center in Amsterdam because of his research in dementia and also, he established the Alzheimer’s Center as a medical center there. And also, Bruce Miller from University of California. So, after that I enjoyed some of the sessions. And in the basic science and pathogenesis section, there was a topic on the Apo-E protein and there was a talk from five different people, so I forgot totally their name, but I remember for the first speaker, she was from Boston University, Professor Julia, she mentioned about how lipidosis is important in the Apo-3 and Apo-4 protein and how that impact in the Alzheimer disease and the dementia. So, she presented the transcripts and proteomics data very well to show how this different form of the Apo-E can actually help to understand the basics of Alzheimer disease and how it can be prevented.

Adam Smith:

Was that… Because I saw when the big announcements coming out of Alzheimer’s Association has been this Boris Kantor research from Duke University and Ornit Chiba-Fallek, who described this new therapy platform based on CRISPR and dCAs9 nine editing strategy to reduce Apo-E4. Is that the same talk, or is that a different one?

Dr Arunima Sikdar:

It’s a different one.

Adam Smith:

It’s a different one. Okay. I’m going to bring that up later. Thank you very much. So, what did you particularly enjoy about it? Is there any relevance to your own work or does this just seem like an interesting area?

Dr Arunima Sikdar:

Yeah, it’s an interesting area. I haven’t found any interesting until… Because it is the first day, I’m looking forward to more for drug development because that is the area in which I am working. So yeah, I’m look forward to the next days in the conference.

Adam Smith:

Oh, I think, are we expecting some more big results from in the drug space? I think is that tomorrow? I think I want to say tomorrow. We did a podcast a few weeks ago with Claire Sexton who highlighted that. So, I’m going to have to check back and see when that was. What about you, Sam? Let’s come to you. What’s your first highlight from the day?

Sam Keat:

So, I suppose being in person, I think you are touched by it, is getting the chance to see some of the brilliant posters in person. And I think the kind of advantages you get being at an in-person conference is being able to chat directly to the researchers about their topics and asking questions about their research and bringing up ideas about your own research as well. And one of the first ones I actually went to, which really stood out for me, was from a person called Eloise Berson who was at Stanford University. And her poster was basically looking at whole genome deconvolution using ATAC-seq. So, looking at bulk ATAC-seq profiles and in tissue samples and basically using reference ATAC-seq profiles for single cells to basically try and deconvolute a bulk ATAC-seq sample, which I’d never heard of before. So, I’ve heard of deconvolution in the sense of cell deconvolution and looking at bulk RNA-Seq in using single cell reference profiles to be able to deconvolute those and look at populations of cells in a bulk sample.

But I’ve never heard of it being done with ATAC-seq. So, it was a very new concept and a very insightful concept for me. Certainly, obviously gave me a chance to talk about my own project, which incorporates bits of ATAC-seq and I’m a bit of an epigenetics nerd, so they gave me the chance to talk about epigenetics as well. So having this conversation with Eloise and a couple of her other people in her team was a really insightful insight into, I suppose, the current technologies that are available and kind of gives me new ideas from my project as well. So that’s one of the kinds of first standouts I had was being able to have these conversations. I think the second kind of standout for me was the first plenary session of the day, so I’m going to absolutely butcher his name and I apologize.

So, Rik Ossenkoppele, who was presenting about PET. So, tau PET. So, the neuroimaging technique to look at tau pathology in the brain and how you can use distinct signals from this tau PET to look at the progression of Alzheimer’s disease and look at the presence of tauopathies within the brain and the kind of diagnostic capabilities of this was really interesting to look at. I’m certainly a very kind of firm person when it comes to early diagnosis, being key in Alzheimer’s Disease. And I think the combination of blood-based biomarkers and neuroimaging would be one of these real kinds of big leaps forward in terms of getting this early and very accurate diagnosis of Alzheimer’s. So that was a big standout, and it was a fantastic talk.

Adam Smith:

Yeah, I saw that one too. I completely agree. We’ve had, Rik was on the podcast with us last year as well talking about his work. So, it was brilliant to see him get the opportunity to present that work. And I mean I know that it’s so often we go to these conferences at the moment and it’s all about blood based and fluid biomarkers, but it’s great to see that that imaging isn’t going away and that it continues to advance just as rapidly. And at least we’re still looking at the combination of those biomarkers and throw in digital as well, that actually it’s not a case of should we use digital or fluid or imaging biomarkers. It’s moving towards using a combination of the three that I think is really exciting.

Sam Keat:

Exactly. I think the more we understand about Alzheimer’s as well, the more different we realize most Alzheimer’s cases are. So, some can be diagnosed using neuroimaging, but some are better diagnosed using blood-based biomarkers, for example. There are not all Alzheimer’s disease cases are the same and we need a rich array of ways of being able to diagnose it to be able to effectively diagnose it. So, the more research into both sides, the better it might be.

Adam Smith:

Absolutely. I think there’s a statistic that certainly that we’re using in the UK at the moment, which is about 30% of diagnosis are also misdiagnosed. And so, anything that also improves the accuracy of that, not just in terms of defining which type of dementia somebody has, but also not to exclude that there could… Because we know there are all kinds of reasons for memory problems that might not be dementia related. And if we can reduce misdiagnosis and potentially treat, particularly if what you discover is something that’s treatable, it is all the better for bringing this on.

And that’s why I imagine the DRI is going to be one of the people bidding for this new, there’s a million pound blood-based biomarker challenge fund open in the UK at the moment between Alzheimer’s Society, Alzheimer’s Research UK, I think the postcode lottery and NIHR were on that as well to work out how we put, because one of the frustrating things is it’s great to go to AAIC and hear about all these lovely validated tau biomarkers now as well and all these biomarkers, but they’re not being used, not in clinical. There might be recruitment to check for recruitment to studies, but not as a real clinical diagnostic tool. So great to see that progressing. Thank you, Sam.,

Mizuki, it’s come to you. Sorry, jumping on you there suddenly, surprised you. Yeah, it’s your turn, go.

Dr Mizuki Morisaki:

My highlight was actually also the same as plenary lecture about the tau PET, but since you summarized everything.

Adam Smith:

No, you can add to that conversation. You might have a different spin.

Dr Mizuki Morisaki:

I could go to a different one. I had several, but I find it quite interesting. So, I would talk about something else. The talks that I watched were beyond the classics, so I can’t remember exact title. But basically, looking at the human neuropathology in the neurodegenerative disease in a kind of new perspective. So, a lot of the talks are basically looking at something slightly from a different perspective. For example, instead of looking at Amyloid-Beta and a tau pathology, they look at the strict disturbance happen in AD patient and they’re looking at the specific nuclei in the hypothalamus or looking at-

Adam Smith:

And the clearance system as well?

Dr Mizuki Morisaki:

Yeah. Or things like what is, the most vulnerable population of the cells within the Alzheimer’s Disease or it’s not just everything, but specifically looking at this cell population is more vulnerable compared to AD and against aging. So yeah.

Adam Smith:

Yeah, because aging, I know it’s your particular, your interest in aging as a whole, aren’t you? That’s your…

Dr Mizuki Morisaki:

Yeah. So, I can’t quite remember the title or that I was watching online, but the reason why I was interested in the circadian rhythm was because I was looking at the stress system and the particular hormone, cortisol is related to circadian rhythm. So, I find it quite interesting because sleep disturbance in Alzheimer’s Disease is quite well known.

Adam Smith:

So, are there new findings emerging from that consideration of stress systems?

Dr Mizuki Morisaki:

They didn’t mention anything about stress, they just focused on circadian rhythm, but the fact that no one really looked at it despite the fact that 50% of neuronal loss happen in that small nucleus, I was like, oh that’s kind of interesting because why nobody has ever looked at it?

Adam Smith:

And that’s the great thing, isn’t it? I mean when you come to this, even yeah, sure you could spend all week going off and looking at talks in your field or you can also go look at other things that are brush up alongside and get those new ideas like you mentioned before, Sam, some new techniques and things. Thank you, Mizuki. So, before we move on and I come back to you all again, I’ll touch on that CRISPR one that we mentioned earlier. So, this was interesting enough to justify a press release from Alzheimer’s Association. So, I’m going to read some of this. Two new CRISPR based strategies offer hope for the next generation of Alzheimer’s treatments, was the headline from this. One of them seeks to dampen the impact of the most common Alzheimer’s risk gene, which we of course know is Apo-E4.

And the other aims to decrease production of a toxin protein in the brain. So, Brent Aulston and his colleagues from University of California, San Diego have developed a gene editing strategy that targets the amyloid precursor protein, so APP, which Aulston calls a gene with a central and indisputable role. Depending on how it’s cooked by various enzymes in the brain, APP can create products that are either protective or pathologic. And this approach hopes to reduce the production of beta amyloid while increasing neuroprotective actions. Testing the process in Alzheimer’s Disease mouse models, the research has found that CRISPR treatment led to a reduction of beta amyloid plaques and associated markers in brain inflammation and an increase in neuroprotective APP products and the correction of brain behavioral and nervous system function deficits. So, this is interesting. In addition, the CRISPR editing did not lead to any undesirable effects in the normal mice.

So that was interesting. And alongside that, the other story was around this Boris Kantor from Duke that I mentioned before, and Ornit Chiba-Falek described an epigenome therapy platform based on CRISPR and dCAs9 editing strategy intended to reduce Apo-E4. They found that their lead candidate can robustly reduce levels of Apo-E4 in both human and induce [inaudible 00:25:17] stem cells, derived miniature brains from an Alzheimer’s patient and humanized mouse models as well without changing levels of other Apo-E variants that are thought to be neutral or protective. So that sounds, quite a breakthrough. I hadn’t come across anything before in that space. So, what they think is they’ve now got proof of concept and evidence to support this approach as a potential new strategy to treat Alzheimer’s. So, reducing that Apo-E4 protein. Did any of you see the session on that? Have you got anything to add to that?

Sam Keat:

I unfortunately didn’t, but that’s definitely one of the ones I need to catch up on because I personally have a very firm interest in CRISPR-Cas9 because I think everyone knows about its potential and what it can do in treatment and gene editing, all this kind of stuff. So certainly, using it for Alzheimer’s Disease is a very promising concept. And I think the recent results and all the conversations that have been had at AAIC about the impact of this APP targeted CAS9, I think is hugely exciting. And another kind of direction in which CRISPR-Cas9 can head down in terms of a potential treatment and a potential gene therapy.

Adam Smith:

Which is kind of got to be a good way forward. Arunima, I’m going to come to you back next, have you got another highlight to share?

Dr Arunima Sikdar:

For the highlights, yeah, as I mentioned earlier that I got that in the basic science and pathogenesis section, I found Professor Julia’s talk about the Apo-E in the glial cells. And there are other talks about the Apo-E4 from other professor, I forgot her name, but she mentioned that Apo-E4 can cause the menopause in females and that that can actually significantly increase the chances of Alzheimer’s in the female, in the woman. So that was kind of pretty much interesting. I didn’t know that before. So that was an interesting talk. I don’t know, have you heard of it or not? And also, there was another talk in the same section by a professor from Southern California. So, he mentioned that the intake of Omega-3, so actually in the earlier ages, in the fifties, if we take more of the Omega-3 protein in our diet, the chance of getting Alzheimer actually reduces when we get old. So that was cool.

Adam Smith:

Really?

Dr Arunima Sikdar:

Yeah.

Adam Smith:

I don’t know, did they also have one after that that talks about red wine being a good protective factor as well?

Dr Mizuki Morisaki:

Eating fish makes you healthy. Is that the message? Really?

Adam Smith:

I know. And I’ve read something recently that talked about plant-based diets, obviously having to say when Sam [inaudible 00:28:17]’s talked about that before as well. I think that when you get into those kinds of dietary things and those, there are so many other factors to play, aren’t there? That it’s so hard to really prove, other than say, do it anyway because it’s a good thing. I don’t know. Anybody, did anybody else see those? Have you got anything to add to that? Actually, that’s a good question. Have you seen anything today that you thought, I don’t believe that that’s just not right. Have you seen any, is there any snake or some kind of snake or presentation you went, yeah, I’m not sure I buy into that? Don’t say any names for goodness’ sake.

Dr Mizuki Morisaki:

Do you mean in this conference like AAIC or any?

Adam Smith:

Oh no, today.

Dr Mizuki Morisaki:

Today.

Adam Smith:

Let’s stick with today. Have you seen anything disbelieving? This is, not that we’re saying that Omega-3 isn’t a protective factor, I feel sure it is. I’m going to go back and backtrack slightly on that and so answer on a postcard if you have any strong views on whether Omega-3 is a good protective factor to reduce risks of Alzheimer’s Disease. And then if you take it, you won’t get it, do reply, and let us know. Sam, have you got anything else to highlight?

Sam Keat:

So, another poster that unfortunately I wasn’t able to catch up with, the amazing Fari [inaudible 00:29:38] who is part of the Christian Steger’s lab in Belgium. I unfortunately wasn’t able to catch up with Fari because he’s a very busy man because he’s been talking about his project all day. But his project which is looking at the integration of Alzheimer’s disease GWAS with molecular QTLs. So, I’m a big kind of GWAS person and a big geneticist and Fari’s a fantastic researcher and a fantastic person in kind of pushing forward this post-translational wealth, this post-GWAS translation, seeing exactly what the kind of GWAS low side translate to in terms of these molecular QTLs, which he refers to. And his kind of ways of being able to translate the findings that we get from GWAS and seeing exactly what these signals mean.

And I’ve done, hopefully going to bump into him tomorrow to talk about his project a bit further and his kind of newest findings. But certainly, his poster was absolutely fantastic. I think it was just, as a bio-physician and a geneticist, it was just mind-blowing how much work Fari’s done and how incredible his work is as well. I think I was absolutely blown away by some of the work he’s done. So, it’s amazing to see it in person.

Adam Smith:

Great. Well, that should definitely be on everybody’s list to go look at. Mizuki any more from you?

Dr Mizuki Morisaki:

It’s again related to aging and neurodegeneration but-

Adam Smith:

Wait a second, what about the postmortem neuropathology one?

Dr Mizuki Morisaki:

I actually-

Adam Smith:

You’ve got to talk to both.

Dr Mizuki Morisaki:

No, I’m not going to talk about postmortem because I thought something else that’s more interesting.

Adam Smith:

Okay, wait a second. You’re not going to tell your boss that, are you?

Dr Mizuki Morisaki:

No. It’s like everything-

Adam Smith:

Lindsay, if you are listening, she didn’t mean that.

Dr Mizuki Morisaki:

No, I mean there’s another thing I was quite interested because we talked about the female having a higher risk of the Alzheimer’s Disease and then there was the talk in the defining frontiers of neuropathologic changes in aging and neurodegenerative disease. And then we actually talked about the sort of potential mechanism because the females are at the higher risk after the menopause. So basically, this was the second talk, talking about the pathways and enzymes. So, focusing on sort of mediator, because when you have Alzheimer’s Disease, it’s not just Alzheimer Disease, you get tau pathology and Amyloid beta. And also, there is overlap and comorbidity with other neurodegenerative diseases. And then they’re talking about, oh, there might be some mediator that increase the risk. So, looking back-

Adam Smith:

That is interesting and also great to see that gender-specific research is actually moving up in profile as well because we know that Alzheimer’s affects more women than it does men, yet all too often there isn’t that focus in on those areas of high concern.

Dr Mizuki Morisaki:

But also, you can’t eliminate the fact that female live longer. So, the chances of getting Alzheimer’s Disease are higher because a male by that point, may not be around. So as much as we focus on hormone and female, but we have to think about those other factors. But it’s still interesting.

Adam Smith:

Of course. Well, do you know what? I think we’re kind of… I really am going to try and keep these down. I’m notorious for making all my podcasts an hour long and I’m determined to make these listenable so that wherever you’re staying in Amsterdam, you can listen to this while you’re walking to the conference or before you start the day to make sure that you can do. So, I’m going to try and keep control over it. There are a few other award winners, Arunima you mentioned, some of, you mentioned Philip and Anne and Bruce Miller earlier. Some other award winners we should mention were Soyoung Chan, who is from Washington University who won the early career researcher award. [inaudible 00:33:50], got an award for basic science and development disabilities. John Schott from UCL where I work, got an award for distinguished service to iISTAART. Cristian Lasagna Reeves from Indiana University won the Inge Grundke-Iqbal Award for Alzheimer’s, and Oscar Hanson, who’s also been on the podcast earlier this year to talk about his work on biomarkers, won the DeLeon prize in Neuroimaging.

Really? Won the DeLeon prize in neuroimaging. Okay. But maybe I’ve got that the other way around. But yeah, Oscar Hanson won the award as well. And Michael Gruff and Alex from London University who were all award winners. And I think some of those have given talks and you can watch that award session as well. Before we wrap up, are there any final thoughts? Any last highlights or I’ll tell you what I will do, we’ll ask you what you’re most looking forward to over the rest of the week. Sam, why don’t you go first?

Sam Keat:

What I’m most looking forward to for the rest of the week is just the opportunity to bump into the 7,000 people that are here. Because I think on the first day, I think you realize how many people are here and there’s so many people you want to speak to that you find out are coming, but the chances of bumping into them are very slim. So, I think what I’m looking forward to is seeing the list of people that are here and being able to potentially have these conversations with some absolutely brilliant researchers at the AAIC. So, I think the kind of thing I’m looking forward to is doing a lot more networking and seeing a few more posters as well.

Adam Smith:

Well done. And you must go to that ECR student lounge. You can get headshots there at lunchtime and they’ve got some good talks going on. And of course, you’ve got the DRI AR UK Alzheimer’s Society reception, which is tomorrow night? Tomorrow night.

Sam Keat:

Tuesday night.

Adam Smith:

Tuesday evening. Yeah. And ISTAART Start reception as well, which is always worth a visit. Anything, what about you Mizuki?

Dr Mizuki Morisaki:

Like I’m looking forward to listening to the talks, of course. There are psychiatric talks as well as information. So, my plan is to get my colleagues to watch it with me in the presentation room.

Adam Smith:

What a great idea. Yeah, go take up a meeting room at work. I was going to say, are you still in the lab tomorrow? But yeah, go take over a meeting room and fill it on the screen. Thank you. And Arunima?

Dr Arunima Sikdar:

Yeah, for me, I will check on those, the CRISPR based, I mean meet talk recording. So, I will go back-

Adam Smith:

And the drug ones for which we are waiting. Yeah, the drug discovery ones.

Dr Arunima Sikdar:

Yeah, so I want to go back those and also special specifically for the clinical trials, some of the drugs from some companies they might present maybe tomorrow or day after tomorrow. I’m not sure. I haven’t checked the full agenda, but I think some of them will present tomorrow. So, we’ll go and check on those. And I will look forward to someone who has sent some questions for my poster. I can answer those. Yeah, interested.

Adam Smith:

Listen, anybody who’s listening, please go and ask Arunima, a question on her poster. Even if it’s just drop her a note and say, great poster, do that. No, don’t wait. Do that right now. Thank you very much, to all my brilliant guests. The incredible last-minute addition to the podcast, who did amazingly well do Sam Keat, nearly called you Dr. Soo. Dr. Mizuki Morisaki from Bristol and the incredible Arunima Sikdar, Doctor Arunima Sikdar, from Carolina.

Dr Arunima Sikdar:

Yes.

Adam Smith:

You’ve all been amazing. I’m afraid that’s all we’ve got time for today. You’ll find profiles on all of our brilliant guests and information on the conference on Twitter if you search hashtag AAIC23, there’s so much there. Of course, if you’ve not already registered, you can, and you’re an ISTAART member, you can still register for the conference even now, even though it’s already started. It’s free of charge for ISTAART members and you can watch it online. Everything that’s already been shown is immediately available like 10 minutes later as soon as it’s broadcast live for you to watch back. So, I hope you’ll do that and have a look at some of the things that our guests have talked about today. We’ll be back tomorrow with three more guests sharing their AAIC highlights. I’m Adam Smith and you’ve been listening to the Dementia Researcher Podcast. Thank you.

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The Dementia Researcher Podcast was brought to you by University College London with generous funding from the UK National Institute for Health Research, Alzheimer’s Research UK, Alzheimer’s Society, Alzheimer’s Association, and Race Against Dementia. Please subscribe, leave us a review, and register on our website for full access to all our great resources. Dementiaresearcher.nihr.ac.uk.

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