Podcasts

Podcast – AAIC 2018 Day Four

Hosted by Adam Smith

Reading Time: 33 minutes

This is our fourth and final podcasts recorded on location at the Alzheimer Association International Conference (AAIC) in Chicago. Each day we have been bringing you news and information from our panellists who are all presenting and attending the world largest dementia conference.

Adam Smith the Dementia Researcher website Programme Lead for the NIHR is again hosting and today is joined by Katy Stubbs from Alzheimer’s Research UK, Nicholas Firth from University College London and James Quinn from THE University of Manchester.

The panel discuss their work, and today’s highlights, including the news from Biogen and Eisai over the exciting trial results of #BAN2401, how the Gut, sleep and environmental pollutants could be important in #dementia – and James talks about Tau.

We hope you enjoyed these podcast, from #AAIC18 – our next podcast will be out on Monday 6th August, when we will resume our usual fortnightly schedule.

Please subscribe to our feed and share with your colleagues and friends using #ECRDementia.


Click here to read a full transcript of this podcast

Adam Smith:

Well, actually, I know Nick and James, you’ve, of course, both been presenting. You’ve not just been having fun and listening to other people’s talks here in Chicago. Maybe Nick, would you like to start by telling us a bit about what you’ve been presenting here?

Nicholas Firth:

Yeah, I had a talk at the Technology and Dementia Pre-conference on Saturday, and I was at a poster today. Both of the things were on the same subject, which was looking at the Amazon Echo and whether or not it could be used to facilitate independence in people with dementia. In particular, we’ve been working with people who’ve got prominent visuospatial and visuoperceptual problems in a disease called posterior cortical atrophy, which is a rare variant of Alzheimer’s disease. We got some people, and we gave them some Amazon Echos, and Spotify, and other cool bits and pieces, and we let them rip for 10 weeks.

Nicholas Firth:

I had these grand ideas that people would be able to navigate their home a lot better and use all of this smart home integration, but the final results came in, and really, people just used it the same as everybody else did. They listened to Spotify and the radio and they set oven timers. The general conversation with participants was that they actually felt like they could do more in their home by themselves after the 10 weeks, so it was positive results.

Adam Smith:

That’s cool and really great to see really readily available technology being used in that way. If that was something that was proven, that would be easy to then replicate and for people to do.

Nicholas Firth:

Definitely. Actually, the guys with PCA have got a really tight knit community and they talk on the Facebook page. The people that were taking part in the study have been sharing their experiences on the Facebook page. Other people have since been in contact saying, “We’ve read about this. Can we have your…” I’ve got a cheat sheet for people to use the devices. It’s been really good, actually. Although we’ve not done a proper study of feasibility or efficacy, we’ve got some really good, promising pilot results.

Adam Smith:

I know all these big companies are, like Google and Apple and people, have got these health departments, haven’t they, that are trying to look at how they apply. Have Amazon got this up?

Nicholas Firth:

They have. They recently started, and I’ve recently got in contact with them, because they were quite a big face of this organization. It’s quite difficult to actually find a human being to talk to. I’ve recently found someone, and they’re really interested in what we’ve been doing, so fingers crossed, in the future we can do more with them.

Adam Smith:

Cool. Thanks, Nick. That was really interesting. I should just say at this point, of course, that Nick, you very kindly came into our studio a few weeks ago in here to record a podcast with Emma Harding, who you’ve been working with on the same subject. I think anybody who’s interested in that should subscribe to our podcast, and then that will be out sometime in August or early September, and you can hear more about that in detail.

Adam Smith:

Coming to James. You’ve had a few… Have you had a poster, an oral?

James Quinn:

Poster and an talk.

Adam Smith:

Poster and a talk.

James Quinn:

I gave a talk on Sunday. It was a really good experience, actually. I talked about the project I’ve been doing surround tau. Got lots of interest in that. It’s been nice to… You get your face out there a little bit, especially. The thing about this conference is not that many early career researchers giving talks, so I felt really lucky to have an opportunity to give a talk, and just talk a bit about my research. It was only 12 minutes, but it was… I ran over slightly, but it was okay.

Katy Stubbs:

Who doesn’t though? I think actually some of the best talks that I’ve heard at the conference have been from the early career researchers who actually put the time in to tell a nice story, keep within time, rather than just tossing out the same old stuff that they have the past five to 10 years.

Adam Smith:

Those people that spend the first five minutes explaining what Alzheimer’s is to a room full of neurologists and neuroscientists. It’s just…

Nicholas Firth:

There’s so much of that. Even the posters. The first box of a poster spends 10 minutes explaining what… Alzheimer’s is an insidious disease. If I see that one more time [crosstalk 00:08:08].

Adam Smith:

Is there anything… What particularly, James, were you highlighting?

James Quinn:

The project I’ve done around tau is I’ve identified a new protease. This is basically an enzyme that comes in, chops up tau, generates some fragments, and we’re showing that these are specific types of dementia. Then, also trying to characterise them, so we’re showing that these chopped up versions of tau, they’re more likely to aggregate, more likely to stick together, more likely to spread between cells. We’re just trying to really characterise the mechanisms of these proteins and just trying to work out what the mechanisms are, and why they are specific to these types of dementia.

James Quinn:

That was one aspect of my work. Then, I gave the poster presentation on Tuesday, and that was surrounding the plasma proteomics. What we’ve done here is we’ve looked at 26 Alzheimer’s and 30 control patients, and looked in the blood. We’ve just basically been able to find 15 proteins that can say 15… Given these 15 proteins, we can say with pretty good accuracy, these people have Alzheimer’s, these people are controls without knowing, and then going back and taking a look at that.

James Quinn:

I got a lot of interest. It was really nice to present the work because a few people came up to us and said, “Oh, we’ve got loads of samples. If you want to you them, get in touch.” Things like this, coming to these kind of events that allows you to meet the people who are the guys running the big cohorts and have all the databases that you need to access.

Adam Smith:

We’re really good in the UK for cohorts, aren’t we? Between the Dementia Platform UK, and we obviously, EPAD is coming onboard now as well. There’s various cohorts where [crosstalk 00:09:49] we’ve got the biobanks as well, and we’ve got the Brains for Dementia Research, and the tissue banks. The UK feels really well-serviced in cohorts.

Adam Smith:

That’s really interesting. I guess, no shortage of work there. If you’re continuing the PhD, you’re going to be fine for a postdoc, right?

James Quinn:

Yeah, hopefully. We’ll [watch the space 00:10:08].

Adam Smith:

Thanks, James. Katy, I know, obviously, you’re not presenting, but ARUK have here again. What have ARUK been up to while you’ve been here?

Katy Stubbs:

We have a stand in the exhibition area. Actually, that’s a really good way for us to get our name out there with international researchers. We’ve got a number of grant teams now that are open to people in other countries outside the UK, as well as our more traditional response, more advanced schemes. It’s a really good way for us to get that out there, but also, we’ve been showing people our virtual reality experience of dementia, A Walk Through Dementia. This always proves popular wherever we go, whatever audience we take it to. A lot of people are saying, “Oh, I think I’ll try and use this with my group,” or a lot of things like that.

Katy Stubbs:

Then, what I’ve been doing is trying to write as much as I can. The UK press is very interested in the conference. Actually, there’s a lot of media stuff going on around what’s been talked about here, so trying to make sure that they’ve got the right end of the stick is part of what we do. Then, I’ve written a couple of blogs too. Today, I wrote one about the gut-brain axis. There were some talks yesterday about that. Actually, it’s something we’ve not talked about with our supporters, so it’s a new area to explore and explain to people.

Adam Smith:

Cool. The virtual reality thing, can people do that themselves? Is this an app that you can download?

Katy Stubbs:

Yeah, so the app is completely free to download and it’s available on Android and on iPhone’s. Just search for A Walk Through Dementia and you can download it. The video’s also on YouTube, and the platform uses the Google Cardboard, it is pretty much the entry level of virtual reality. It’s cheap. It’s about six pounds to buy one of these boxes. It’s a really good thing, and we try and push it as much as we can.

Adam Smith:

It’s really interesting. Thank you, Katy. Again, just coming back to James and Katy, I guess if people want to know more about your work… Obviously, for Nick, there’ll be the podcast in a few weeks, but maybe we can just capture everybody’s Twitter names now, just to get you out there. Nick, you are on Twitter?

Nicholas Firth:

I am on Twitter. My Twitter handle is PiMan314, and that’s the Greek letter, pi.

Adam Smith:

Not because you ate all the pies?

Nicholas Firth:

No, it is because when I was 18 years old, I got a tattoo of pi on the back of my head, so that stuck with me.

Adam Smith:

I’ve seen that. I can confirm that. As you start thinning…

Nicholas Firth:

Yes, it’s an area of concern for me at the moment.

Katy Stubbs:

I’m glad I’m not the only one with a science tattoo.

Adam Smith:

You’ve got a science tattoo? What’s yours?

Katy Stubbs:

I’ve got a mitochondria.

Adam Smith:

I’m not going to ask where it is. James, isn’t it about time you got tattooed?

James Quinn:

I haven’t got a tattoo. I want to get a bee.

Adam Smith:

A bee?

Katy Stubbs:

Oh, for Manchester.

James Quinn:

Manchester.

Adam Smith:

Oh, okay.

James Quinn:

But that might have to come after my PhD, but now I’ve set it on this.

Adam Smith:

Maybe a bee on a brain or…

James Quinn:

That could work.

Adam Smith:

[crosstalk 00:13:05]

Katy Stubbs:

That would be cool.

James Quinn:

A bee tangled up. There we are. A bee caught in a web. That’s a bit deep, but yeah.

Adam Smith:

Well, if you want to…

James Quinn:

If you want to find out about potential tattoos, you can find out on Twitter, and I’m @TweetwithQuinn, so it’s Q-U-I-N-N.

Adam Smith:

We’re going to go find a tattoo place in Chicago to sort that out.

James Quinn:

We’ll see after the early career event tonight if that happens.

Adam Smith:

How about you, Katy? I don’t know. Are you going to give us ARUK or do you tweet in a personal capacity?

Katy Stubbs:

Well, so we have two work accounts, so @ARUKnews captures pretty much everything. It’s our general account. We’ve got @ARUKscientist, where all our research facing stuff, so opportunities, training schemes, grants, that sort of thing. Then, my personal one is @KatyLStubbs, and that’s Katy spelled with a Y. Last night, I did one of my most popular tweets, after a few glasses of wine, about imposter syndrome, and have been laughed at all day.

Adam Smith:

Fantastic. Well, there’s no such thing as bad publicity, is there?

Katy Stubbs:

No, not at all.

Adam Smith:

I had a poster today talking about the Dementia Researcher website and the work behind what we did to develop it, so I just shared some statistics on how the site’s been used so far, because we’ve been really pleased. It’s out of the 500, the registers which we set our self as an objective for the first year, and we’ve hit that in the first view months, so we obviously need to be more ambitious for the rest of the year. We’ve really enjoyed having a booth here to talk about the Dementia Researcher website and showing how it can help early career researchers from across the world, not just in the UK as well.

Adam Smith:

If anybody’s interested in knowing more about how we set about this, or if anybody’s interested in contributing blogs to the website from the UK or overseas, you can find me on Twitter @BetterResearch.

Katy Stubbs:

Question.

Adam Smith:

Yeah?

Katy Stubbs:

Do other disease areas have something like Dementia Researcher, or is this the first in class?

Adam Smith:

Not that I can find. I’ve had some people from primary care and different areas of research come back since and say that they thought it was great. This is a good idea. I recently said we’d be quite… There’s another charity that was interested, so we said we’d let them potentially take a copy of it, not obviously the content, but the format, the layout. Save some money not having to reproduce the entire site themselves. That was for, I can’t remember what disease area, so I think it was for rare diseases, researchers working on rare diseases.

Katy Stubbs:

I just think it’s amazing. If you think of this, and you think of things like Join Dementia Research. Often seen as the underdog area, dementia research is, but actually, we’re leading the way in a lot of initiatives.

Adam Smith:

Yeah, I completely agree. These public facing issues are there. Of course, I have to say working for the NIHL, the NIHL with Alzheimer’s Researcher UK and Alzheimer’s Society are really pleased to be able to bring these to help people.

Adam Smith:

Let’s move on. Today was the fourth and the last full day of the conference. Is it on tomorrow morning as well? [crosstalk 00:15:57]

Katy Stubbs:

They just start at 8:30, extra half hour in bed everybody.

Adam Smith:

Extra half hour in bed. Today was the last full day of the conference, but it seems like some of the big announcements came today, they were held back today, and I’m grateful for you all to join us today, because I know you’ve had to miss the last session of the day. I know Professor Linda Clare from Exeter is presenting right now, but my colleague Piers is there, so we’re looking forward to getting more about that. Some of the big announcements came today. I’m thinking of the Eisai and Biogen news.

Katy Stubbs:

Currently, taking Twitter by storm.

Adam Smith:

Yeah. Then, there was the work on the effects of pollution. Then, the study which showed, which I know I don’t think any of us managed to get to it, but there was a study that showed intensive blood pressure control could reduce risks of MCI. Katy, I know you’ve managed to make those big talks. Maybe let’s… What is Twitter saying about Eisai and Biogen? Well, what did they say?

Katy Stubbs:

Well, they said that this was the largest trial of its type that has shown support for the amyloid cascade hypothesis. It’s an anti-amyloid antibody called, let me get this right, BAN2401. It was a Phase 2b, and they were doing multiple different doses in an adaptive trial design. They were talking up how they planned out the study and how it was different. They’ve come up with a different metric to measure change. Because their cohort is MCI and very early stages of Alzheimer’s disease, you need a metric that’s an outcome that’s going to be sensitive enough to detect that change.

Katy Stubbs:

They were talking up this one that they’ve made. I don’t know if it’s that good, but basically what they’ve said is that they’ve been able to detect the change on the highest dose of this BAN2401 drug.

Adam Smith:

That’s over 18 months.

Katy Stubbs:

Over 18 months, it cleared amyloid from the brain, so they were doing PET scanning to show that. 80% of the people on the highest dose became amyloid negative having been on it, so that is really quite astounding. In hand with that, they did see some cognitive benefits as well using the… Let me get this right. It’s called ADCOMS. They sourced 30% reduction in the cognitive decline, so a slowing of the cognitive decline by 30% in the 10 milligram, twice a month dose.

Adam Smith:

I made a few notes as well. That was 856 people on five doses.

Katy Stubbs:

That is the biggest one we’ve had.

Nicholas Firth:

Is that ADCOMS FDA approved?

Katy Stubbs:

I don’t know. I’d have to do some desk research.

Nicholas Firth:

I wonder whether or not it actually counts as a positive, or whether or not they’d get approval based on the back of that…

Katy Stubbs:

I guess if it’s a Phase 2b, they’ve got to show… They also, they did use on their secondary outcomes, they had ADAS-Cog and CDR Sum of Boxes, which the other ones are using. I think CDR Sum of Boxes is what aducanumab was using, so they’ve compared it with that. They’ve also seen benefit in those, but as they showed in the graphs, the change wasn’t as steep, so it hasn’t got sensitivity to detect that much milder change at the early stages of the disease.

Adam Smith:

They’re saying it wasn’t showing an improvement after 12 months, was it? It’s 18 months. Well, that’s what the announcement said. The drug didn’t seem to be working at 12 months, but the trial in the new custom end point in 18 months.

Katy Stubbs:

I took pictures of the screen.

Adam Smith:

There’s also a new adaptive design as well?

Nicholas Firth:

I think the most take home thing for me is that it’s a monoclonal antibody, so it’s going to be massively expensive to produce and put into people. If it’s going to be 18 months, then an MCI, you’re going to have blanket give it everyone with MCI to see any approval. Then, it’s still got be approved in the UK. I can’t see that NICE… Because the amount of money that it would cost to get it into people is [crosstalk 00:19:58].

Adam Smith:

It would also mean, particularly for the UK, I know because obviously working and running Join Dementia Research, and I worked on supporting some recruitment of these drug studies, but we’re going to have to then get better at identifying people with MCI, because MCI is just not consistently used as a diagnostic term in the UK. People don’t come to get checked out until they’ve gone beyond MCI, and we’re into early Alzheimer’s disease.

Katy Stubbs:

If we have drugs on the market that can do this change, it can have these benefits, will that drive diagnostic rates?

Adam Smith:

That would finally address some of those sceptics and people that are saying, I know it’s an argument we don’t like, but what’s the point of an early diagnosis if we’ve got nothing to offer? Well, if you have got something to offer, maybe that would drive…

Nicholas Firth:

If it’s an early diagnosis, then the cost of it’s going to be so high, the NHS won’t be able to afford it.

Katy Stubbs:

I guess that’s all that health economics stuff. I know that our policy teams are going to work on that, trying to work out what the evidence we’ll have to get to show the benefit, because at the moment, dementia isn’t on medical costs in the UK, it’s a social care cost and it’s a hidden cost as well. It’s trying to provide the evidence to say, “You know, actually, there are a lot more costs associated than the NHS is currently seeing, so we are going to have to spend more, but overtime, we’re going to save more.”

Adam Smith:

I think, actually, I know from my work… What’s interesting at least is that at least that conversation’s going on now, is that everybody’s hoping that there’ll be some treatment coming through. ARUK have said that you want a treatment by…

Katy Stubbs:

Our mission is inline with G7 declaration of a disease modifying treatment by 2025. We say a life-changing treatment because, actually, new symptomatic treatments can still provide a lot of improvement in people’s quality of living, so a life-changing treatment by 2025. I think it’s possible.

Adam Smith:

The cool thing is, well I think, that at least we’re being smart in anticipating that that’s going to come at a cost. There are conversations going on to say that when this treatment does become available, how is it going to be able to be implemented and afforded, because you can imagine the outcry if there suddenly was a treatment that is unaffordable from the public. There’s 450 some thousand people with a diagnosis of dementia in the UK.

Nicholas Firth:

It happens in cancer as well. You see people that have got late stage cancer, but NICE look at quality of years lives, and they say there’s a press release that comes out of maybe some right-wing newspaper that says there’s this new, amazing drug out, and lots of people with cancer then want to go and use that drug, but NICE have said actually, the quality of life years that you get is so minimal that they’re not going to approve it for the cost.

Adam Smith:

Absolutely, so I guess we should all really… By the time people are listening to this podcast, I’m guessing that this news might have already hit the headlines, tomorrow maybe?

Katy Stubbs:

Yeah, so with the press release having gone out… I think it went out to the UK press on Friday, so they’ve had the time to work it up. They’ve all been tapping in and listening in to the presentation that just took place. It’ll be, I would expect, prominently in the UK press, tomorrow morning.

Adam Smith:

The news is that they’re working on how to make that into more trials, aren’t they? Eisai and Biogen are working up for more trials, hopefully, that they’ll also be trials that are going in the UK. I know when the aducanumab Biogen study results were published in Nature two years ago, that created a massive spike for Join Dementia Research of people.

Katy Stubbs:

I wrote up, the comment is [inaudible 00:23:46] my time at ARUK, and I wrote up the comment for that, and we put in our Dementia Research info line number into that, which is how people sign up to Join Dementia Research. The express printed off our number, and we had an influx, a deluge of people wanting to get involved with the trial. Actually, we know that people that we spoke to the day and the day after the announcement then, subsequently, were entered into that trial. I think it recruited much faster than Biogen were expecting.

Adam Smith:

It definitely did. I worked on that as well. Let’s watch this spiff tomorrow when people suddenly jump in.

Katy Stubbs:

One interesting thing. The first question in that talk today was from Eric Karran, who used to be our Director of Research at ARUK. He said that the preclinical data in mice, this antibody didn’t clear plaque, so were they surprised that it cleared plaque from humans, and why didn’t it clear plaque from the mice? Apparently, it’s all to do with the model being quite severe. It has this Swedish mutation in it, but I just think that’s quite an interesting thing because everyone always says we’ve cured Alzheimer’s in mice multiple times.

Adam Smith:

Now, they’ve cured Alzheimer’s in people, but not in the mice.

Katy Stubbs:

I think it’s this difficult thing. No model is perfect, but it’s having that broader understanding of the disease to get it to that stage of clinical trials.

Adam Smith:

It’s exciting news, isn’t it? This is, having had a year of this has failed, that has failed, having something that’s coming forward which is something to cling to and say, “Well, this is… We’re making progress,” is exciting. I think if there is a tick away from the public from this whole of the conference, it will be that that captures their interest.

Katy Stubbs:

That would be the one.

Adam Smith:

You’ve also, moving on, there was a big talk this morning about environmental factors and pollution.

Katy Stubbs:

Environmental factors. Pollution. This is again, something the public’s very interested in. There was a study out in January 2017 that was looking at busy roads and the proximity with which you lived a busy road effected your dementia risk. I went along to the session, and there was four talks about pollution, three about particulates, so air pollution, and what about noise pollution.

Katy Stubbs:

The one that I’m going to probably focus on actually came from a Scottish study out of the Dementia Research Centre in Edinburgh. This was led my Tom Russ there. It’s using the 1936 Lothian Birth Cohort, which is a pretty cool cohort because it was in 1947, all 11 year olds in Scotland were tested for their intelligence. Then, they’ve been followed now, over their lifetime, so it’s a really rich dataset that they’ve got from these people born in 1936.

Katy Stubbs:

Then, they’ve done some cool modeling. We don’t have data on air particulates and pollution dating back then, but you can put it together based on other measures. They did all this modelling to work out what air pollution was like and how it varied depending on where people were living. Then, looked at did it increase people’s risk? I don’t think anybody would be surprised to hear that air particulates do increase the risk of dementia. It’s here probably through inflammatory pathways or maybe a direct action, but they found that it was the accumulation of air pollution over a lifetime that seemed to be the important factor. The early life exposure seemed to be the really crucial thing there.

Katy Stubbs:

Then, actually, the talk after that was on noise pollution. The poor speaker had audio feedback and issues with her microscope, which is I just thought was really, really ironic.

Adam Smith:

Across this conference, and before, risk factors, risk factors, risk factors, every time. Do you think… There isn’t going to be a single cause of this in the end, is there? It’s just going to be, how do we explore the combinations of all these things, not just any one thing? I don’t know. You’re the one here, James, that might argue that you’re going to find the science solution to this, rather than a whole group of different factors.

James Quinn:

I really think it’s going to be a mixture of everything. I think we’re going to need to deal with the lifestyle factors that reduce your risk. You’re going to need to take all these different drugs targeting amyloid, targeting tau, targeting your inflammation. It’s going to be a much bigger story, and I think, unfortunately, it’s going to be an expensive story to really fix it. I think the field is only going to develop, and as it progresses on, I think these drugs will get cheaper and cheaper with time. I really don’t think there’s going to be a single science.

Adam Smith:

That and clearly just the lifestyle end up changing society as a whole, or you have to end up just agreeing that it’s something that a certain percentage of the population will live with if we don’t change things individually.

Katy Stubbs:

I think it’s really interesting that incidence in the UK is going down because of our changing lifestyles. The fact that everyone is educated is really protective. Also, I think it’s the CFAS Cohort, they found a drop, or how our brains work from Cambridge, they found a drop in incidence. They attributed it to men improving their heart health, and that was reducing the incidence of dementia.

Katy Stubbs:

I think there’s a lot to be said… Nothing really new is coming out in the epidemiology. It’s heart health risk factors, it’s social interaction, it’s keeping your brain active, but if there were ways that we can get people to adopt these changes, then we can see huge benefits.

Adam Smith:

The population’s appetite for risk I guess. We know that there are lots of things related to other diseases and people still do them. There was the thing on 30%, on Sunday, was related to hypertension, and lifestyle, and education, and things like that, but I suppose some people might say, “Well, I can live with a 30% risk.” Oh my gosh. If it’s a 10% risk, I’m okay. Where do you balance off that? Smoking’s bad for you. Lots of people do it.

Nicholas Firth:

I don’t know. It’s a personal decision I guess on how much you enjoy smoking and how much you value those extra five minutes of life you kick off every cigarette you have. It’s really personal choice, isn’t it?

Adam Smith:

I know one of the other talks you went to, Katy, was about the gut. Are you going to tell us we can’t eat bad stuff now as well?

Katy Stubbs:

It wasn’t really…

Adam Smith:

We can’t have television, no fizzy drinks.

Katy Stubbs:

The thing is with the gut-brain axis stuff, there’s only really been researched, as a whole, for less than 20 years now. It’s still in its infancy, it appears, with dementia. They know that people with Alzheimer’s disease have a different profile in their gut microbiome, but… It seems to be a shift towards more pro-inflammatory bacteria and a lower level of anti-inflammatory bacteria, but then, we don’t really know the next steps after that.

Katy Stubbs:

There’s a change. Is that change because people have Alzheimer’s disease and there’s something else going on there, or is it that changes in driving high levels of inflammation, driving with damage in the brain? More research is needed, is the phrase I probably say the most in my job. It is quite interesting. I think, again, if we can understand, can you influence your gut microbiome? What is it that lays yours down? Do we need to work out who has the best one, and is it that we just have to have faecal transplants at various points in our life to maintain a really healthy gut biome?

Katy Stubbs:

There was one guy that was talking, and he said that if you took the microbiome from a lean woman from Africa and put it into a mouse, everything was fine. If you put the microbiome from an American woman, whether or not she was lean or obese, it had detrimental effects to the mouse’s health. There is something really interesting in there, but we don’t yet know what the ideal microbiome is. We don’t know if there’s a different fingerprint for different types of dementia. All that needs to be understood, but it’s more of the inflammation message, and it’s another way that inflammation could be effecting the brain.

Adam Smith:

Something to inspire our podcast listeners. If they’re thinking of something to research, that sounds like it could be a hot topic.

Katy Stubbs:

One of the core themes at the UK DRI at Imperial College is looking at the gut-brain axis in dementia.

Adam Smith:

I don’t know if they’re looking for people right now, but there is jobs advertised on their website.

Katy Stubbs:

Yes, I think they are. There’s lots of… UK DRI, as it picks up speed, as it grows, as it establishes, there’s always jobs it looks like coming out.

Adam Smith:

I did actually see, I think, Imperial advertise three rules while we’ve been out here in the… I don’t know if it’s in that same line. Let’s move on, Nick, because we’re already, we’re 30 minutes in. Time is getting away from…

Katy Stubbs:

It’s my fault. I’ve been talking.

Adam Smith:

No you didn’t at all. Nick, what have you seen today?

Nicholas Firth:

I guess the most interesting session for me, which has also been popping up quite a lot, consistently across the conference, was on sleep and how sleep can effect dementia or is effected by dementia. It’s one of those things, again, we don’t quite understand whether it’s one way or the other. Whether it’s sleep that can cause a higher risk factor in dementia, or whether it’s early causes of dementia cause sleep.

Nicholas Firth:

A lot of things on circadian rhythm and how people that have got different circadian rhythms can have these very different patterns of cognitive abilities, which is quite interesting. Also, the first feasibility study run by someone at UCL, Gill Livingston, at UCL. She ran a big study looking at whether sleep interventions could be used to improve quality of life for people with dementia. More care focused than basic research focused, but she saw that it was feasible and that she actually saw some slight efficacy. People were actually getting a higher quality of life and were happier because they were getting more, better quality sleep using these quite simple interventions, like going to bed a bit later rather than napping during the day, light treatments and things like that.

Nicholas Firth:

It’s really varied between the basic science circadian rhythm type stuff through to the care, but it’s been popping up at lots of different sessions, sleep. It’s really interesting.

Adam Smith:

Cool. We could all do with some extra sleep.

Katy Stubbs:

Yeah, sleep. I would like a few hours from last night I think.

Adam Smith:

You’re getting another quiet night tonight though, of course.

Katy Stubbs:

No. I always behave.

Adam Smith:

Was there anything else, Nick, particularly?

Nicholas Firth:

I think, from that session, that was basically it, but I’ve just realised actually, just saying about napping. There was a session on excess napping and how it’s really bad for you, so actually, napping too much increases your risk of dementia.

Adam Smith:

Because doesn’t it just lower your night time sleep quality because you just can’t get the same depth? I recently started using a sleep mask. Big fan. Highly recommend.

Nicholas Firth:

Me too.

Katy Stubbs:

Really, really changed… The last three weeks, it’s changed my life.

Adam Smith:

Really?

Katy Stubbs:

Yeah.

Adam Smith:

What, the…

Nicholas Firth:

Yeah, the big ones you get on airplanes, but I’ve gotten a silk one as well, so it feels delicious.

Adam Smith:

Everything I enjoy has gone out the window this week. I like a good nap. Did you see, there was a whole conversation the other week about, what’s the definition of a… How long is a nap? How long is too long to be defined as a nap?

Katy Stubbs:

Wasn’t it where you don’t want to hit a deep sleep cycle because you’ll wake up feeling worse? You want to go just into light sleep [crosstalk 00:35:08]

Nicholas Firth:

Do it in 20 minute bursts.

Adam Smith:

20 minutes, half an hour, I thought was a nap, but some people said two hours.

Nicholas Firth:

Yeah, I’m a two hour kind of guy.

Adam Smith:

You’re a two hour napper? James never sleeps. I can tell. He doesn’t believe in a nap. He’s too young.

James Quinn:

They do, just talking of nothing, they do have a zen room here where…

Katy Stubbs:

Colouring books.

James Quinn:

One of friend wanted to show me the zen room. We open the door and there’s just six people just asleep, having a nap.

Adam Smith:

No way. I’m just discovering that today. Where is the napping room?

Katy Stubbs:

It’s next to the student lounge.

James Quinn:

Next to the student lounge.

Adam Smith:

Do you have to be a student to use it?

James Quinn:

No, it was entirely usable by anyone, but I think it’s just whatever space you can find, you just take that space, because people were lying on sofas. It was a sight to behold.

Adam Smith:

I’m really in… I’m surprised you didn’t find yourself in there today, Katy.

Katy Stubbs:

I’m too busy. I’ve got all these blogs to write, Adam, all these tweets to send.

Adam Smith:

Okay. James, what have you picked up on?

James Quinn:

There was two things that stood out most to me. There was a plenary session. These are the big sessions where they introduce the speakers with music. It’s an impressive way of getting your attention, but there was a talk by… I’m going to annihilate his name here, but [Gua Jun Boo 00:36:18], and he is from the Washington Mayo Clinic in the States. He was looking at APOE and presenting, which is quite rare for this conference, extremely, really, really new data, and on a lot of things as well. It was really exciting.

James Quinn:

It was nice to see where he’s looking at the different isoforms of APOE. You have E2, E3, E4. E4 gives you an increased risk of Alzheimer’s disease, and E2 is a lower risk, and E3 is normal level. Showing that, looking at E4, APOE4, and then looking at, not just in the brain where it’s normally been studied, but looking outside of the brain, and showing that by doing changes to APOE outside of the brain, it was effecting things happening in the brain. This is the whole idea that outside this, dementia is not just purely related to the brain. It’s the whole body system.

James Quinn:

That was linked in the next session I went to, which was the Emerging Concepts in Basic Science series, which was a panel discussion. Unfortunately, it wasn’t as packed out as they were hoping. I think there was another big news story going on, which we’ve just talked about, but it was very interesting. They summarised the main emerging concepts. There’s one on circadian rhythm, one on oligodendrocytes, one on the microbiome, so lots of things that we’ve just been discussing there.

James Quinn:

Then, again, this whole idea of Alzheimer’s or different types of dementia as being a whole immune system and whole body thing was really, really coming up. It was a very interesting day, but it was a lot more not focused entirely on the brain, which is good because we need to start thinking about it in a more global view.

Adam Smith:

That’s because a theme that’s come through this podcast is the importance of collaborations between different diseases. It’s interesting then, to talk about as well, not just different diseases, but different parts of the body. It’s the whole thing.

Katy Stubbs:

Holistic. Needs to take a holistic view.

Nicholas Firth:

The APOE talk was… I was in that one in the plenary session, and it was great. He covered everything from the structural biology of how the isoforms are actually different, going through to the heterozygosity and homozygosity risk factors. Then, talking about the pathways in the cells, and then he built up to all this new data as well. Whereas, normally these talks are quite difficult, he gave a really nice overview and worked his way up to this new data, so I think that a lot of people would have learned a lot from that.

Nicholas Firth:

In all of the studies we do in the modelling side, we just use or we’ll throw in APOE as a covariate and we’ll regress out that effect, or we stratify populations based on whether or not they do or don’t have the alleles, but now, I feel like I’ve got a much better understanding of what’s going on, on a more basic biology level.

Adam Smith:

That’s really great. We’re running short of time I think, but as this is the last day of the conference, just in very, very quickly, what do you we think? Has it been a good conference? Would you recommend this to people who haven’t been before next year? Have you had a good time? Have you learned lots?

Nicholas Firth:

Yes.

Adam Smith:

This is why I didn’t ask anybody that question in particular. Everybody’s just nodded. I shouldn’t been more specific. Nick.

Nicholas Firth:

This is my third AAIC, and I’d say the quality has probably been the highest that it’s been so far, and the most positive outlook. For the first time, we’ve had an AAIC where we can actually almost see some positive results happening, whereas the previous one, it’s been a lot of negative trial results.

Adam Smith:

Cool. James? This is your first, right?

James Quinn:

This is my first even AAIC. It was an experience, definitely. The science, in parts, has been really, really interesting, but I think you get that with every conference, where there’s a few of the talks that they’re basically just a repeat of the previous talk, but it was good to see such a diverse range of research being presented. The good thing and the bad thing… I don’t you. You pigeonhole yourself a little bit, because you go to the sessions that you’re most interested in. Then, you’re like, “Oh, I’ve just read that paper,” because they’re presenting [crosstalk 00:40:32].

Adam Smith:

But that’s the cool thing about this conference I think. If you want to go learn about something else, because there’s something for everybody, so if you wanted to come and spend a little bit of time in your comfort zone, and then, you could go to different things, which I think inspires that different way of thinking and those new ideas.

James Quinn:

I think I’m just the final year PhD student who’s thinking tau, tau, tau, tau, tau.

Adam Smith:

Well, and I know from talking to [Ulsa 00:40:55] and Isabelle that were here yesterday, they’d be trying to persuade you that next year, you should be applying to be an ISTAART volunteer [crosstalk 00:41:01]

James Quinn:

I can’t be an ISTAART volunteer because I won’t be a student anymore. However, I would highly recommend other people to apply for that scheme because I think you get a lot more out of the conference than you do just being there, because you’re there with a big group of people and you’re trying to make the conference happen.

Nicholas Firth:

Also, PhD chat for, it forces you to get out of bed in the morning, rather than just missing all of [crosstalk 00:41:23]

Katy Stubbs:

I loved, there was one guy, who I saw was in a couple of sessions, who was so good with the don’t take photography sign, and was really actually enforcing it when people would ask for no photography.

Nicholas Firth:

I saw somebody put it in front of somebody put it in front of someone’s camera today to stop them from taking it. They were actively like, “No, you just take a picture of this instead.”

Adam Smith:

I’m pretty sure that I know that a lot of what’s been talked about over the last few days, that we’ve picked up on the podcast, and then, Katy, you’ve talked about today is going to be in the ARUK blog I expect.

Katy Stubbs:

Yeah, so we’ve done… I will have done, in total, three blogs. The one that we’re going to do, probably next week actually, because we want to do some cool graphics for it. We try and blog as much as we can. Also, we try and do more on social media, so little videos. There’s a video where we walk through from the outside of the exhibition hall, all the way in, in warp speed. Then, I appear into frame at warp speed. Then, it goes to the normal speed, and I start talking. [crosstalk 00:42:16]

Adam Smith:

That’s quite flashy.

Katy Stubbs:

Yeah. We’ve done some more stuff like that to try and draw people in, snappy little videos.

Adam Smith:

Brilliant. Well, and I know lots of what’s of we been talked about today is all over Twitter using #AAIC18, so I think, don’t take our word for it. Have a look for there for yourself, and all of those pictures of the posters, despite some of the rules, and some pictures of some of the presentations. I think that’s all we’ve got time for today. None of you did the 5K run, right?

James Quinn:

I did the 10K instead. No, legitimately did. The 5K was running, and then, me and a guy who used to be in my lab did the 10K. It was quite nice because I’ve just finished my Running Down Dementia challenge.

Adam Smith:

You did a 10K run today?

James Quinn:

No, not today. It was yesterday.

Adam Smith:

You did the 10K yesterday and finished running dementia at the same time?

James Quinn:

Running Down Dementia, yeah.

Adam Smith:

Fantastic.

James Quinn:

It’s a… I’m sure Katy [crosstalk 00:43:07]

Katy Stubbs:

It’s a virtual running participation event, but it’s a great way for people to hit a target, but also raise money for a fantastic cause.

Adam Smith:

Well done, James. Thank you very much. Okay, so thank you to our panellists Katy, Nick, and James. Listeners, don’t forget to visit our website to check out profiles on all of our panellists, where you can also pose questions to them in the comment section. You’ll also find details of their Twitter feeds. I know they’re all happy to interact with everybody here. Please do subscribe to this podcast, which is available in iTunes and SoundCloud, and tag us using the #ERCdementia.

Adam Smith:

Thank you for listening. I hope these recordings from the AAIC have been interesting. As I said earlier, this is the last one for Chicago, and we’ll be back to our normal schedule, with our next podcast recording coming on the 6th of August. Thank you very much everybody, and I hope these have been interesting. Thanks.

Voice Over:

This was a podcast brought to you by Dementia Researcher, everything you need in one place. Register today at dementiaresearcher.nihr.ac.uk.

END


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