Podcast – 2020 Dementia Roundup Christmas Special

Adam:

Hello, and welcome to the Dementia Researcher podcast. Seasons Greetings wherever you are. It’s that time of year where we usually bring you a show of clips and highlights from the year that’s past, to celebrate and highlight the great work of all of our contributors, as well as to reflect and prepare for the year ahead. 2020 has been a difficult and tragic year. The Pandemic has effected everyone’s lives. On behalf of Dementia Researcher I want to take a moment to thank everyone who has worked hard to keep research going this year. As Francis of Assisi once said, “Start by doing what’s necessary, then do what’s possible and suddenly you are doing the impossible.” I feel that, as a scientific community, you’ve done exactly that.

Adam:

I try to find the positives in every situation, so here are my thoughts. The world suddenly feels a little bit smaller, as webinars and online conferences came into their own, I’ve seen more science shared than ever before, and seen talks and posters from people I would never otherwise have had a chance to see. In developing a vaccine, we’ve seen what just can be possible when the scientific community has money and time and resources. This is inspiring and has demonstrated what could be done if that same focus was placed on Alzheimer’s Disease and dementia.

Adam:

At Dementia Researcher we’ve been enthused to see organizations waking up to the importance and contribution of early career researchers and to see the support systems for you all growing. We’ll continue in 2021 to do what we can to help, and to build the community and encourage more people to take up a career in dementia research. So from me, Adam Smith and everyone at Dementia Researcher, keep calm, jingle all the way, and enjoy our 2020 highlights reel.

Megan:

Okay, so we had a podcast last year I think it was called 50 Shades of Microglia, so hopefully our listeners have all listened to that, so they know the general role of microglia, but maybe we could hear from you Maria about quite how awesome microglia are?

Maria:

Sure. In my personal experience, I always think of microglia as your very own personal ninjas avenging any kind of threat to your brain and all of the central nervous system. In more scientific terms, microglia service your [hypocetic 00:03:02] sentinels, so the key effector cells of the immune system, patrolling the brain, maintaining homeostasis, making sure that everything works just fine, pruning any unnecessary connections and also clearing out pathogens and cellular debris. They’re not just smart and capable, they’re quite the looker, because they’re really fascinating to observe and study under microscope.

Maria:

But, for me personally, what I really appreciate about microglia is that their function and disfunction in the brain represents sort of an [inaudible 00:03:33] territory. Secrets behind an open door if you will, because it really stirs hope for new discoveries and treatments. The brain has been studied for decades from that cup, and it was almost always as if the brain doesn’t function in unison with the periphery and other cell types around ignorance. The term glia literally derives from Greek glue, reflective of how the microglia were long thought of. Basically it was just a support to the main star of the game, the neurons. So, for me personally as a neuroscientist, it’s really encouraging and exciting to see the growth of the interdisciplinary approach and the efforts to understand neuronal function in the context of everything else that’s going on in the brain.

Megan:

Hello everyone and thanks for joining us. I am Megan O’Hare and I am delighted to be hosting our first daily Alzheimer’s Association International Conference special podcast. We will be sharing news and our favourite moments from each day of the AAIC like we do normally, but as you probably know, the conference was due to take place in the Netherlands this year, but the Pandemic has changed all that. So this year’s conference is taking place virtually, with every talk and poster still being shared online, and there are live scientific sessions and pre-recorded and on-demand videos as well.

Megan:

Okay, shall we start with the Plenary session, which was delivered by Ralph Nixon on proteostasis failure in Alzheimer’s Disease and related dementias and new clues to pathogenesis and therapy.

Speaker 4:

I came to the Plenary from a completely non-lysosome specialist perspective. I normally work on things like depression and anxiety as manifestations of Alzheimer’s Disease or risk factors for the development of Alzheimer’s Disease. So nothing to do with lysosomes in my daily work. But, what I particularly liked was the way that he was able to make it understandable for someone like me, who didn’t really know an awful lot about autophagy and lysosomes and I really liked the way, particularly from a clinical perspective, that he was able to relate it to other similar diseases. I thought that was really good. I particularly liked the inside-out model of where neuritic plaques come from, because that made a lot of sense to me, so that was great.

Adam:

Today I am joined by three amazingly talented early career researchers, bigging them all up there, to discuss day two of the Alzheimer’s Association International Virtual Conference.

Speaker 5:

There was one bit I really liked that didn’t really have anything to do with biomarkers today. It was from [Lee Gow 00:06:25] at Harvard on sleep disturbance and incidents and Alzheimer’s Disease. In this study they followed patients for 12 years and looked at their self-reported data. I was really fascinated by their findings saying that, if you sleep more than nine hours, your likelihood of having Alzheimer’s Disease or developing Alzheimer’s Disease increased. In my head, I’m always telling people you need to get as much sleep as you can, whereas I think instead you have to find that nice balance. They did talk about a potential mechanism in there, so I think future studies in that will be really fascinating.

Adam:

I found that talk really fascinating too. I saw that they used UK Biobank data, which particularly caught my eye, because where I work at UCL has a biobank. They had 502,000 data sets people to look at, which is just such a huge number. Anybody whose interested in data sets should definitely look at the UK Biobank and given this study was taking place at Massachusetts General Hospital, this just show you can access this data elsewhere in the world. It was fascinating. So six to nine hours sleep were, two per thousand were going to go on to develop cognitive impairment, whereas for the nine hours plus sleep, it was 6.6 per thousand. So, more than three times as likely which, I agree with you. Who thought more sleep was better? That’s not the case at all. Obviously it’s going to be complex. There’ll be more factors to play into that I’m sure if you wanted to unpick and find fault with this, I’m sure you could. But also sleep apnoea was a factor, and daytime sleepiness.

Adam:

Once again, I’m joined by three special guests, who have all been emersed in the third day of the Alzheimer’s Association International Virtual Conference. The focus for day three of the AAIC was the clinical manifestations and drug development. So that will be what we’ll talk about today. Anna, I’m going to come to you first though, because that’s a… well two fold. First of all, people will now know that we’re not the same person, because we’re actually in a podcast at the same time. You and I talk all the time, but we’ve never actually been in a podcast together before I realized.

Anna:

I’m glad that we can now differentiate between us. Yep, that’s really significant.

Adam:

And, the first time I’ve gotten to introduce you as doctor. Congratulations.

Anna:

Thank you very much. I’m going with evil doctor Volkmer. I think it works well with my surname.

Adam:

It does. You’d be a character with some minions, I imagine.

Anna:

Yeah, I was going for a Bond villain, and I’d like some henchmen, but you know-

Adam:

Isn’t that what the children are for? Are the children your henchmen?

Anna:

Yeah, precisely, that’s right.

Adam:

Danielle, you’ve been quiet. Let’s come to you first of all. So what did you see and hear yesterday that caught your eye?

Danielle:

Yeah sure, so my previous work within dementia has been around clinical trials, recruiting patients into trials and running really big prevention studies. Only being within the DRI for the past five weeks, I wanted to go and see what was happening within technology, and I really focused my attention there. So, something that caught my eye was a presentation by Professor Ipsit Vahia at the University of Harvard where he outlined mapping behavioural symptoms within dementia using passive radio sensing and how the digital phenotyping makes this work possible. By that he defined that as moment by moment quantification of the individual level human phenotype in situ. So, using data from personal digital devices, to enable us to study perhaps how people move around their homes, and what that then says about what might be happening clinically.

Danielle:

He used quite a good example of a patient with a depressed mood for example, and being able to use voice analysis, perhaps using an Alexa device or your mobile phone, to be able to track that, but also using actigraphy, which is the study of movement to perhaps track sleep, appetite or slow code motor symptoms. He then applied that to dementia, so could we perhaps manage, track agitation, or at the other end apathy?

Danielle:

So, his group have been working with MIT, Massachusetts Institute of Technology to monitor this movement and behaviour and using AI to then map these movements. What I really liked about his presentation was his use of this technology, which is still fairly experimental, and then using it to try and help clinicians facilitate earlier intervention. They’ve been able to demonstrate that change of movement or odd patterns of movement could be used to make adjustments to medication or behavioural interventions. They’ve used it in COVID-19 patients as well, living in an assisted living facility, where they were able to measure breathing rate of those that were diagnosed with COVID-19 and the changes between day one for example versus day four. Obviously not having to have very close contact to be able to do that.

Danielle:

So, I really liked the evolution and the quick nature that that could be used within COVID-19 patients. I found that really interesting.

Adam:

Once again, joined by a new panel today of Dementia Researchers to discuss day four of the Alzheimer’s Association International Virtual Conference. I’m going to come to you next [Rina 00:12:43]. The racial disparity session with Lisa Barnes was talked about a lot online yesterday. Could you give us a summary of that session?

Rina:

Yeah, it was really interesting. Lisa Barnes was talking about racial disparity between African Americans and white people. She was talking about how African Americans are twice as likely to develop dementia but they’re less likely to get a diagnosis or be represented in clinical trials, which I think is something that was talked a bit last year as well, and is steadily getting more into the narrative of research that we really aren’t including minority groups into clinical trails.

Rina:

But, she also mentioned that there didn’t seem to be any difference in the rates of the actual cognitive decline in comparison to the white population, but they seemed to start at a lower set on the cog test. They’re getting lower scores going into any studies, which could be influenced by factors effected by race, such as the socioeconomic status, or the literacy, and also the fact that they’re less likely to get a diagnosis at those early stages, so it’s hard to compare them I think.

Rina:

It’s interesting that they didn’t really find any particular differences. There was a few differences in pathology. So they found that people with dementia in African American communities were more likely to have mixed pathology, but she also mentioned that actually they go to memory clinics for other problems than memory problems, and that might be why we’re just seeing a more representative group of people who might have also got hypertension or other factors.

Rina:

Then she went on to talk about how just the experiences of discrimination in their youth was actually impacting their health and the presentation of their cognition. For example, they found using SMI studies that there was less functional connectivity in places that were related to trust in people with dementia from African American descent, and that they seemed to be linked to their experiences of discrimination in schools, particularly if they had grown up in the south of America. I just thought that was a really interesting idea that I’d never thought of. It also got mentioned then later on in an LGBTQ session as well, that perhaps that was something that would feed into LGBTQ experiences as well, that they felt more discrimination in their youth, and that might be effecting their later cognitive status. It was really interesting.

Adam:

It was. Does anybody else have anything to add to that?

Speaker 9:

I made a link as well with the something… It was a bit got smacking sort of thingy. Like when she said about the integrated the schools. So you’d think, I think as maybe as policy makers, especially at the time, you think “Oh that’s a great thing”, but actually now it turns out it has some adverse effect later down the line. Who could have thought that? Yeah, that’s just really interesting to see also for future policies I guess, that you thinking you make the right decision on one level, but on another level it might actually got the other way. Yeah, it just shows the complexity.

Speaker 9:

Also, you’re right, I picked up as well about the LGBTQ population. My goodness, and if you have a double, that’s really… It gets really complex that way.

Rina:

Yeah for sure.

Adam:

I think a podcast panellist from an AAIC, I think it might have been in 2019, Nika Seblova, whose now at Columbia as well, she also had a post yesterday looking at African American populations and educations yesterday which was very interesting. So please go have a look at that. She’s N-I-K-A S-E-B-L-O-V-A, Nika Seblova, and that’s under the public health sections in the posters.

Adam:

Isabelle, what are your circumstances right now?

Isobelle:

I’m also funded by [inaudible 00:16:38], and I consider myself more 50/50, so 50% lab based, and 50% biophranetics and analysis. I’m lucky in the way as I still have work to do. I was running experiment and optimizing thing. All of that is delayed because we had to pause all of that, but I still have lots of work that I can do from home. I was used to working from home anyway. I usually try to do it once a week, and actually I think 99% of my PhD thesis was written at home.

Isobelle:

However, this is different. I find that right now is a really challenging time. Everything just changed in an instant, and I’ve been… Well one, there was this high expectation as well when we started that, oh we now have so much time in our hands. I started with, oh I’ll write papers. I’ll write grants. I’ll do all the webinars, all the courses. I feel I’ve hit, I’m just against the wall in a way. I’ve been feeling quite unproductive, unmotivated and I don’t want to feel this way, so in a way it’s a bit exhausting. So, I’m trying to take one day at a time and see the small achievements as small successes. So doing an analysis, reading a paper, submitting a report, instead of just looking at finishing this big experiment or this big analysis. I’m trying to look at the small steps more and more.

Adam:

Today, I’m delighted to welcome my friend Eric [Dyne 00:18:25]. Hi Eric.

Eric:

How are you doing?

Adam:

I think it’s fascinating because it is some of the most amazing science, in fact verging on science fiction from my little knowledge of this. So, Eric is going to talk about his research into magneto-thermal destruction of beta amyloid plaque.

Eric:

So hi everybody. I’m Eric Dyne. I am a graduate student at Kent State University and today we’re going to talk about using hypothermia via magnetic nano particles to disrupt beta amyloid plaques. As Adam said, it is quite a fascinating approach to targeting amyloidosis and Alzheimer’s however I think this has a lot of very interesting implications and we have a bright future for us. So, where can we go with nano particles? The future is vast. They can be made out of many different materials. We can stimulate them using various manners. They’re now working, using these for contrast agents, drug delivery and I think I said kind of sitting in with the brain. But yes, they’re looking now into using nano particles for glioblastoma, they’re using it for Parkinson’s Disease. They’ve found some success with delivering drugs for oligodendrocytes and Multiple Sclerosis and some Leukodystrophies.

Eric:

Then, the question I get constantly is, what about Tau Protein? We’re focused on the amyloid hypothesis. What about the Tau hypothesis? Luckily there’s already groups that are looking at targeting Tau or using nano particles to negate the effects of Tau Protein. So the field is growing. It’s relatively small at the moment, but it is a very exciting field and the cancer therapeutics that come with nano particles and mild hypothermia, it’s just fantastic.

Eric:

What am I doing after I graduate? I don’t really know.

Adam:

So hello, and thank you for joining me for Dementia Researcher online. I’m Adam Smith and for the next 12 hours I’m going to be your host through what I hope will be an interesting day. In this marathon session I’m going to be interviewing 56 researchers, four special guests, discussing their research, what motivates them and how their work is helping people with dementia. The whole event is in aid of Alzheimer’s Research UK. They’re an amazing charity. They fund a significant amount of research and through this day we hope to raise 5,000 pounds.

Adam:

Together we are the Dementia Researcher podcast.

Megan:

Dementia Researcher podcast.

Adam:

We’re here today, Megan and I, to celebrate episode 100. That’s right folks.

Megan:

100 episodes. Woo hoo!

Adam:

Since February 2018 we recorded 100 episodes and I was having a look, across those 100 episodes we’ve also had, guess how many guests?

Megan:

400.

Adam:

No, nearly. 370 different guests across 100 episodes.

Megan:

Wow, that is a lot of very nice people.

Adam:

It is, we’ve had a lot of them more than once, but absolutely. It’s 370 guests and it’s fantastic. So we thought we’d join you today, drop into the podcast stream just to celebrate episode 100 and just talk a little bit about the show, just for 10 minutes to give you a few insights about what happens behind the scenes.

Adam:

So, Megan. I’m going to ask you a question first. Which is your favourite episode?

Megan:

I like the ones where I have been to their places of work and then interviewed various researchers, because I think they open up slightly differently. Although, I do also have to say, recording in the studio was nice because Patrick, the sound guy was there. He was really nice and helped me learn about levels. I liked him a lot.

Adam:

Patrick is awesome. If you’re listening Patrick, we love you. We really miss you. He is still editing the podcasts for us, but he’s stuck working at home in London as well.

Adam:

I’m delighted to be joined by three amazing people, who I’m sure many of you will have met before. Hello to Wendy Mitchell. Hi Wendy, and Chris Roberts and Jane Goodrich. Hi, hello.

Jane:

Hi. Good to be here. We had to come on the same device because of internet access problems. We’re on a camp site in the middle of Somerset somewhere.

Adam:

That’s brilliant. I’m very envious, although it’s sunny in Oxfordshire as well. Wendy, you’re muted. I don’t know if you’ve noticed. You might just need to unmute yourself. That’s okay.

Wendy:

Well that won’t do will it? Well, it probably would.

Adam:

I can guarantee Wendy, you won’t be the first person I say that to today, almost.

Jane:

It’s the phrase of 2020. You’re on mute!

Wendy:

Yeah. Oh yeah, I’m Wendy Mitchell. I’ve got mixed dementia too, although I only found that out by looking over the consultant’s notes. Because they told me I had Alzheimer’s, and then one day I looked over the consultant’s notes and it said mixed dementia. I said, “Why has nobody told me that bit? Don’t you think it might help me a little bit?” Anyway.

Wendy:

I was diagnosed five or six years ago, something like that. As Chris said, you’re given no hope whatsoever. They way diagnosis is medicalized, you just have all the negatives thrown at you, and no hope whatsoever. I wanted to be involved in research from the start, because I saw that as the chink of hope, just as Chris said. Because you have to have something to cling onto when, at the beginning you know nothing else. Just being involved in research just made me feel valued again, and gave me that sense of, yes I still have something to give here. So that’s how I started to be involved in research and have continued ever since, just like my lovely friends.

Chris:

When I found out that research didn’t involve people being invasive and stealing your body parts, a lot of projects are just filling in surveys and questions and assisting that way. Then I realized that that’s something that I could do, and I could do quite well. I could take my time and it really does make me feel, like Wendy says, it makes you feel like you’ve achieved something and you’re helping other people.

Wendy:

Yeah, I think, social and technological research is equally important as medical, clinical research. We have to find the best ways to live for those of us living with it now, and we have to find the best ways to care for those who can no longer care for themselves. Technology is… I didn’t use technology before dementia, so don’t give up hope of learning technology just because you’re diagnosed with dementia, because everything I’ve learned, I’ve learned since being diagnosed. I never had an iPad before dementia came into my life. Now, it’s an extra appendage on me.

Chris:

I’ve got one of them.

Wendy:

Yeah. Yours is called Jane.

Chris:

An iPad. An iPad. Terrible people. Terrible people. But we can’t… If we can do this, and join in and help, after a diagnosis, then anyone can, and everyone should be doing that. I didn’t realize at first that research also wants, not people just diagnosed with dementia, but also healthy brains for comparison and stuff like that. So this is why we need money for research and all the money at the moment has disappeared because of this horrible time we’re in. So now, you’re back at work, give us the money.

Wendy:

That’s right. Absolutely spot on.

Jane:

Now more than ever. The big pharmas are all concentrating on going for the cure, the holy grail. As Chris often says, which one do you cure? There is so many different types of dementia. As Wendy alluded to, the psychosocial research is enabling us to live to the best that we can, whilst we can, because the holy grail cure will not come in time for best benefit for Chris and Wendy and everybody else out there like them. It is extremely important, but there’s all the other pieces of research in between, that enable us to carry on, to enable us to learn how to use the iPads and the technology, which has been absolutely completely invaluable during this last four, six months, because the way the Pandemic has effected people with dementia has been exponentially overburdensome, but this at least has given people with dementia hope and been able to reconnect, and also we’ve taken a part in research during the lockdown, by having the iPads and things.

Wendy:

Yeah.

Megan:

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

 

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