Podcast – AAIC 2023 – Day Four

Voice Over:

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

Adam Smith:

Hello, and thank you for joining us for our fourth and final AAIC highlights podcast. Yes, I know there is one more day of conference, but we swamped you enough with news all this week, so we thought we’d give you a break tomorrow. I’m Adam Smith. I’m the program director for Dementia Researcher, and it’s my delight to be sitting in the host chair today again. Today, as with the rest of the week, we’ll be sharing a snapshot of some of our best bits from the day’s presentations, and weren’t there so many today? To bring you highlights, I’m joined by three brilliant researchers. We have Vyshnavy Balendra, Dr. Iain Hartnell, and Dr. Helena Popovic. Hello, everybody.

Dr Helena Popovic:

Hello, Adam.

Vyshnavy Balendra:

Hello.

Dr Iain Hartnell:

Hi.

Adam Smith:

Let’s do some proper introductions. Iain, why don’t you go first?

Dr Iain Hartnell:

Hi. I’m Iain. In a former life, I was a dementia researcher looking at FTD and inflammation, but now I work for the Alzheimer’s Society in the UK as a research communications officer. I basically translate technical research language into words that everybody without a science background can understand. So, they know all about the exciting scientific advances that happened in dementia research.

Adam Smith:

Great. Where did you do your Ph.D.?

Dr Iain Hartnell:

I did my Ph.D. at York, University of York in the UK.

Adam Smith:

Yorkshire, People’s Republic. As a proud Yorkshireman, I’m quite pleased to see that you went to Yorkshire.

Dr Iain Hartnell:

Yeah. I lived in York for four years and absolutely love York and the surrounding county is great. It’s probably my favorite county in the UK.

Adam Smith:

How soon after finishing your Ph.D. did you jump ship?

Dr Iain Hartnell:

I did a postdoc after my Ph.D. in Southampton, and then out following that postdoc I started Alzheimer’s Society.

Adam Smith:

Well done. It’s a great place to work, I imagine. I mean, not that I worked there, but I work with. They’re great. Helena, why don’t you go next?

Dr Helena Popovic:

I’m a general medical doctor, a health educator, and author of three books, two of them related to dementia risk reduction, and I teach patients the public, and health professionals’ evidence-based strategies to boost their brain and reduce the risk of cognitive decline and dementia. I depend on all of you brilliant researchers to provide me with essential information to pass on to my patients and colleagues. I’m very excited that on my return to Australia, I’ll be investigating whether a ketogenic diet can reduce cognitive decline in people with either type two diabetes, subjective cognitive impairment, or mild cognitive impairment.

Adam Smith:

I can’t help but think that Australians and their love of avocado will have far less trouble with the keto diet than some other places in the world.

Dr Helena Popovic:

Well, I’m low carb anyway, and I’ve tried the ketogenic diet. I did it when my partner had lung cancer because it augments the effectiveness of chemo and radiotherapy, and it wasn’t that hard. It’s just about planning and knowing what to do.

Adam Smith:

Brilliant. Well, thank you very much for joining us. V, I’ll come to you next.

Vyshnavy Balendra:

Hi, my name is Vyshnavy, but it’s V for short, and I’m a medical student pursuing dementia research. I take a more integrative medicine approach, so my research is on non-pharm interventions as well as pharmacological interventions. I focus on diet, exercise, lifestyle changes, health and wellness that may help to prevent and treat AD. I am also part of the Alzheimer’s Association as a student representative for the Nutrition, Metabolism, Dementia PIA, as well as the Clinical Trials PIA.

Adam Smith:

Anybody wants to know more about the PIAs, all last week we did a PIA podcast each day on our relay podcast, in which we talked about the PIAs and their work. They make amazing contributions to bring people together. Thank you very much, V, not only for being here but also for all that voluntary work you do with the PIAs. That’s brilliant. I know that none of our speakers have been presenting at this conference today, so we’re going to get straight on with the highlights. Helena, why don’t you go first?

Dr Helena Popovic:

This was actually the last presentation of the day. It was definitely one of my highlights though everything was brilliant. It was implementation of plasma biomarkers in clinical practice. Now the whole conference has been all about biomarkers, but this particularly impressed me because it was Henrik Zetterberg from Clinical Neurochemistry Lab in Sahlgrenska University Hospital, Sweden. I apologize if the pronunciation was incorrect. He looked at the potential co-founders in interpreting Alzheimer’s disease blood biomarkers, and it just made the whole topic of biomarkers even more complicated than I realized it would be. I mean, we know that age, kidney function like creatinine levels, and BMI do influence NfL, GFAP, and to a lesser extent pTau, but not to a great extent. However, firstly, they found that individual drugs that a patient may be taking can have really strong effects like a tetracycline antibiotic used to treat pneumonia called minocycline.

It also affects microglial activity and so it increases plasma NfL several fold. That would result in a false positive. There’s also a hypertensive drug used in heart failure. It decreased plasma amyloid beta 42 to 40 ratio by 30%, which is actually greater than that caused by amyloid plaque pathology. So that would be another false positive. Then there was a chronic myeloid leukemia drug that also reduced pTau after 12 months of treatment. Number one, we’ve got to be really careful on what other drugs the patient is on.

The other really interesting finding was that a standardized meal reduced plasma NfL, GFAP, and pTau by 10% to 20% after two hours. That’s similar to the reduction seen in anti-amyloid beta antibody drug trials. It definitely seems we’re going to need fasting samples. Basically, the takeaway from that was to be on the lookout for confounding factors. If you have really unusual, unexpected results when you are doing a biomarker test, really start to investigate what else could be in play with that patient. We need to keep looking for unknown factors that influence biomarkers and can either give false positives or false negatives.

Adam Smith:

That is interesting, isn’t it? There’s some of the big questions that I think this new grant, there’s a funding call open in the UK at the moment for 5 million pounds to test out the practical application and use of blood-based biomarkers. You’d imagine that’s got to be a hot topic for those as well, knowing it has to be fasted? How do we capture and understand what the drugs? Because I can’t imagine that they even know yet, even though we’ve been talking about blood biomarkers for a decade, there is a full comprehensive understanding of what other drugs-

Dr Helena Popovic:

No way.

Adam Smith:

… will affect us until we start using them on a scale.

Dr Helena Popovic:

Yeah. Some co-founders may be assay-specific, so there’s still a lot more to learn.

Adam Smith:

Did you see that session as well, Iain?

Dr Iain Hartnell:

I did, yeah. It showed me that there were some things that I never even imagined could affect plasma tau concentrations. I know that Henrik was saying the ratio, they don’t know if the ratio was also affected and whether it’s just pure concentrations but seeing that and seeing how other diseases can also impact. I think kidney diseases quite often impact the reliability of these markers too. It’s just things that I’d never even thought about before, and I’m very glad that there are people out there that are thinking about this stuff.

Adam Smith:

Yeah, I completely agree. That ties in nicely actually with, there was a press release from Alzheimer’s Association today which talked about the promise of this finger prick test as a way to test for amyloid quickly and easily potentially at home rather people do for diabetes at the moment. This was Hanna Huber also from Gothenburg, so I’m guessing she was probably connected to Henrik, I imagine, and Sebastian Palmqvist from Lund. They had results from a single fingerprint blood test that were promising and a blood test that was more than 80% accurate in identifying Alzheimer’s related changes, which was significantly better than the doctors who didn’t have access to the test.

I guess if all you’re relying on is manual cognitive testing, which we know certainly in the UK, I mean, once you’ve got your diagnosis anyway, you’re discharged from healthcare, you might come back for titration to manage your drug. Other than that, you come back if things get worse. Being able to continuously monitor your onset particularly I guess also if you’re going to be taking a new treatment, being able to do that through one of these home testing kits has lots of potential.

Dr Helena Popovic:

There was another presentation also on that topic comparing the accuracy of blood biomarkers and clinicians. It was quite shocking that 50% I think of true Alzheimer’s disease cases are not receiving symptomatic treatment, and 30% of non-Alzheimer’s disease cases are incorrectly receiving symptomatic Alzheimer’s disease treatment. It’s a big deal. The diagnosis is still pretty poor in clinical practice.

Adam Smith:

Yeah, absolutely. There’s a stat. I think this has come from Alzheimer’s Society actually that 30% of diagnosis in the UK is inaccurate anyway. Not only is not good enough that we just got to push for improved diagnosis, but then you’ve got to get it right as well with so many misdiagnoses out there. I mean, that’s not necessarily to say they don’t have some form of dementia, but it could be mistyping or misunderstanding what somebody’s disease is. That’s brilliant. Thank you, Helena. I mean, we haven’t really talked much about blood biomarkers in these highlight podcasts this week. As I’m not there in person, I don’t get a sense of how big a topic is… Whenever I go to the AAIC, there’s a hot thing. I remember one year was you felt like everything was about microglia or everything was about anti-amyloid. Where have blood biomarkers sat in that hysteria of there’s a lot going on in this space this week?

Dr Helena Popovic:

I didn’t even know that there were that many different just tau alone blood biomarkers.

Adam Smith:

That just emphasizes the importance of cracking on with this program in the UK to understand which tests to use, how you might use them, where they can be applied. It brings up that tricky awkward question of screening again, doesn’t it? Screening programs, middle-aged screening programs, which are so difficult to consider but inevitably might have to be. Thank you very much, Helena. That was fantastic. Iain, why don’t I come to you next?

Dr Iain Hartnell:

I’m not really going to shift very far from biomarkers. I went to a really good talk by Rosie Watson from the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia. Her talk was about fluid biomarkers in dementia with Lewy bodies. I think generally because there’s just so much talk about Alzheimer’s disease because we know so much about the vast majority of… Most people get Alzheimer’s disease, people that get dementia, and then the vast majority of funding is in Alzheimer’s disease as opposed to the other ones. I find it really important to think and consider and look at the other types of other diseases that cause dementia.

I learned some really interesting things about DLB in her talk and some really hopeful things for the future in terms of blood biomarkers. She was saying that about 50% of people who are diagnosed with dementia with Lewy bodies when we were talking before about misdiagnosis, about 50% of people diagnosed with DLB. Before that diagnosis, they had a different diagnosis that was corrected to DLB. I think because she went on a bit later on about why that could be. She’s also saying that it takes about 200 days more for somebody to get a diagnosis of DLB than Alzheimer’s disease because it’s, I don’t know, more complicated to diagnose it.

She outlined how in the diagnostic toolkit that they have for dementia with Lewy bodies, there aren’t any markers that actually track the cause of the disease. They’re all things like EEGs, sleep studies, MRIs, that downstream effects of the disease rather than earlier markers. There isn’t currently a good reliable PET tracer of dementia with Lewy bodies. In bringing hope from that perhaps slightly unnerving picture, she was talking about alpha-synuclein seeding assays, and these seem to be an assay where you take a patient sample and then you put it in with some native alpha-synuclein. If you have some aberrant alpha-synuclein, it will start to aggregate and that will be detected.

They found that about 9 out of 10 people had a 90% success rate in detecting dementia with Lewy bodies. She was talking about how this is a really important step in the diagnosis and early diagnosis of dementia with Lewy bodies. But in the aspect of complicating the field and why some people might have that horrible diagnosis journey where they get misdiagnosed to start with is that there’s so much comorbidity. I think in a previous talk I’d heard that 50% of people with dementia with Lewy bodies also have either cerebrovascular disease or amyloid beta pathology or tau pathology. It’s very rare… Well, it’s just as common to have it purely as it is to have it with something else. Somebody at some point in their talk said, comorbid pathology is the rule, not the exception, which I thought was a really interesting thing that we need to consider.

But then another thing that Rosie talked about in a talk was that people that have taught in their brains as well as alpha-synuclein in DLB. About between 30% and 60% of people also have tau, but it reduces diagnostic accuracy if you have tau because it masks some symptoms. Having tau, people that have tau in their brains too have reduced visual hallucinations and reduced motor parkinsonism, which are two of the four classic symptoms of DLB. That could be a big reason why some people get this misdiagnosis. I just found out that this talk taught me a lot about DLB and showed me that there is hope for the future, but there are also lots of complications that need addressing as well.

Adam Smith:

That is interesting. Do you have any sense of whether this varies according to where in the world you are as well? Because in the UK where the majority of diagnosis happens through psychiatrists rather than in neurology. So, we know that there’s a standard sets test that they have, whereas neurologists tend to get the different people who present with slightly different symptoms in the first place are more likely to be referred to a neurologist than they are a psychiatrist. I wonder whether neurologists were better at picking up on Lewy bodies than psychiatrists were. In which case maybe I look to V because I’m guessing in the US, in the States, it’s very much a neurology-led service, isn’t it? Do you get a sense whether there’s an improved diagnostics for Lewy bodies in the States where they have that different clinical focus?

Vyshnavy Balendra:

I agree. There’s more focus, and the test screening process is much more detailed for Lewy body because we have subcategories within that as well.

Adam Smith:

Whether the improved… It’d just be interesting to look at how that varies across the world about improved diagnosis from one country, and in Australia, Heliea, it’s different again, isn’t it? Is it mostly elderly care physicians that were in secondary care?

Dr Helena Popovic:

It’s either a geriatrician or a neurologist who is most likely to diagnose that.

Adam Smith:

It shouldn’t matter, should it? I mean, fundamentally, the diagnostic cue tools you see when a patient comes through the door should be the same, but you just know that a neurologist and a psychiatrist, and a geriatrician might all take three slightly different approaches to how they deal with that.

Dr Helena Popovic:

Sorry to interrupt. I just found it interesting. Somebody in the audience asked a question and made the comment that all psychiatrists in Germany learn to do lumbar punctures and it’s part of their standard treatment. There’s no way a psychiatrist in Australia is ever taught to do a lumbar puncture, for instance.

Adam Smith:

Interesting. Thank you very much. That is good. We’ve actually talked about Lewy bodies on the podcast recently. We did an ask your mentor podcast last week with somebody that works in DLB blood biomarkers. So go check that out there what are the risks against dementia, fellows. V, you’ve been very patient. Thank you very much for waiting. Well, you give us your first highlight from today.

Vyshnavy Balendra:

First highlight from today. This whole process, I had FOMO the entire conference because I was like, “I wanted to go.” I couldn’t go because I’ve had prior obligations. I’ve been following the conference since day one. Initially, it was the science aspect to it, Dr. Rik with the welcome, and then we had the tau PET study and that technology. Then we had the clinical trial data release from the anti-amyloid therapy. I think I went full circle with day four, which was caregiver burden. For me, that spoke a lot to me because we do have medications and pharm treatments, but caregivers are the force behind the survival of dementia patients and they’re integral to how the patients are living and living through their symptoms. But at the same time, I think it was today’s talk, it was novel approaches to address caregiver burden and stress and its assessment presentation with Dr. Glover.

There were two sub-presentations within that that really spoke to me, which was addressing Black caregiver stress. There was, I think it was Dr. Brewster who was talking upon that and how she had implemented a six-step program which works at how to take care of the family member who’s suffering from Alzheimer’s disease. But what I liked about it is that in that program they also try to incorporate self-care. What they found from that study is after the six weeks, these Black caregivers, they had mastered the skill, and it actually lessened their overall stress and burden. That was very important, and they’ve tried to now implement that in Jamaica as a pilot study. So, catering to cultural differences there so that they were working on that. One more thing in that sub-presentation that I liked; I think there’s something called Care Ecosystem in UCSF that is done by the university there. What it is, it’s also a program but then it’s, I want to say a global village to help take care of that patient.

What they found is when you have a caregiver, a caregiver is usually in their maybe 15 years younger than the patient that they’re caring for, they’re also stressed, and they probably have their personal health issues, and they’re also highly likely depressed. What they’ve noticed is that when caregivers take care of severe dementia patients, the number of emergency visits goes up. This program has helped to actually see that there’s been a reduction in emergency visits and also the program costs, I believe $100 a month, but they’ve seen in the US $500 reduction in Medicaid claims.

It’s also helpful because taking care of someone with dementia is also very costly. I found it very interesting that this program that they’ve implemented and also, it’s occurring within the US right now, some states have adopted a system that it’s not only decreasing the amount of emergency visits, but it’s also decreasing the inappropriate use of medications that caregivers end up doing. So, I thought it was for me eye opening.

Adam Smith:

It sounds brilliant. What were the well-being interventions for the carer that they were in the program? Did they say?

Vyshnavy Balendra:

I think it was that they also implemented self-care. There was a team that could call a helpline if they needed help, and then it would be triaged. That’s what it was. Actually, the stat is the number needed to treat one potential inappropriate medication was three. So, I thought that was overall. If you look at the cost of $100 a month and you’re saving $500 every month, that’s pretty good overall.

Adam Smith:

I love that care is being discussed so prominently particularly, I mean, at the AAIC as a whole. It’s only really in the last few years that cares found its way onto this particular program. But it’s great this year. There’s been so many carer and care-related talks. I still think there is one particular aspect that I think is overlooked because even though we’re getting there on carers, professional domiciliary care still doesn’t seem to be an under-researched area. Particularly, when it’s provided by two people living in their own homes. In the UK, we’ve got a challenge about how many of these people there are, how much time they have with people, how much training they have, and what they do when they’re in somebody’s own homes. I think that the whole field, that whole profession about the training they get, what is an appropriate of time, what activities, how they interact with somebody when they visit somebody or in their own home is really under-researched.

I love that this is going on in care. I’d like to see it carry on into domiciliary care as well. Care homes have done really well in the last few years. We’ve seen lots of care home research moving towards improved support for family carers, but I think domiciliary and professional care as well could do with a good look at. In fact, I’m going to have a trawl through, have a look, and see if I can find some posters on that topic just to see if there were any. Thank you, V, which was great. Do you know what? I’ll give you all a little break while I pick up on one. I don’t know if you saw this today, Helena, there was another press release today from Alzheimer’s Association which talks about the experiencing less bowel movements are associated with cognitive decline. These were two new studies that have identified specific gut bacteria associated with increased risk of dementia as well as bacteria that may be neuroprotective.

Previous research has established a connection between the gut microbiome and the community of microorganisms in our digestive tracts and various bodily Functions. But these studies were from Dr. Yannick Wadop from UT Health San Antonio and Dr. Chaoran Ma from University of Massachusetts Amherst. They emphasized the interconnection of bodily systems and highlighted the need to address dysfunction for overall health. I’m going to read this now. It was the US POINTER study investigating how behavioral interventions impact the gut-brain axis to better understand the relationship between gut bacteria and brain health. The first study revealed that chronic constipation characterized by infrequent bowel movements is linked to worse cognition indicating a healthy gut is crucial for brain health.

I’m always, without seeing the full data on this, it’s one of those ones where I’d really want to see the full data because that’s got headline written all over it, but when you start to scratch below it, you find that’s an oversimplification of what is clearly a more complex issue, so I can see that.

Dr Helena Popovic:

It’s long been known in Parkinson’s disease that you get dysregulated bowel function and more constipation preceding the disease. Weird studies have found that if you cut the vagus nerve, you will reduce your risk of Parkinson’s disease. But no, thanks.

Adam Smith:

Also, I’ve talked about this, I feel like I’m constantly plugging this podcast. We recorded one early this week talking about hydration, which will come out I think on the 4th of September, although I made the connection between hydration and constipation, and they all corrected me and said, “Actually, that’s not entirely true.” But I always understood that was the case. So, listen to that podcast, 4th of September [inaudible 00:27:01] going to join us from [inaudible 00:27:04]. The second study in this highlight suggested a correlation between specific gut bacteria and the buildup of Alzheimer’s biomarkers providing potential avenues for therapeutic approaches. There was also a third study that looked at low levels of certain gut bacteria that were associated with poor cognition, highlighting importance of maintaining a healthy gut microbiome and diet.

I’m not going to talk about this a great deal. We’ve actually done a whole bunch of podcasts on guts and microbiomes and diet and dementia in the past. Sam Moxon’s recorded a series for us called Food for Thought and he’s had two people that have talked really well to this, which is Alan Desmond from the US and Neal Barnard who’ve been on the podcast to talk about this topic about different foodstuff, some plant-based diets, and things. So have a listen to those or my Helena’s books.

Dr Helena Popovic:

Exactly.

Adam Smith:

I got that plugin for you there. While you’re there, Helena, why don’t you tell us about these two books because it sounds like they’re relevant to this topic.

Dr Helena Popovic:

Very relevant. The second one, the most recent one, is the more detailed one for health professionals as well as the public. It’s called Can Adventure Prevent Dementia? A Guide to Outwitting Alzheimer’s. As well as going through the 12 modifiable risk factors listed in The Lancet report. I go through obstructive sleep apnea, dental hygiene, the microbiome, the importance of meaning and purpose, the importance of time spent in nature, the importance of the caregiver relationship, and to change that language to call them a care partner so that you realize that you are getting something out of it as well. Because our perception of our role is really important. I also talk about the importance of beliefs and attitudes and how our negative stereotypes are really damaging. When you improve people’s perception of aging, it’s that old adage, if you feel young, you are young, and it actually is born out in a lot of science.

The second one takes a really deep dive into how to reduce your risk of Alzheimer’s, how to best care for somebody with dementia. We’ve got to start our risk reduction strategies in midlife. It’s not too late, but the longer you leave it, the harder it is. It’s a book for everyone who wants to look after their brain. The first one was more about; it’s called In Search of My Father: Dementia is No Match for a Daughter’s Determination. It was really my journey learning to be his care partner. That’s more for carers and getting tips on how to manage being thrown into the role of caring because it almost seems like you’re thrown into it overnight. That’s how it happened to me. Mum died of lung cancer and there was such a stigma around dementia in my Serbian family of origin that they didn’t tell, my parents did not tell their only child, their loving daughter, who was also a doctor that her father had Alzheimer’s.

I found out because after mom died, I was clearing out the fridge and I found a box of rivastigmine in the butter compartment of the fridge. I said to dad, “Oh, what’s this doing here? Who’s taking this?” He said, “I am.” I said, “Why?” He said, “Your mom said I needed to take it for my memory. I don’t think it does much good, but happy wife, peaceful life, so I take it.” Then I went and tracked down dad’s GP because I was living interstate. That’s how I found out my father had Alzheimer’s disease. I realized, “I’ve now got to look after this man.” I didn’t realize that I wasn’t going to be able to leave him. The first book talks about that journey.

Adam Smith:

What a story. I need to read that now. Is that available in Waterstones and Amazon and all good bookstores?

Dr Helena Popovic:

Amazon. They’re both available on Amazon, yes. Or through my website, but it’s probably cheaper if you get it through Amazon.

Adam Smith:

No, go to your website.

Dr Helena Popovic:

Yeah, exactly.

Adam Smith:

Thank you, Helena, that’s fascinating and a good highlight to pick up on. Iain, we’re going to come back to you for your second, is it your second? I think your second.

Dr Iain Hartnell:

Mine’s not like second highlight isn’t a single talk. It was the closing section of the plenary today. The plenary was speakers from Biogen, Roche, Eli Lilly, and Eisai all talking about how the various drugs that they have been testing in clinical trials changed biomarkers in their participant groups. For starters, they were all very interesting talks, but Cath Mummery did a small summary towards the end of it that was looking more towards the future. She was saying how right now we’re in an era of amyloid immunotherapy, but we’ve got more to do. She said we need to step on the gas and not take our feet off because explaining how early diagnosis important to get people eligibility for these drugs, we need to have the provision of scalable biomarkers that can detect and then segregate out different participant groups as well as improving service implementation for how people will actually get these drugs.

But then following that, there was a really interesting mini-question session because I didn’t attend, I’m virtual, so I’m still in the UK, and they didn’t have the main Q&A session virtually, it was only for people in the room. But they did a couple of questions, and they were both really interesting because the first question was how do we go now from knowing that decreasing amyloid beta improve clinical benefit? What extra learnings do we have to understand? They were talking about how we need to understand what’s better. Is it the speed at which amyloid is decreased? That’s important. Is it the eventual level that amyloid is decreased to? Or is it the amount of amyloid that’s removed? The difference between the number of amyloids that simply starts with compared to the amount that the drug ends with because they still see benefit in people that don’t have complete amyloid removal.

Is amyloid complete removal being all and end-all? Other questions they had were about the lag of amyloid removal with some people taking a while before the amyloid starts to come down. The dose and accumulation as well. Then the other question was more on biomarkers and whether the biomarkers can protect one who will benefit most from these drugs and two who may suffer the side effects of amyloid-related imaging abnormalities and whether biomarker can help us to then alter treatment strategies for those people. My whole day, everybody in various different talks has been saying that one, we won’t be having one biomarker for everybody. It will be a panel of biomarkers, and the treatments will be, it may end up that we’re in a situation where treatments are more tailored to the individual as opposed to one-size-fits-all, especially when we’re talking about DLB with 50% of people having a different comorbidity. I think-

Adam Smith:

Yeah. Also, to throw in that controversy you mentioned there about you can get different levels of amyloid removal and have different benefits, you can also have all amyloid removal and no benefits. I love Cath Mummery’s talks because she’s so honest and transparent about this. Well, I think she does an amazing job at balancing being positive but also being very realistic about the potential benefit from these drugs as somebody who’s led clinical trials delivering these to people, she knows firsthand whether they’re really beneficial or not and accepting that there’s going to need to be more an anti-amyloid therapy alone isn’t going to fix everybody.

I think that’s one of the issues with pharma companies isn’t because they’re all businesses at the end of the day. The first thing they’ll do is to try and jump on this to get their own anti-amyloid and then gradually work on improving the side effects that come from those. What you want them to do is to continue to explore other treatments as well or vaccinations. I know we’ve had vaccination talk with ADI last week from Vaxxinity, which was fascinating. Sorry, interrupted you. By all means, carry on.

Dr Iain Hartnell:

With the biomarkers, I think Rachelle Doody from Roche was saying that they have an algorithm and a blood test that they’re developing that they think can predict who will be a high risk of ARIA, which is really interesting because that could revolutionize the safety aspects of these drugs and the bad side effects. Other companies-

Adam Smith:

ApoE was on that as well, wasn’t it? They needed to introduce some ApoE testing which they don’t routinely do right now.

Dr Iain Hartnell:

Yeah. Because I think it was from the donanemab trial by Eli Lilly, they showed that at least people with ApoE4 had less, it was less effective for those people. I think lecanemab has shown the same as well.

Adam Smith:

Yeah.

Dr Helena Popovic:

I think they’re more likely to get side effects when ApoE4s are more likely to get ARIA.

Adam Smith:

But then there was the other study we’ve talked about on day one which said it can reduce ApoE4. You needed that as well as that. That’s where this whole thing is about, it’ll be a combination of therapies rather than how we deal with cancer these days. You don’t just get one thing; you get a whole range of different treatments which are personalized care. Personally, you were mentioned at the start there, Iain. Sorry, we interrupted you for a second time. Do carry on.

Dr Iain Hartnell:

I was just going to say this. I and everyone else is seeing a field where we’re going to get a better and better amyloid immunotherapy until that’s what we’ve got and that’s doing the job. I think it will be with tau, perhaps a tau-removing drug, maybe even something that targets neuroinflammation or metabolic changes or something as well. The other thing I wonder is whether we are going to get further and further to slowing down the disease that then we hope that it stops, but whether diagnosis will get better and better that we can see people in prodromal stages of the disease so that they never actually, and through the screening and things, it’s maybe me pipe dreaming it, but screening programs and things to at a certain age to see people who have got higher risk and then giving them drugs that will stop them actually having any memory and thinking problems in the first place.

Adam Smith:

Prevention was always going to be the main, wasn’t it? I mean, yes, sure you can make, Helena talked to, those lifestyle changes in middle age and then combine that with a very, very early biomarker of some kind that can then mean you could receive some form of treatment that would also prevent you getting it maybe. That seems most likely at the moment, isn’t it the way this is going? Unless we suddenly all find out that there’s one particular cause and that’s it. It’s easy. Gum disease causes. Thank you, Iain. It must have been a busy week because you’re Alzheimer’s side, must have been a busy week for you as well with all the press around the news. I imagine you’ve had a stressful week.

Dr Iain Hartnell:

Yeah. Monday was particularly busy, well, putting out the information for our supports and stuff and then fielding various requests and our team was just running around crazy-

Adam Smith:

Well, I know your team are off having fun in Amsterdam, while you are dealing with all the work back in London.

Dr Iain Hartnell:

Yeah, I’m sweeping up back here in London.

Adam Smith:

Thanks, Iain. V, I’m going to come back to you for your next highlight.

Vyshnavy Balendra:

I just wanted to touch upon the vaccine that you were saying. I think it was today’s talk as well where I think the name was Dr. Pascal Geldsetzer, and he was talking about the shingles vaccine, the herpes zoster vaccine, and how he was… What he did was I think it was September 2nd, 1993. Everyone who took the vaccine after that, and it was just a one-week difference, and how that vaccine and just before that week and after that week is what they gave these participants. They found out that it was preventative towards AD. He was talking about a study is AD, maybe there’s a viral component to it because that’s what they saw. How does that one week, September 2nd, 1993, 1,000 people before this week received it and the other 1,000 didn’t receive it, and they, I guess, followed them. They saw I guess the benefits of that vaccination so when he talked about that.

Adam Smith:

It’s interesting, isn’t it? I mean, it’s hard to replicate.

Vyshnavy Balendra:

Right, exactly.

Adam Smith:

I mean, you’d like to replicate that on a much larger number of people, but then we’d have to wait another 30 years before we see what happens.

Dr Helena Popovic:

Sorry, on Saturday I went to the PIA Day because it was my first time. I went to the inflammation infection PIA, and they spoke about that particular group is quite convinced that the herpes zoster vaccine is protective against Alzheimer’s and several mechanisms are proposed. One of them is that it’s not actually the zoster virus that is the risk factor, but it’s herpes simplex I reactivation that has been found to significantly increase the risk of Alzheimer’s disease. That reactivation occurs because of stress, lowered immunity, sun exposure, whatever. But having the shingles zoster vaccine has been found to… This was what was presented, stops reactivation of herpes simplex. It’s via reduction in herpes simplex that the herpes zoster vaccine works.

Adam Smith:

Iain, as our official science communications person, not officially from Alzheimer’s, what would you make of that? This story comes to you, you’re Alzheimer’s Society, it’s in the news tomorrow, what are you going to make of it? What are you going to say?

Dr Iain Hartnell:

When the Daily Mail or whoever it is says herpes-

Adam Smith:

They pick up on this tomorrow.

Dr Iain Hartnell:

… causes Alzheimer’s disease.

Adam Smith:

No, herpes vaccine can prevent Alzheimer’s disease. Nobody routinely gets vaccinated against herpes, do they? Not in the UK anymore.

Dr Helena Popovic:

In Australia, it’s highly recommended that in later life you get the zoster vaccine.

Adam Smith:

Is this one of the vaccines that’s only really been applied in the UK in the last few years, and they’re given it to younger people now? There’s been a few in that space, hasn’t there? No? Am I imagining that?

Dr Helena Popovic:

Oh, the chicken pox vaccine has been around for ages.

Adam Smith:

I know we don’t give that in the UK either.

Dr Helena Popovic:

Oh, we do in Australia. Then later in life, you’ll get the zoster vaccine.

Adam Smith:

We don’t routinely vaccinate for herpes in the UK.

Dr Helena Popovic:

Okay, interesting.

Adam Smith:

I don’t think so. Do we, Iain?

Dr Iain Hartnell:

Because if this plays out on a much bigger scale, countries where they routinely vaccinate should have lower levels of Alzheimer’s disease in theory.

Adam Smith:

They should.

Dr Iain Hartnell:

Now there is a good study. Is anyone interested in researching that?

Adam Smith:

I can feel a funding call going out from the Alzheimer’s Society. Can you see his brain working away right then there?

Dr Helena Popovic:

That’s an easy fix. If that really is the case, what an easy fix.

Adam Smith:

Finding a country where that’s been routinely used, though on a large scale I think, would be interesting. Wow, thank you, V, you’ve caused our controversial one of the days, but I like it. I mean, that sounds brilliant. That’s got lots of potential. Can you remember who… Sorry, remind me again, I think you said at the start. Who presents that?

Vyshnavy Balendra:

He’s from Stanford University, Dr. Pascal Geldsetzer. G-E-L-D-S-E-T-Z-E-R.

Adam Smith:

Go look that one up. I know I’m going to be. Do you have another one to add?

Vyshnavy Balendra:

Yes. Then like I said, I was doing caregiver, I feel like I was going through in a museum. First, it was science, and then it was biomarkers, then it was drug development. Today was a caregiver and public health. This session was a lightning session, and it was lightning presentation, and it was public health. I forgot her name, but she was looking at the life after 90 cohort. We usually, when we think of AD, we only probably hit 90, but this is 90 plus. They were looking at a cohort of ethnically diverse population and cognitive decline, how fast it is after that age. What they found was white participants had significantly greater decline in executive functioning and then followed by Asian participants. Executive functioning scores among Black participants and participants who identified as the other had very similar as Latino participants. What it is the disparities in cognitive aging after 90 didn’t mirror the disparities seen in the younger elderly groups.

Adam Smith:

That’s interesting too. Sorry, who was that?

Vyshnavy Balendra:

That was… I’m just looking. That was by Claire Meunier from University of California Davis, and she was a session presenter under the lightning presentation round for today for public health.

Adam Smith:

Brilliant. Thank you, V. I’m going to come back to you, Helena. I’m conscious of time, so I’m going to give you and Iain one more chance to pick up anything or give you all one more chance to pick up on one more thing before we wrap up today. Why don’t you give us your next?

Dr Helena Popovic:

Okay. I was really interested in sex and gender-specific risk factors for cognitive decline and neurodegeneration. There were a lot of talks about that topic. The ones that stood out was the sex-dependent effects of air pollution on longitudinal changes in CSF and plasma biomarkers of Alzheimer’s disease. That one was presented by Natàlia Vilor Tejedor, Ph.D. from Barcelona Brain Research Center. She looked at 195 middle-aged cognitively unimpaired people. She measured their CSF, amyloid beta 42, 40 ratio, and CSF phosphorylated tau both at baseline and then at follow-up. Basically, she found that high levels of exposure to air pollution as measured by particulate matter 2.5 that indicates the size and nitrogen dioxide, the higher those levels, the greater the reduction in plasma amyloid beta 42 and 40. But here’s the thing, women are much more sensitive to air pollution than men. There were also effects on interleukin-6 pro-inflammatory cytokine and similar effects on plasma NfL, especially as levels of nitrogen dioxide increased.

It was particularly significant in women. That was then followed by… We could speculate on the mechanisms, but they weren’t offered. Then Matt Nosworthy, who is a Ph.D. student from the University of British Columbia in Vancouver Canada, looked at whether biological sex moderates the association of residential nature exposure with brain volume. The basis for that was favorable associations have been found between green spaces and brain structure. Green spaces reduce dementia risk. What he looked at was they defined exposure as having a natural environment, the percentage within 1,000 meters of a person’s home. How much green space did you have and nature exposure? It’s just phenomenal. I think that’s partly due to various phytoncides which are chemicals released by plants that help regulate our immune system and various things like that. But basically, the greener space, the greater your total gray and white matter volume and the greater your average hippocampal volume, so get out there.

This is the unfairness of it all. Men benefited more from living closer to green spaces than women. From the previous study you would’ve thought the opposite because women are more sensitive to pollution. You would’ve hoped that they would benefit more from having green spaces around them, but they didn’t. I mean, both sexes benefited, but men benefited more. The argument was maybe that if you live in a green space, maybe women still spend more time indoors perhaps, maybe men tend to exercise more outdoors perhaps. So, they did try and control all that. But there was a good news story that came out of gender differences. This was looking at the vascular system and things that mitigated cardiovascular risk on Alzheimer’s disease. Cheer for this one, women benefited more from aerobic exercise than men in terms of executive function and as measured by their ADAS-Cog score and Stroop test. Finally, we come to something that benefits women more than men.

Adam Smith:

If you do that outside, it is even better.

Dr Helena Popovic:

Even better indeed. Apparently, not. Apparently, this study found that only females have an increase in brain-derived neurotrophic factor after six months of training, men didn’t seem to have that increase. We love BDNF, it’s a fertilizer for brain cells that stimulates the growth of neurogenesis, synaptogenesis. It promotes learning neuroplasticity. We all want more BDNFs. My take home from that was I will really, really encourage. I mean, I always have, but now even more so make the case for women to go out and exercise because you will benefit even more than men if you go out and move. I did ask the question, why do we think women benefit more from cognitively, more from physical exercise than men? They didn’t really have an answer, but one speculation was when women go out and exercise, they tend to do it in a more social way. They tend to join classes, so they’re not just getting physical benefit, but they’re also getting social benefit. Whereas men might just go out for a run or something. But I don’t know if that’s necessarily the case.

Adam Smith:

No. I mean, it’s great that this has been looked at. I think this is one of the fantastic areas about dementia at the moment because there are so many factors that are still in play because we haven’t fully decided on exactly what causes it, what prevents it and things, which means they throw out this really wide net of research that really captures and encompasses everything. I love that’s the case although because you could argue as well that’s not necessarily spending the money in all the right ways, but I love that and that’s important. But the point about being, if women spent more time inside than outside, you’d imagine that when they lived in polluting areas, they’d be more advantaged because they’d be inside, not outside.

Dr Helena Popovic:

That’s true. But remember this study… Yeah, that’s true too.

Adam Smith:

Fascinating. I mean, we could chat about that for ages anyway because I just particularly on the pollution side of things. I think I saw several talks at the AAIC last year and the AD/PD that talked about particulate levels, and I learned so much from that talk and things I hadn’t thought about at all.

Dr Helena Popovic:

Yeah. One more quick thing, I want to make the point. I think one of the reasons women benefit more from physical exercise than men are they start probably at a lower baseline, and they have less muscle mass. I think even just aerobic exercises helps to increase muscle mass in women. We now know that grips handgrip strength, the lower your handgrip strength, the lower your cognition and the greater your risk of cognitive decline in Alzheimer’s. That strength training is really, really important. If you start doing any form of exercise, you’re going to improve your strength. I think that might be a reason that women benefit more.

Adam Smith:

It’d be interesting to see then more of that work carried out in places where we know that there is higher prevalence right now. Because, of course, the issue with those studies is that they’re all often carried out in wealthy and middle-class populations of people in these parts of the world where you want to see that happening in more diverse populations. To look at those sex and gender differences in Sub-Saharan Africa where we know that there is a higher incidence or prevalence rates right now, but where people fill different roles traditionally, they do different jobs, they have different activities, and pollution levels are variables. It’d be interested to see that same work replicated in other parts of the world in India maybe or in South America. Thank you, Helena. Iain and V, have you got one more?

Vyshnavy Balendra:

Just to add on to Dr. Helena’s. That whole green space study, someone did present I think earlier where she did a prospective study on 350,000 participants. What she did was she put them their green space into quartiles, like quartile one, two, three, and four. The fourth had the largest green space. So, the fourth quartile had a 10.9% lower risk of Alzheimer’s than the first one, which was 3.2-

Dr Helena Popovic:

Yeah, I was in that. I think I was [inaudible 00:55:05] Brilliant.

Adam Smith:

So aerobic exercise and go live in the countryside. We’d all like that. Iain.

Dr Iain Hartnell:

I’m going to bring it all the way back to biomarkers again. One of the big questions I have and that we are thinking about Alzheimer’s society as well is that whether in somebody’s dementia diagnosis or Alzheimer’s disease diagnosis journey with the improvement of blood-based biomarkers, whether that would be a suitable test to give somebody in replacement for another test that shows that they have amyloid or something in their brains. I think people often don’t have any biomarker test at the moment. It would be a memory test and a structural brain scan. Then if there’s more uncertainty, then they would be offered further tests.

Adam Smith:

They’re not even given the structural brain scan, are they? Not routinely. It’s in the Royal College guidance but not routine. Even in the UK, it’s variable.

Dr Iain Hartnell:

Yeah. It seems that the gold standard or the best standards for diagnosing that somebody has amyloid in their brains, for example, is to give them a PET scan or a CSF test. One of the questions I have is with these blood-based biomarkers, I know that the idea is that before I’ve heard that the idea could be that somebody has a blood test that suggests that they might have elevated levels of amyloid or tau that suggests that they might have Alzheimer’s disease to then have another test like a CSF test for a PET scan to confirm it, which is problematic because for PET scans, at least in the UK, there’s just not the infrastructure to be giving everybody that may have dementia or may have Alzheimer’s disease, a PET scan, and CSF tests. I think compared to other countries in Europe at least, I know that the UK is more squeamish about testing CSF in the general population, whereas I think it was the Netherlands, I heard that it’s very routinely done that people in there get lumbar punctures for various things.

There was a talk by a guy called Sebastian Palmqvist from Lund University, and he was talking through a blood test that combines phosphorylated tau 217 and the Abeta42/40 ratio. But the interesting thing about his talk was that he was looking at the people who then ended up having amyloid in their brains by a PET scan and didn’t, and the overlap and seeing which tests showed that was discriminatory. From that, he proposed having a three-tiered level of testing. You do give people a blood test and then they’d not even show that they have amyloid in their blood.

They would have a low probability that they have Alzheimer’s disease. You perhaps would watch them, or you’d follow them up. Then there was a group who it was quite distinguishable that the people that had this, it was called PrecivityAD2, the blood test, that were positive for this then did have Alzheimer’s disease, and the overlap was very small. Rather than having a black and white blood test, it would be more of maybe a… I know in diabetes there’s the idea of seeing that somebody has pre-diabetes before they are then diagnosed with diabetes. Maybe the same thing can happen in the UK.

Adam Smith:

That was on their press release as well, wasn’t it? They use this amyloid probability score, the APS2 apparently.

Dr Iain Hartnell:

Then in the questions because I was in the same session as Henrik Zetterberg, in all of the questions, there was asking about whether they could be used, the blood test could be used alone just to diagnose Alzheimer’s disease without further tests. I think from the panel, at least the general consensus was yes, but taking extra care and to say, to add caveats to the certainty of the test and perhaps in this three-tier diagnosis system of the blood test, the people with the low probability might have a second test, whereas the people that have the high probability of having amyloid in their brains, it would be distinguished that they did have Alzheimer’s disease.

Adam Smith:

I think it would certainly help with this challenge. We know that talking to psychiatrists right now, that there’s this particular challenge where the public health messages that have come out of the likes of Department of Health, the NHS, Alzheimer’s Society telling people to don’t wait. As soon as you think you’ve got a problem, go to your doctor’s. The problem is that then they get referred to a memory clinic and the sensitivity of the test we’re using right now just mean that the doctor just doesn’t know. They’re slightly reluctant perhaps to give somebody a diagnosis and say, “Oh, you’ve got Alzheimer’s disease,” because that’s a pretty bad diagnosis to give somebody.

They might say they have mild cognitive impairment, or they might say, “Just go away, we’re not sure, come back if things get worse.” I think I like the idea of potentially using that as a tool to address those don’t know people where if you could give them a blood test at that point and then schedule in perhaps over the course of the next year, quarterly blood tests like you do in cancer, you watch them wait, we’ll come back for another scan in three months, but come back for another blood test in three months and do another one.

You can see what’s happening with amyloid or tau levels to help inform that decision as to how do you proceed. I think that would potentially at least address this awkward limbo that so many people find themselves in, which is either getting told, “You’ve got a disease that you don’t actually have,” or getting told, “We are just not sure you’ve got a memory problem come back later.” Or being put on a medication that they don’t need or not getting treated for something else that they could be getting treated for. I think it has got real potential power in that space, but that’s just my view. I’m not a clinician.

Dr Iain Hartnell:

It was interesting that you’re talking about the tools that the current clinicians have to make these diagnoses. Because in that talk he did compare… I don’t know what tools they were using, but he did compare the current diagnostics from him and then some of his colleagues, they tried to diagnose based on the information they already had. They found with this new blood test, it was 82% accurate at diagnosing Alzheimer’s disease, whereas their current tests alone were only 54.8% accurate. He even alluded to the fact that’s not very much better than just flipping a coin and saying it was distinguishing Alzheimer’s from non-Alzheimer’s disease. But he was saying that clinicians know, they know that the tools aren’t good enough and there’s a bit of uncertainty.

Adam Smith:

But that brings it back to that usual thing. I mean, I’ve got a background in NHS service improvement and change management. That brings us back to this old problem that even if we know we’ve got something better, actually implementing that in a healthcare system is a challenging issue. I mean, first of all, getting everybody to agree on what is a good digital cognitive test, for example, or which biomarkers to use or what’s the process for this. But then actually taking what we know is there available now and actually getting it out there and making it work is so frustrating and takes way longer than it needs to do. These things are there now, let’s just crack on, make use of them. But the NHS is an amazing organization. It’s brilliant for that, but it’s also bureaucratic, I think, and you can’t suddenly crack on and some lone physician somewhere decides that they’re going to do something differently.

It doesn’t work like that. I think it does slightly more in Australia. I think you’ve got more potential for that in Australia. If you’ve got the money, you can certainly do that in the US. I think that’s enough with… That’s it. We are way over. Do you know what? I was determined to make this podcast 40 minutes and here we are at one hour in and that before we edit. You’ve all been amazing and the reason why this is so long because you’ve all had such amazing talks and you’ve talked about them so passionately as well. That’s really coming soon. Thank you so much all of you for-

Dr Helena Popovic:

Thank you.

Vyshnavy Balendra:

Thank you.

Dr Helena Popovic:

One thing, Adam. Can I just say? You don’t record this. One for you. I think it was the first podcast you had a little fun chat about omega-3s, one of the guests-

Adam Smith:

I know. You’re going to tell me off now, aren’t you?

Dr Helena Popovic:

No, I’m not going to tell you off. I’m going to tell you about a really interesting post-it. It wasn’t a presentation. Hussein Yassine, basically, he’s looking at the effect of ApoE on lipid metabolism, and he found that ApoE4 carriers with age, their response to omega-3 fatty acids gets less and less. The more fish, the higher their DHA diet is, on population studies, the better their cognition tends to be. Supplementation is really controversial, but with ApoE4 carriers, they’ve got to get their omega-3s early in life because once they get past middle age and once, they have any cognitive decline, omega-3s are no good. ApoE4-

Adam Smith:

Which spells doom for people like me who was a child of the ’70s, who was brought upon everything, in my house, was beige. I had a lot of beige food during the ’70s and ’80s.

Dr Helena Popovic:

If you’re not an ApoE4 carrier, you remain responsive to omega-3s. It’s only if you’re an ApoE4 carrier that you lose your responsiveness to omega 3.

Adam Smith:

I think that’s a good question about omega-3s, isn’t it? Because if you are having a good, filled omega-3 diet, the chances are you’ve probably got a pretty good diet anyway rather than somebody who doesn’t. You are going to offset that risk factor where we know diet is important. It’s up there in that list of Lancet modifiable risk factors.

Vyshnavy Balendra:

Shameless plug. I was just going to say that’s nutrition, metabolism, dementia. He was [inaudible 01:05:35] Dr. Hussein, right? That was [inaudible 01:05:38].

Dr Helena Popovic:

Yeah, he’s wonderful. He’s wonderful.

Adam Smith:

All those talks are available to watch back on the platform for the next few… Certainly, I think if you’re an A star member, you get it for slightly longer, but these are all available-

Dr Helena Popovic:

30th of August, I think.

Adam Smith:

… for you to go back and watch on the platform. I think you do have to have registered by now, so you can’t register after the conference closes, but I think, up until today, tomorrow, it’ll be your last chance to register and still watch everything. But once the conference is finished, you can’t register retrospectively. So do go away and catch up on some of the talks we’ve mentioned. As we said, there were over 800 orals, 6,000 or 8,000 posters. We haven’t been able to talk about everything we’d like to, but I think we’ve had a bloody good go at it today if I’m honest. Thank you to my brilliant, brilliant guest V Balendra, Dr. Iain Hartnell, and Dr. Helena Popovic. You’ve been amazing. Thank you so much. You’re all welcome to come back to the show and we’ll be back. Our next conference highlights show will probably be from Alzheimer Europe later this year.

You can find profiles of myself and all my brilliant guests and information on the conference shared by attendees on Twitter using #aaic23, and of course, on our website at dementiaresearcher.nihr.ac.uk. The podcast will be taking two short week break just to allow you all to catch up on the shows that you’ve missed over the last couple of weeks, but we’ll be back on the 7th of August talking about reshaping misfolded enzymes, and if you just can’t get enough, we also have a separate podcast called Ask Your Mentor, which will be having the last in that podcast’s 10 episode run with Aitana Sogorb. That will be coming out next week, so if you have a look for Ask Your Mentor, there’s 10 brilliant podcasts there, 9 at the moment, 10 from next week where you can listen to mentees interviewing their mentors, talking about their careers and how they’ve changed over time, and some top career tips from some amazing researchers in that series.

My last plea, because I wrote a blog on this week, is, however, if you’ve been attending the conference in person this week, I’d encourage you to consider offsetting your carbon footprint from that. I know carbon footprints are often a little bit controversial as to whether they’re beneficial or not, but if you find the right program through one of the gold standard frameworks, it’s really worthwhile and not necessarily as expensive as you’d think, and it’s a great way to set an example to other conferences. I think in-person conferences are very important but do take a look at that and just give some consideration to potentially offsetting your carbon. As we’ve heard today, air pollution is important, the world is warming up, and we can all play our part to contribute to reducing that. Thank you very much, everybody, again, Helena, Iain, V.

Dr Helena Popovic:

Thank you.

Dr Iain Hartnell:

Thank you.

Vyshnavy Balendra:

Pleasure.

Adam Smith:

I’m Adam Smith and you’ve been listening to the Dementia Researcher Podcast.

Voice Over:

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.

END