Welcome to the seventh season of the Dementia Researcher X ISTAART PIA Relay Podcast. Across six episodes, leading early career and senior researchers hand the mic from one ISTAART PIA to the next, giving you an honest, peer-to-peer tour of where dementia research is actually heading, from wearables and biomarkers to policy and trial design, in the run-up to AAIC.

Lewy body pathology shows up in roughly 30% of the brains of people who had dementia, yet it gets diagnosed in only about 5% of cases. Closing that gap has shaped much of Dr Joe Kane's career. Joe is a geriatric psychiatrist at Queen's University Belfast and outgoing Chair of the ISTAART Lewy Body Dementias PIA, and with host Dr Patrick Lao he traces his work from the Diamond Lewy programme to consensus diagnostic guidelines built by Delphi process. They discuss the symptoms clinicians often miss because they don't think to ask, from constipation to loss of smell, the cardiac scans and seed amplification assays now detecting pathology in CSF and even skin, and the TOP HAT trial repurposing an anti-sickness drug for hallucinations. Joe makes the case for a Lewy body specific rating scale, explains why the prodrome may be psychiatric or delirium rather than cognitive, and runs through the PIA's biggest AAIC programme in years, including a PIA Day panel on seed amplification assays.

Takeaways

• Lewy body dementia is heavily underdiagnosed: pathology appears in about 30% of brains but is diagnosed in around 5%.
• Much of the disease shows outside the brain, in constipation, blood pressure and smell, so it gets missed if nobody asks.
• Seed amplification assays, now usable on CSF and even a small skin biopsy, are changing how the pathology is detected.
• Trials can fail on the wrong yardstick, which is why the PIA is building a Lewy body specific rating scale.
• The prodrome is not only cognitive; the first sign can be depression, psychosis or delirium, and those gaps need data.

--

The Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART) convenes the global Alzheimer’s and dementia science community. Members share knowledge, fuel collaboration and advance research to find more effective ways to detect, treat and prevent Alzheimer’s and other dementias. Professional Interest Areas (PIA) are an assembly of ISTAART members with common subspecialties or interests.

There are currently 30 PIAs covering a wide range of interests and fields, from Neuroimaging to Diversity and Disparities and everything in between.

Find out more at https://istaart.alz.org/

--

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(upbeat music)

- [Voice Over] Hello, and

welcome to season seven

of the Dementia Researcher

ISTAART Relay podcast.

In this series, members of the ISTAART's

professional interest

areas interview each other

about their PIAs and the

hot topics in their fields.

Each guest then becomes

the next episode's host,

passing the conversation along

from one researcher to the next.

We're releasing one episode a day

in the run-up to the

Alzheimer's Association

International Conference, this

year in London and online,

showcasing the work of the ISTAART PIAs.

Thank you for listening.

(upbeat music)

- Hi, and thanks for tuning in.

I'm Patrick Lao, and I'm

an assistant professor

at Columbia University, and

I work on the Down syndrome

associated Alzheimer's disease

professional interest area.

I'm the current programme chair

and the incoming vice chair.

So today I'm excited

to be talking with Joe

from the Lewy body dementia

professional interest area.

So hi, Joe.

Could we start with you

introducing yourself?

- Sure.

My name is Joe Kane.

I'm a geriatric psychiatrist

and a researcher

from Queen's University,

Belfast in Northern Ireland.

And I am the chair of the PIA.

I will be handing over the reins

to your incoming chair,

Federico Rodriguez-Porcel

at AAIC this summer.

So it's been really exciting.

It's been really fun, but

it's time to hand it over.

- That's great.

So before we talk about

your work with the PIA,

could you tell us about your own work?

- Sure.

I've been working in Lewy body dementia

for about 10 years.

And one of the things about

working in this disease area

is that you really do get to

experience the whole breadth

of the topics that make

up Lewy body dementia.

And you get to bring all

those strands together.

So I started off with

a very clinical angle.

I worked on a programme

called Diamond Lewy,

which was a kind of multi-step programme

to look at how Lewy body

dementia was diagnosed

and treated within the UK

National Health Service.

That was my introduction

to Lewy body dementia.

And one of the things we did

was we did a large epidemiological study

of clinical diagnosis of LBD.

Even though we see pathological evidence

in about 20 to 30% of brains

of people with dementia,

really it's diagnosed in what

we find was around about 5%.

So we then kind of set out to try and see

what we could do about that.

We did, amongst other things,

we developed a consensus

around how to best diagnose

and treat Lewy body dementia.

And we did a cluster-randomized trial

where we introduced these toolkits,

these consensus advice pieces

in the different services

and saw if they helped people.

And we did find that there

were some improvements

in people's lives there.

And then I complemented that

with a bit of work with biomarkers.

I used a scan, a cardiac scan,

called MIPG, and we used

that to differentiate

Lewy body dementia from

Alzheimer's disease.

And that was pretty cool,

that was pretty exciting.

And it's something I've

continued on as well,

some of that type of work.

And then once I returned to Belfast

and returned to clinical work,

I found myself doing a

lot of clinical trials.

And that's what I've been

doing a lot of locally,

as well as doing a bit of biomarker work

and as well as doing the work with the PA.

So I'm a local lead for

a few different trials

in Lewy body dementia.

I recruit patients from my clinic

and both organise and collect the data.

And it's really great because I get to see

where research sits in the life cycle

of someone coming into a service,

understanding their diagnosis,

maybe doing a bit of patient

public information work

with us or advisory work with us,

and then maybe coming into a trial.

So it's great for me because

it's also clinically aligned.

And although I can do, try

to work with scientists

that really help develop my

understanding in other areas,

I really find that the patient

and their care partners

are at the middle of what I try to do.

And what we see when we go

to conferences like this,

like AIC, is that we benefit from people

with loads of different expertise

that maybe they brought from the likes

of the Alzheimer's world,

but maybe they've brought from

completely different places.

We work closely with them to

try and develop new projects

and new angles on this.

So it's a really exciting field to be in.

I've been very fortunate to work on it

over the last 10 years

and I'm really excited

to see how things develop

in the future.

- Yeah, that's great.

That's an incredible range of

different types of studies,

doing clinical to clinical work,

to clinical trials and

epidemiological studies.

So when you mentioned that

there was about 30% of brains,

or was it 30% of individuals diagnosed

with Lewy body dementia,

but only 5% of them had

a pathology at autopsy?

- So when we do autopsy studies

of people with dementia,

we find good going Lewy body pathology

in about 30% of those brains.

Now, in a good percentage of those brains,

there's also a good amount of

Alzheimer's pathology there.

And we know that Alzheimer's pathology

interacts with Lewy body pathology

and in different ways

that we're only just really

starting to understand.

But it's such a big jump

from that huge proportion of people

who have that pathology

to the clinic whereby,

5% in a Lewy body

dementia research clinic.

You know, in other services,

you know, there are some services

that might not see people

with Lewy body dementia

for months at a time.

And our argument has always been

that a big part of that is,

yes, starting to co-morbid pathology

and how it influences the

expression of that pathology,

but also the fact that

there are symptoms there

that not everybody is

accustomed to looking for.

And, you know, these are symptoms

like REM sleep behaviour disorder,

in which someone acts out their dreams.

And we keep telling people

that if they're not comfortable

asking about these symptoms,

you won't detect it.

And if you don't detect the symptoms,

you're not gonna make the diagnosis.

So we feel that even though the pathology

is a big part of it,

we feel that the detection

is also a really significant part of it.

So we need to approach it

from both angles, really.

- And you mentioned that the

guidelines that you published,

they helped, the clinical

guidelines that you published

really helped sort of fix that gap.

- Yeah, I mean, it's great

when there's a huge body of evidence

on which you can draw in a clinic

and when you can rely on really good

randomised control trial

data and, you know,

phase four studies.

But the reality is for a lot

of the less common dementias

and for lots of different

conditions in general,

you're relying on different study designs.

You're relying on a little

bit of expert opinion.

You're relying on some

anecdotal data as well.

So that was where that came

about, how that came about.

Rather than just do a systematic review

and dredge the really,

really good quality,

robust data there, we were able to go out

into our Lewy body dementia community.

We were able to gain

consensus through this process

that we call a Delphi, where

everyone or a good proportion

of people needs to agree

with a certain statement

before it gets accepted

into the guidelines.

And whilst it's not perfect by any means,

and even just today, I

shared those guidelines

with colleagues that were approaching me

and asking me for advice.

So yes, you can throw somebody

a really good journal article

which tells you about this

or tells you about that,

but to be able to say to somebody,

here are consensus guidelines

on how you should diagnose

and treat this condition,

it's just so invaluable

for busy clinical staff.

So that's been really rewarding,

and we're actually in the

process of updating those.

- Oh, that's great.

Yeah, and I think that's where biomarkers

can really come in handy

if the clinical diagnosis

is tricky.

So you mentioned using

cardiac scans to differentiate

between Lewy body disease

and Alzheimer's disease.

Could you tell me more about that?

- Sure, one of the things

that has always struck us

about Lewy body dementia is that we see

in the patient's symptoms

evidence of pathology,

not just in the brain,

but throughout the body.

A large proportion of people

with Parkinson's disease

and a large proportion of people

with Lewy body dementia will

not necessarily describe

cognitive problems as their first problem.

And what you see is a lot of constipation.

You see a lot of autonomic dysfunction.

And there is some good

autopsy data to suggest

that in a fair proportion of people

with Parkinson's disease and

other Lewy body diseases,

that there is some degree of spread

from lower down in the

peripheral nervous system

up in eventually to the

central nervous system.

So the idea behind the cardiac scans

is that we leverage that

fundamental difference

between Lewy body dementia

and Alzheimer's disease

and try to identify pathology

in the peripheral nervous system.

And theoretically as well,

doing that at a very early stage.

And the cool thing

about this scan is that,

you know, in Japan, for example,

nearly everybody suspected

of having Lewy body dementia

gets this as one of their first scans.

So there's really good data out there.

And what we did back in my PhD work

was we compared this cardiac scan,

which demonstrates adrenergic dysfunction.

Due to Lewy body pathology.

And we compared that with

the other famous biomarker

we have, which is the dopamine DAT scan.

So which does look at the

dopamine uptake in the striatum.

And we find that even though

it was very good biomarker

in the UK population,

wasn't quite as effective as the DAT scan.

But there's been a lot that has changed

in the Lewy body dementia

sphere since then.

And that we're now looking at disease

earlier and earlier and earlier.

What we are starting to think

of is these cardiac scans

and these DAT scans, dopamine scans,

as being complementary rather

than head-to-head biomarkers.

And we also think that, you know,

certain phenotypes may demonstrate

that the biomarker may be more effective

in certain phenotypes.

So it's still very much there.

It's still part of our

diagnostic criteria.

It's something that we're

learning a bit more about,

but it's always been a cool angle.

I find that not only

researchers and clinicians,

but patients really buy into that

because they, as soon as they hear that

constipation is a symptom

or urinary incontinence

or heat or cold intolerance is a symptom,

they will inevitably say,

"Oh yeah, I had that.

"I've had that for a few years."

And it's crazy once you start going

and systematically asking

people about their bowels

or systematically asking them

about their sense of smell.

There's a huge proportion of older people

that are affected by that.

While they're not

necessarily the best means

of discriminating Lewy body dementia

from Alzheimer's disease,

it does show us that there's different

pathological processes,

and we need to somehow leverage those.

- Yeah, I've heard about some

alphabetically in biomarkers,

maybe some PET tracers

at an early development,

as well as the seed amplification assay.

And that seems to only

work in CSF right now,

but not necessarily plasma.

How would those change the field?

- Well, the seed amplification assays

have really sparked so

much interest in the field.

They have been really useful in CSF, and

the USDLB Consortium and

some of our colleagues

in the likes of

Newcastle-upon-Tyne and Amsterdam,

they've really lent into the CSF analysis.

But what's also interesting

is that you can use

the seed amplification

assays on other tissues.

My understanding is that in

blood it's quite difficult

because it's quite easy

to get false positives

because of the clumping together.

But what a lot of my

colleagues in the States

have been using, and something

that we're really looking

forward to talking about on our PA day,

is the use of skin biopsy.

So with a very small

punch biopsy in the skin,

we can put them into these

seed amplification assays.

For those that don't understand,

it's basically a mechanism of growing

the alpha-signed eukaryotic fibrils

until they're detectable.

And even in very, very small

quantities in the skin,

they can be grown and detected,

and they can indicate

that there's evidence

of this pathology.

And you're right, although

there is promising data

around markers that we

can use in neuroimaging,

those aren't scalable yet,

they have their issues.

The idea of a skin

biomarker or a CSF biomarker

is just so much more

seemingly within reach

to clinical practise, and it's

something we're finding out

more and more data about.

And until we get that

really good PET tracer

that's really stable and really scalable,

I think we're gonna continue

looking into this evidence

of pathology through places like the skin,

but also CSF and elsewhere.

- And you mentioned with clinical trials,

what are the targets for those?

- And there's different targets for them.

They're not necessarily the places

where you expect to look for.

So one of the trials that we're looking at

led by University College London

is called the TOPHAT trial.

So it's using ondansetron,

which is a very widespread use

as a anti-sickness, anti-emetic drug

in cancer and oncology

practise in particular.

Although we have long thought

of the Lewy body dementia

as a disruption of dopaminergic systems,

and then later on, cholinergic systems,

and the likes of the use of ondansetron,

it's actually serotonergic.

So it's looking at the upstream effects

of the dopamine degradation

that causes hallucinations that we see

in Parkinson's disease

and Lewy body dementia.

So in some of the other studies,

they're looking at

different targets as well.

And it's a really exciting time

in Lewy body dementia research

because these targets are emerging

and because they are quite diverse.

And that's before we even get to that idea

that we hope is coming

later on down the line

of somehow modifying that

Alzheimer's pathology

in people with Lewy body pathology.

So range of targets, all it

takes is one of them to work

for it to transform the field,

but there's certainly

plenty in the pipeline

and plenty of cause for

optimism as a consequence.

- Yeah, that's great to hear,

especially because you mentioned

the different clinical subtypes

and so there might be different strategies

for different groups.

- It's no secret in

Parkinson's in particular,

there's different clinical phenotypes

represent very different symptom groups,

prognoses and different

responses to medication.

We're fairly confident

it's gonna be the same

in Lewy body dementia,

but we need the big sample sizes

and the big studies to do that.

- Great, so thinking more broadly,

are there any emerging topics at the field

that you wanna highlight?

- Sure, I mean, the real thing

that's on everyone's lips

from my perspective is the trials

and because so many of us

are working in clinics,

we're working closely with participants,

working closely with

advocacy groups and charities

and it just totally

transforms the conversation

when you can talk about

interventional trials

and not just observational ones.

Obviously, we've still got a lot to learn

from observational trials,

but it really transforms

the dynamic in the clinic

when you talk about,

there are new treatments on that,

that might be on the horizon,

do you want to be a part of that?

The thing is with the trials

becoming more and more

of an issue is that they

really made us reflect

on the trial environment

and their trial design.

One of the things that

PEA has done really well

has been to examine trial design.

So we've always relied

very heavily on things

like outcome measures for

things like Parkinson's,

for things like Alzheimer's disease.

We use the likes of the CDR, for example,

that are designed for Alzheimer's disease

and don't always necessarily

reflect the experience

of the patient.

And we were also

conscious that some trials

might be failing because

their outcome measures

aren't specific to Lewy body dementia.

So it's really made us think

very hard about trial design.

It's made us think about

how we leverage biomarkers

in trial design,

how we look towards the start

of kind of stratified medicine process

of maybe using some of

the Alzheimer's biomarkers

to work out when someone's

got mixed pathology.

And the other thing that

we really identified

as a very significant need has been a DLB

or Lewy body dementia

specific rating scale.

And that's what we've been working on

over the past few years.

I'll be presenting at AAIC

some of our work with that.

It's been really exciting

because it's allowed us

to engage the Lewy body

dementia community.

All of us working together

on this one question

with many kind of sub questions to it.

And we've made really good progress

but we do have some way to go.

So that's been something which has really

captured people's

imagination in the field.

And I think it's brought

us together as a community.

And we're hopeful that if

we develop the right tool

that it will actually catalyse trials

and encourage some of these novel targets

to be investigated.

And for the regulatory authorities,

people like the FDA, for example,

to buy in to these treatments

if they do appear to be effective.

So obviously I'm biassed

because it's something

I've been working very heavily in

but I do think that's

generated a lot of interest.

- Yeah, totally agree.

When you can start talking

about interventions

to patients and participants,

it really changes the entire conversation.

So that's been really

helpful to set the scene

for what I wanna talk about next,

which is the work of your PIA.

So you mentioned a little bit

of how you've been reevaluating

the design of clinical trials.

But are there some other examples

of how the work of your

PIA supports research?

- Sure.

Sorry, I'll just take a brief pause there

'cause I don't have more on me to.

Yeah, we in the PIA have

had a quite diverse approach

to our work groups.

And we've got four different work groups

and one of them is really heavily invested

in trial design.

We also have work groups on biomarkers,

on developing research consortia,

and also on prodromal Lewy body disease,

which is, I suppose, analogous somewhat

to mild cognitive impairment.

And Alzheimer's disease.

And one thing that these things,

one thing that these

working groups have all done

is they've acted as a lightning rod

for the international Lewy body community.

And it has provided such a great vehicle

and such great exposure.

And it's allowed us to move beyond

the three or four or

five traditional giants

in Lewy body dementia research,

to diversify, to

democratise our community,

and to bring more and more

people into the community.

And we have had people

that have started off

doing some of these projects,

like a publication for

the trial methods group,

for example.

And in the case of my colleague,

Dr. Rodriguez Purcell,

he started off doing a systematic

review on trial methods

and now he's about to lead the PA.

And then in other working groups,

we've got really experienced colleagues

working on biomarkers

and really forwarding

the conversation there.

And again, what they've done really well

is just energised the broader community.

So where you previously looked at

some of these great reviews,

you had maybe four or five people

from the same groups, same

centres, contributing to them.

And you look at some of our PA papers,

and there's loads of authors

from all over the world.

And the people that have

worked on these projects

have stayed in Lewy body dementia,

stayed in the PA,

and they developed projects of their own.

So the exposure and the

ability to grow our network

has been something quite different

from anything we've been able to do

in the Lewy body dementia community.

- Yeah, I've always

appreciated the ability

to participate in working groups

generated by the PAs.

And exactly what you're saying,

bringing groups together

from all over the world,

giving early career researchers

a chance to sort of contribute

and work with some of

the giants in the field.

You mentioned a prodromal working group,

and I'm interested about that.

How long is the disease

force in the prodromal stage?

- Great question, and the

answer is we don't know.

One of the things that

we've been really lacking

has been longitudinal

Lewy body dementia data.

And again, there's been a

few well-resourced centres

that have really got their act together

and put really cool

longitudinal projects in place.

But the fact of the matter is

that we don't fully understand conversion

from prodromal disease to

full-blown Lewy body dementia.

We don't fully understand the role

that the biomarkers have to play in that.

We don't fully understand what things

like Alzheimer's pathology

has to play in that.

And then the other big huge

thing is that we believe

that the prodromal phase

of Lewy body dementia

isn't just a cognitive one.

And although we think of

MCI in the context of AD

to be very much driven by

the cognitive symptoms,

we also believe that there

are significant groups

of people out there ticking along

without much in the way

of cognitive symptoms.

And the first evidence of their disease

is psychiatric disease.

So the first time somebody

has to ask the question

is this Lewy body dementia

could be their first depressive symptom,

could be that they get psychosis

or new hallucinations.

And then there's also another group

whereby we think that people get delirium.

We know that people with Lewy

body dementia, for example,

get delirium more frequently

in the lead up to diagnosis

than people with Alzheimer's disease.

So we also don't know

how that delirium onset

prodromal disease then interacts

with the full-blown dementia diagnosis.

And it's a little easier

and we've got a little bit more data.

And in the PA, we've produced

a couple of really nice

systematic reviews on the conversion

from mild cognitive impairment to dementia

and the neuropsychological characteristics

of those patients.

But huge, huge gaps remain

around the psychiatric

and delirium prodromes.

And that's something which is something

we've got to really work on as a community

and get the data and that's not that easy.

- Yeah, and I think that

really highlights the need

for early intervention,

if those are some of the earliest signs.

Those are really impactful

on patients' lives.

- Yeah, I mean, different clinicians

have different blind spots.

And I'm a psychiatrist

and if I see somebody

with psychiatric symptoms,

focus on the psychiatric symptoms

and I'm maybe not always

looking as closely

as I could do about the

likes of cognitive symptoms,

even with disease progression.

So we need to work out how

this changes the behaviour

of clinicians in different services

with their different blind spots.

And we've achieved so much in the realm

of dream enactment behaviour,

REM sleep behaviour disorder,

kind of sleep physicians

are now really, really good

at identifying people at a high risk

of the Lewy body dementia.

And we could probably do better

when it comes to psychiatrists,

old age psychiatrists and

neurologists and geriatricians,

maybe asking a bit more systematically

about some of these psychiatric symptoms

and scrutinising for

delirium a bit more closely.

But we need the data, we need the studies

and we can't really move

forward until we've done those.

- Yeah, and I think that's

why these focus areas

are so important, bringing

together different scientists

with different backgrounds

to cover those blind spots.

So what brought you to the PIA

and how did you get first involved?

- I didn't rack my brain about this

because I've been involved in

the PIA for many years now.

And I first got involved with

one of the PIA working groups

just after the pandemic.

And I had paused my research work.

I had moved from Newcastle,

which is one of those traditional giants

and moved back to Belfast,

didn't have the same and

doesn't have the same pedigree

for Lewy body dementia research.

And I really wanted to carry on the work

that I'd done in my PhD.

And this call went out saying,

do you wanna work on a paper

about international consortia?

I co-led that with Fabrizio D'Antonio

and we worked really

closely with Dag Arsland

and Jim Nevins,

who are some of the absolute

giants in the field.

And it was so much fun

putting that together.

It was hard work, but

as part of that project,

we basically had to reach out

to all Lewy body consortia

that were occurring throughout the world.

And it really gave me an idea

of what the network looked like

and really put me in contact

with people I would never

have had contact with either.

Shortly after that, I was asked

to be communications chair.

And at the time I was tweeting a lot

and that worked really well

with tweeting about some

of my favourite subjects.

And it was a really nice way

and a really exciting time

to get people that were interested

in Lewy body dementia interacting.

And we ended up going

out for drinks at AIC

and social media and getting out there

has become a big, big part

of who we are as a PA.

Definitely not because of me,

but because of my successors.

And then it was shortly after that

that I became vice chair and then chair.

So it's been absolutely

transformative for me

as someone who,

although I've been fortunate enough

to work with some of the

real luminaries in the field,

I am a little bit isolated,

it could be argued.

And the PA just changes that,

the PA just put me in the

middle of these networks.

And it gave me the opportunity

to work on some really exciting grants,

to collaborate with people

I would never have

collaborated with before.

And sounds trite, but

they're all my friends now.

We go to AIC and we look for each other

and we have fun together.

And yeah, it's been such a privilege

and such a boon for my

career and for my life.

So I'm very, very grateful.

- Yeah, speaking of AIC,

you mentioned you have one presentation.

Does the PA have any

other activities going on?

- Yeah, we're really

excited that this is maybe

our biggest AIC for many,

many years in the PA.

We have lots of activities going on.

We were in PA day after

a brief hiatus last year.

We're back to PA day

and we're really happy with the

programme we've got lined up.

We've got a kind of a panel discussion

that's gonna look at not only the data

around the seed amplification assays,

but also how they might start to influence

our decisions in the clinic

and how you might start

figuring out clinical dilemmas

using those biomarkers.

We also, as part of that PA day,

are really looking forward to awarding

our first PA publication

of the year award,

which is an amazing paper.

I'm not gonna let the cat out of the bag,

but we're really excited

that it's such a quality

paper for our first award.

Then straight up after that,

we always really engage enthusiastically

in the postdoc and student prizes.

Probably one of my

highlights of AIC every year

is visiting the Lewy body posters

and seeing the early career researchers

and the great work that they're doing

and sharing it far and wide.

So there's that.

And then I think we've got

three featured research sessions.

I'm in one of them.

And one small part of a

really exciting session

that's going to talk about the integration

of some of the new biological frameworks

that have been developed

in Lewy body disease

and in Parkinson's disease

and how it might relate

to not only trials,

but also practise and our cohorts as well.

Then the last thing I'm

really excited about attending

is a clinical toolbox session,

which I think is on the last day.

As a clinician, you're

looking every bit as much

for some really good

clinical presentations

as much as breaking research.

And our PM members, Bhavna

Patel and Kate Wyman

are gonna be sharing a really

broad multidisciplinary look

at how to manage some of the

more troublesome symptoms

in Lewy Body dementia.

So I'm really looking forward to that.

And I'm really looking

forward to seeing everybody

and being face-to-face.

And I'm really looking forward to seeing

what my colleague Federico has in store

for the next few years of the PM.

- Yeah, congrats.

That sounds like a really

productive programme at AAIC.

And I'll have to stop by

and check some of those out.

- Please do, please do.

You'd be very welcome.

(upbeat music)

- All right, well, thank

you so much for your time.

I think it's time to end today's podcast.

Before we go, I do have a final question.

So what advice do you have for someone

who's just learning about ISTAART

and how has it helped you being involved?

- I think one of the things

that ISTAART has helped with

is to provide,

we talk about providing a platform,

but it's actually a bit of a pedestal.

It kind of raises you up.

It's really levelling

and it really puts you

at the same level of

some amazingly talented

and experienced people.

So my advice is to take that

opportunity with both hands.

And what always surprised

me earlier in my career

is that when I went up,

I'm usually quite nervous in doing so

and kind of gingerly

approaching really experienced,

really important researcher in the field.

How keen they were to speak

with just about anybody on our topic.

How keen they were to provide

people with opportunities.

And how keen they were to,

especially with ISTAART,

involve people as much as possible.

So my advice would be, it's

such a great opportunity.

Use it, try and set

your shyness to the side

and ask that question

because I guarantee it's

not a stupid question.

- Yeah, completely agree.

So thank you, Joe, for

taking time to join us today.

- Thank you, Patrick.

Really nice to speak with you.

- So thank you for listening.

You can find profiles of

myself and my brilliant guest

and information on how to

become involved in ISTAART

on our website.

There's a link below in the show notes.

So I've been Patrick Lao

and you've been listening

to the Relay podcast

from Dementia Researcher

and Alzheimer's Association.

Hit subscribe on YouTube or

in your favourite podcast app

to ensure you don't miss an episode.

Thank you.

Goodbye.

(upbeat music)

- [Voice Over] You have been

listening to the Relay podcast

delivered as a collaboration

between Dementia Researcher and ISTAART.

This podcast is made at

University College London

with generous funding from the NIHR,

Race Against Dementia,

Alzheimer's Association,

Alzheimer's Research UK,

and the Alzheimer's Society.

Please like and subscribe

and share your thoughts in the comments.

(upbeat music)