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.

Almost everyone born with Down syndrome overproduces the amyloid precursor protein from birth, which makes it one of the clearest natural windows we have into how Alzheimer's begins. Dr Patrick Lao, Assistant Professor at Columbia and Programmes Chair of the ISTAART Down Syndrome and Alzheimer's Disease PIA, comes from a medical physics background and uses multimodal neuroimaging to map the disease across its genetic and sporadic forms. With host Lillian Morgado, he explains amyloid and tau PET, Thal phases and Braak staging, and how chronological age can stand in for disease stage in this population, with a typical symptom onset around 54. They talk about why people with Down syndrome were long left out of anti-amyloid trials and how that is now changing, and the risk and resilience research asking why some people fall off the expected timeline. Patrick also previews the PIA's AAIC PIA Day session on returning results, plus the separate DSAD/ADAD conference coming to London next year.

Takeaways

• Genetic forms of Alzheimer's, including Down syndrome, let researchers study the earliest disease pathways before symptoms appear.
• In Down syndrome, chronological age can approximate disease stage, with symptoms typically expected around age 54.
• Imaging shows where amyloid and tau sit in the brain, the spatial detail a blood test cannot give.
• People with Down syndrome were historically excluded from anti-amyloid trials; that is shifting, with a lecanemab safety extension now underway.
• Not everyone follows the population timeline, and risk and resilience work asks what pushes onset earlier or later.

--

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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(light music)

- [Moderator] 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 are 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.

- Hello and thanks for tuning in.

I'm Lillian Morgado,

a research coordinator

at Georgia State University

in Atlanta, Georgia, USA.

I'm also the Social Media

and Communications Chair

for the Health Policy PIA.

Today, I'm delighted to be

talking with Dr. Patrick Lao

from the Down Syndrome and

Alzheimer's Disease PIA.

Hello, Patrick.

Can I start by asking you

to introduce yourself?

- Hi, Lillian.

Yeah, so I'm Patrick Lao.

I'm an assistant professor

at Columbia University.

I'm the current Programmes Chair

for the Down Syndrome-Associated

Alzheimer's Disease PIA

and the incoming Vice Chair.

- Congratulations on your vice chairship.

- Thank you.

- And then before we talk

about your work with the PIA,

can you tell me a little

bit about your own research?

- Sure.

So my background is in medical physics,

and I do a lot of neuroimaging.

Yep, so I use multimodal biomarkers

to look at the disease course

across different forms

of Alzheimer's disease.

So that includes genetic forms

like Down syndrome-associated

Alzheimer's disease

or autosomal dominant Alzheimer's disease,

as well as sporadic forms,

so like late-onset Alzheimer's disease.

And even within the different

clinical presentations

of Alzheimer's disease,

there are certain subgroups

like posterior cortical atrophy,

where there's more

visual-spatial impairment

and more posterior

involvement of brain regions,

or logopenic variant

primary progressive aphasia,

where there's left temporal involvement

that leads to language impairments.

And so looking across

all these different forms

of Alzheimer's disease allows

us to compare and contrast,

see what pathways might be generalizable

and essentially a target

for therapy for everyone,

or which pathways are

specific to specific subtypes

where more of a personalised

approach might be warranted.

And so by doing this work,

we can use the unique aspects

of each form of Alzheimer's disease

to kinda gain new insight.

So for example, adults with Down syndrome,

they have Trisomy 21,

which is the triplication

of Chromosome 21,

and that's where the amyloid

precursor protein gene is encoded.

So from birth, they're overproducing

the amyloid precursor protein.

And this is happening in every

person with Down syndrome.

And a lot of our work has shown,

we've mapped out the amyloid

cascade in these individuals,

so starting from amyloid, going to tau,

going to neurodegeneration,

and finally, cognitive impairment.

And since I do a lot of multimodal work,

I've been really

interested in incorporating

vascular and inflammatory

pathways into these cascades.

And by doing so, several

groups across the world

working with cohorts of

adults with Down syndrome

have put out a lot of cross-sectional work

and, more recently, longitudinal work,

essentially showing that this happens

in a very stereotypical pattern

and we can use chronological

age to essentially approximate

disease progression in this population.

And so now we're starting to characterise

the timeline of the

natural history of disease,

and this will really help

inform clinical trial design.

- Okay, that is really cool.

And I have some questions because this is,

I mostly do qualitative research,

so some of this is outside

of my normal stuff.

You had mentioned that you work

in medical physics, I believe.

Is that correct?

- That's correct.

- Okay.

That sounds like a very niche field.

Which side did you start on,

the physics or the medicine?

- Well, I did a dual degree

in biology and physics in undergrad.

And so they always kind of

came hand in hand for me.

I was originally thinking

about going to medical school,

and then I had heard about

medical physics as an option,

so then I ended up going that route.

So yeah, I think it's simultaneous

in this case. (chuckles)

But yeah, it's essentially leveraging

kind of the properties of radiation

and how they interact with human tissue

to generate either meaningful images

or to treat things like

cancer with radiation therapy.

- Actually leads to my follow-up question.

You had mentioned doing

multimodal imaging,

and I was curious what that means.

Are we talking about

looking at brain scans

or tissue samples?

What sort of images are you comparing?

- Right, yeah, I guess

multimodal could mean

a whole host of different things

depending on what type of biomarker.

But since I normally do neuroimaging,

I'm just talking about

different brain scans.

And so some of the ones that

we use are amyloid PET scans.

And this will show you how

much amyloid is in your brain.

And these are really useful

for clinical trials right

now that target amyloid.

So all the anti-amyloid antibodies,

to show eligibility for the study,

a participant has to be amyloid-positive,

and so they'll get a scan

or a blood test prior to enrollment.

And then after treatment with the drug,

they're gonna scan them again to see

if there was treatment-related

amyloid clearance.

And so imaging is the gold standard

for this type of stuff

just because we can get

that spatial information

that we're used to getting from autopsy.

Whereas a blood measure

will kind of just tell you

a global burden of amyloid.

And so in the amyloid cascade,

after amyloid comes tau pathology.

And so we have these tau PET scans.

Only one of these tracers is FDA approved.

The rest are still only for research.

And so these methods are

still being developed

in terms of visual

reads and quantification

and harmonisation across tracers.

But tau PET is really,

really useful in showing

how the tau pathology

spreads across the brain.

So for amyloid, it's more

important how much you have

in these Thal phase regions,

which is kind of a global phenomenon.

But for the Braak staging,

it's really the tau spreading

across the brain that

gives you information

about the progression of the disease.

- Question.

- Yeah.

- What is Braak staging?

- Sure, so I mentioned that PET imaging

is sort of the gold standard

because it relates to autopsy.

And so autopsy is how

we kind of definitively

show pathology at end of life.

And so while a person is

alive, we can't do that.

And so we have to use imaging biomarkers

to kind of get a sense of that.

And with the spatial

information from imaging,

it sort of maps onto autopsy best.

And for amyloid, the

spatiotemporal progression

of amyloid plaques across the brain

was first characterised by Dietmar Thal.

And so we call those the Thal phases.

And so those go from one to six.

And then for tau tangle

pathology across the brain,

that was first characterised by Dr. Braak.

And Braak, I think, is

a husband-wife pair.

And so Braak staging essentially describes

the progression of tau across the brain

from stages one to six.

- Okay, thank you so

much for clarifying that,

'cause I was like, ooh, that

sounds really important.

So it sounds like imaging is really cool

because it tells you where

the biomarkers are deposited,

whereas if you do a blood draw,

it just says if they're there or not.

And another thing you had mentioned

was that through using

this imaging technology,

you're able to figure out the

Alzheimer's disease staging

for people with Down syndrome

based on chronological age.

So does that mean you can say,

all right, when someone

who has Down syndrome is,

I don't know, 40 years old,

we can expect this level of accumulation

and they may need this level of support?

- Right, I think that's the ultimate goal,

to be able to place them

on the disease timeline

based on something as

simple as chronological age

in order to give guidelines

to these individuals,

their families, their

caregivers, their clinicians,

to know what to screen for at

a particular stage of life.

And when we start to

look at these different

genetic forms of Alzheimer's disease,

I think it's been more widely studied

in autosomal dominant AD,

where there are mutations

in the amyloid precursor protein,

Presenilin 1 or Presenilin 2.

But essentially, what comes out of that

is a concept called estimated

years to onset, or EYO.

And this is how predictable

their clinical symptom onset is

based on their parent's symptom onset

if they had that mutation.

So for example, if someone

has autosomal dominant AD

and they're 45 years old,

and their parent with the

mutation got symptoms at 55,

they would be negative 10 on EYO,

or essentially 10 years away

from their clinical onset.

- Okay, so it's like a countdown clock.

- Mm-hmm.

And yeah, and that differed across

the different mutation types.

But here for Trisomy 21,

we tend to use a single

age for symptom onset.

- And another thing, and I apologise

'cause you may have already answered this,

but you do such cool work,

I wanna learn more about it.

One of the things that

I do know about folks

with Down syndrome is that

people with Down syndrome

are living longer than ever

due to a lot of really cool

medical advances and additional supports

that people are able to offer.

Does that mean that Alzheimer's disease

for these folks is a growing concern?

- Yeah, absolutely.

So the life expectancy in the 1960s

was around 10 years old,

and that was limited

by the high incidence of

congenital heart disease

in this population.

And it wasn't till the '80s

or so where the surgeries

were developed to fix

these congenital defects,

and even later for being offered

to the Down syndrome population

because they were concerned

about how they would tolerate surgery.

And so with that, life expectancy

is now in the '60s to '70s,

depending on what country

you're looking at.

And now Alzheimer's disease represents

sort of the upper limit

on people's lifespan.

The single age of onset

that I referred to

earlier is 54 years old.

So that's when you can

typically expect symptoms.

- Yeah, that's rough because it's early.

But I think it's really important

that you're able to figure

out a typical age of onset

because that probably allows

people and their families

to better plan for what they'll

need to support themselves

and have the best quality of life.

Thank you for doing that work.

- Yeah, and something else

that we're looking into is,

I am kind of talking about this

in terms of like stereotyped process

or what happens on the

overall population level.

But we do see individuals that

might show some resilience,

and there's actually a

range around that 54 years.

Some people can get it as

late as their '60s or '70s.

And on the flip side of that,

there might be some individuals

showing increased risk

where they could get it as early as 30.

And so we're trying to

look at those extreme cases

and see what's different about them

to see what kind of pathways

we can target for therapy.

And so while there is this

population-level progression,

there is still some

inter-individual variability

that we're hoping to leverage, yeah.

- Didn't the Down Syndrome

and Alzheimer's Disease PIA

publish something about

resilience research?

I think it was in 2024 or 2023.

- Yeah, it might've been 2024.

Yeah, that was a product of

one of our working groups.

And so that working group is still active.

There's a paper investigating

risk and resilience mechanisms

in Down syndrome-associated

Alzheimer's disease,

because for a lot of our early work,

we were focused on

developing these timelines

that apply to the population overall

to sort of inform clinical

guidelines and clinical trials.

But as we're doing more and more work,

we're realising that not every individual

falls onto these timelines perfectly.

And so some people will get it much later,

and maybe they're doing different things

like in terms of lifestyle,

or maybe they have some

other protective factors

in terms of comorbid

co-occurring conditions,

or maybe their overall

morbidity rate is lower.

And so we're trying to

figure out what factors,

even in a genetically determined form

of Alzheimer's disease,

might push these timelines

apart for individuals.

- Very cool.

And are there any other really hot topics

or exciting things in your field right now

that you wanna talk about?

- Yeah, so I've been talking

about sort of these timelines

and all of this data coming out

to really support clinical trials.

And so we're really now

just at the start of that.

So there are three in the pipeline

that are going to be including

individuals with Down syndrome.

So even though they're

at this ultra-high risk

for Alzheimer's disease,

they've been excluded

from all of the previous

anti-amyloid therapies

due to safety concerns or protections

for individuals with

intellectual disability.

But because these people

are at such high risk

and there is no other way to treat it,

we've been advocating a lot

through our work in the PIA

for individuals to be

included in these trials

so that we can get the safety information

necessary for them to enrol.

And so one of these trials, for

example, is using lecanemab,

which is an FDA-approved anti-amyloid

that was tested in the

non-Down syndrome population.

And so they're doing a phase IV

sort of safety extension trial

in adults with Down syndrome.

So we already know it works.

We have a general sense of the safety.

We have additional safety guards

for the the participants

with Down syndrome,

like stricter inclusion criteria,

but we are allowing them to take the drug.

And so we'll see what other

special considerations

we need to make for

people with Down syndrome

when we're providing these treatments.

And so I think that's a

really critical step forward.

- That's really cool.

And another follow-up question.

I know one of the issues

with clinical trials

is getting enough people of

certain populations in it,

and people with Down syndrome

are a pretty small

portion of the population.

Were you involved, or do

you have any knowledge

of the recruiting process that

was used to get those folks

into the clinical trial

or any of that part?

- I'm not super familiar

with the entirety of it,

but there are clinical trial-ready cohorts

that are being established

to where we do this multimodal

characterization over time.

So we essentially have all

their baseline characteristics,

and we can use themselves at baseline

compared to them after treatment

as the comparison group.

And so one study that I'm involved in

called the Alzheimer's Biomarker

Consortium-Down Syndrome,

or the ABC-DS study,

is one of those clinical

trial-ready cohorts.

And so a lot of our participants

co-enroll into this TRC-DS,

and then they can be recruited

through that mechanism

into these ongoing clinical trials

based on what they wanna do.

- That's so exciting,

and I'm so glad that you're able to use

that information you're

getting all the imaging

and being able to do the stereotyping,

to moving it to seeing

the specific situations

and how things can be

done to make it better.

That's gotta be really satisfying.

- Yeah, it's been a really

influential time in the field

to see how much has changed

in the last 10, 15 years,

especially even with the most recent

revised criteria for the diagnosis

and staging of Alzheimer's

disease that came out.

Previously, this was

essentially to establish

a way to diagnose Alzheimer's

disease with biomarkers

and not have to wait the 20 years

until cognitive symptoms appear.

And so they established this amyloid-tau

neurodegeneration framework

in order to stage individuals.

But still, the starting point

was someone had to be amyloid-positive.

And if we really wanna

know what's driving amyloid

in the first place, we have

to look earlier than that.

And so in these genetic

forms of Alzheimer's disease,

like autosomal dominant AD or

Down syndrome-associated AD,

they have now been included as

stage zero in this framework.

And so we can study the

earliest pathways in the disease

because we know that they

will eventually develop it.

And so that was a huge

change in the field as well.

So both on the research and

clinical trial areas, I think,

there's been a lot of progress.

- Very cool.

(light music)

That's really helpful to set the scene

for what I wanna talk about next,

which is the work of your PIA.

So how does the work of your PIA

really support your field of research?

And I know we talked about

you guys had that workgroup

that had that awesome publication.

I'm sure you're doing

other cool stuff too.

- Yeah, so in addition to the risk

and resilience working group,

we have another working group

in development where we're expanding

to other forms of intellectual

disability and autism.

And so we had a all-members meeting

about a month ago to engage

sort of all the members,

not just our executive committee,

in these regular meetings.

And we broke out into working groups,

and this allowed for smaller interactions.

And each of the breakout rooms was tasked

with talking about where

we wanna go with this PIA,

what kind of new working

groups do we want,

what would they like to see us do?

And so one of those was about

the broader umbrella of

intellectual disabilities.

And someone had been working,

Eric Rubenstein had been working

with electronic health record data,

and they started noticing

that a dementia diagnosis,

dementia, all-cause, as in

sort of an umbrella term

in the health record,

was maybe being overused

in certain cases.

For example, in individuals

that were too young

for that to be a possibility.

And now we're developing a survey

to send out to clinicians to get a sense

of what their level of experience

with people with

intellectual disabilities is

and whether any additional

clinical training

or guidelines would be more helpful

in terms of understanding when to use

that diagnosis or when to use that code.

And similarly, for our first working group

for the Risk and Resilience,

Dr. Lydia Vasquez and Sigan Hartley,

they have been developing

this survey to send out

to get a better sense of the risk

and resilience factors in Down syndrome.

So following up on that first paper.

- Very cool.

Two questions about the new working group.

So the first one is you're

saying that the code

for dementia is being used potentially

more liberally than it should

by healthcare practitioners

on folks with autism

specifically, is that correct?

- Yeah, autism spectrum disorder

or intellectual disabilities, yeah.

- And I understand that this

still needs to be researched,

but is the hypothesis or the suspicion

that the healthcare

providers are doing this

because they don't know

what the appropriate

baseline is for these folks?

- Yeah, I think that would feed into it.

Or there are things

like regression disorder

in adults with Down syndrome

where it's kind of like

a very sharp decline

and they might mistake that for dementia.

And so it's really getting a sense

of how many patients have they seen

with these baseline conditions

and how did they sort of handle it

when they suspected dementia.

- Right.

That's really cool,

because then you guys can,

like you said, we can see, all right,

do these folks need extra training?

What else can we do to help these people?

So who are you looking to join that group?

'Cause you said it was still being formed.

Are you looking for members

still, or is it closed?

- Yeah, absolutely.

Yeah, it's still in its very early stages,

and we're actually still

developing that survey.

The target audience for that

survey would be clinicians only

since we're interested in sort

of getting at that diagnosis.

- And then the other one you're working on

is the group that did that

great publication on resilience.

And now you're working on another survey

where you're looking at

the resilience factors.

Correct?

- Yeah, I believe so, yeah.

- Okay, that's so exciting.

- Yeah, I think it really

helped shape the message

that we can provide

back to the participants

in the community when

we can start to focus

on these resilience factors and

what people can do about it.

Like for example, in

relation to enrollment

in clinical trials rather

than just sort of this

inevitable progression, yeah.

- What initially brought

you to join the PIA?

- A colleague reached out and

asked if I wanted to join.

And at the time, I wasn't

doing any networking at all.

I was pretty shy, but they

just told me about it.

I figured why not?

So I joined as a student member.

And then from there, it just

turned into a really great

opportunity for engaging

with more senior scientists

and really hearing the way

people think about certain topics

or how they sort of plan or

organise different events.

And so after that, I signed

up to be programmes chair,

and then will be the new vice chair.

So it's been a really helpful,

successful collaboration.

And then I'm in it for the long term.

- I love that, and I cannot overstate,

as someone who also joined

as a student member,

the importance of just being in the room

and listening to the people

who have been in it for longer,

their thought processes

and what their thoughts are

on the trajectory of things.

I feel like I should say

that there's something

more structured about

the PIAs that is useful,

but I think that is one of

the most useful experiences,

'cause, you know, different

places do webinars,

but to get actual time with senior people

that's unstructured is really valuable.

- Yeah, absolutely.

(light music)

- What does your PIA have

planned for the coming year?

- Yeah, so earlier this year,

I guess I forgot to mention

how this would be another way

that the PIA contributes to,

I guess, the field of research

is that through our ISTAART,

we applied for funding

from the Alzheimer's Association

and we got funding for a conference.

And so this conference is called

the Down Syndrome Associated

Alzheimer's Disease/Autosomal Dominant

Alzheimer's Disease Conference,

or essentially the DSAD/ADAD Conference.

And it's essentially to bring together

researchers from different fields,

studying these different kinds

of genetic forms of Alzheimer's disease.

And we just had our third meeting,

third annual meeting earlier this year.

And the fourth one has been announced

for London in next fall.

So if anyone's interested

in attending that,

that one's a really great

small-format conference

that engages the audience a lot.

And so conference planning for that

will be ongoing this year.

We're also going to have a PIA Day event

on July 11th, I believe.

And there, we're gonna be talking about

the return of results for

observational research studies

as well as some of these clinical trials.

And what's the best way of doing it?

Are the participants able to understand

this scientific information

because it's a risk,

not really a diagnosis?

And are there any sort of

like psychosocial factors

that we need to consider in

how we relay this information?

So there'll be pre-disclosure

and post-disclosure surveys,

interviews, and engagement with

MDs throughout the process.

And so that'll be a

really interesting topic.

That's already a big topic

in the non-Down syndrome

field on how to do that best.

And so it'll be very interesting

to see that panel discussion.

And we have two featured research sessions

for the conference.

One will be on these general timelines,

and the other one will be on

the risk and resilience factors

that pull individuals off

of those general timelines.

- Okay, so your PIA Day,

you're doing return of results,

and is that focused just on

the Down syndrome community,

or is that in general?

- We're gonna be bringing

experts in general

to help inform how we're going to do it

for Down syndrome specifically.

- Okay, that's so exciting.

I know that's a big new thing

everybody wants to make sure

they're doing it correctly.

So I'm really excited you

guys are looking at that.

And then you also said you guys

have a featured research session.

Do you know what day that's going to be?

- I believe they're both on the

first day of the conference.

First or second day, yeah.

- Okay.

You're opening things up,

and then you have your whole

own conference happening separately.

I don't think you're as excited

as you really should be about that.

Like that's a big deal. (laughs)

- Yeah, it has been super successful.

That is the brainchild of

Dr. Juan Fortea in Barcelona,

and he's hosted it there

the first three years.

- What a lovely venue.

And if somebody wants to learn more

about that conference

you guys are planning,

what should they do or who

should they reach out to?

- Yeah, they can reach out to

anyone in the Down Syndrome

Associated Alzheimer's Disease PIA,

or they can do a Google search

with that great acronym,

DSAD/ADAD. (laughs)

And then we have a

dedicated conference website

where they can find more information.

(light music)

- Before we go, I have one final question.

What advice do you have for

someone who's just learning

about ISTAART and how has it

helped you with being involved?

- Yeah, that's a great question.

I think, because I was

so shy at the beginning,

just getting involved.

So reaching out to people.

They are way nicer than I ever expected,

especially with the sort of

professional stage difference.

But everyone was willing

to help answer questions,

respond to emails and

just, like we said earlier,

just being in the room with them.

It's just getting involved early,

and that really

accelerated my career path.

- Thank you so much, Dr. Patrick Lao,

for taking the time to join us today.

- Yeah, thank you.

- Thank you for listening.

You can find profiles on

myself and my wonderful guest

and information on how to

become involved in ISTAART

on our website at

dementiaresearcher.nihr.ac.uk,

and also at alz.org/istaart.

There's a link in the show notes.

I'm Lillian Morgado, and

you've been listening

to the Relay Podcast

from Dementia Researcher

and the Alzheimer's Association.

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in your favourite podcast app

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Thank you so much.

Goodbye.

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Alzheimer's Association,

Alzheimer's Research UK,

and the Alzheimer's Society.

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