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Doctor de Emma Davenni, Welcome to Projec one hundred.

Thank you.

So our normal proces is we ask our guest if they wouldn't mind explaining their qualifications, because, particularly when they have a medical background, I'm so important for our audience to know who they're listening to, because I am by no means any what near an expert in any of the topics that we discussed here.

I'm just an interviewer and you're the expert.

So could you please sell us where your qualifications are?

Yes, of course, thank you.

So, yeah, I have a medical degree.

I went to medical school back in Ireland and Northern Ireland actually and they and since then I trained in neurology, so I am a cognitive neurologist, and I also did a PhD.

So when I came to Sydney almost thirteen years ago, I came to do a fellowship and then fell in love with the police, fell in love with the work and all of that, and decided to stay.

And so then I did a PhD here at unsw You so I have a medical degree and then also a.

Doctorate and you're currently at NEURRA at new So what do you do in euro.

Well at EURA have a variety of rules that includes the sort of clinical work, so you know, clinical neurology, particularly in the cognitive field, and looking after people with dementia, diagnosing people with dementia, looking after them also in my role, I am now leading a international project.

I'm leading the Sydney site.

The international project is called DIANE.

That stands for Dominantly Inherited Alzheimer's Network.

So that's funded through Washington University in the US, by the NIH which is a National Institute of Health, and a variety of other funders.

And that's a project that's been going on about twenty years now.

So it's like a long longa judinal study and started off as a longitudinal study back in two thousand and eight.

In fact, Sydney here was one of the first sites in Europe.

And what that aims to do is that aims to track people with a genetic form of Alzheimer's disease.

This is a rare form of Alzheimer's disease.

It usually affects people in their thirties, forties, fifties, well yeah, I know.

And what it does is it tracks them before they develop the disease.

So these people give their time and effort up when they're in their twenties and thirties and we're able to follow them over time looking at biomarker's, looking at neuroimaging to try and understand how the disease progresses, and that's been really instrumental actually and how we understand Alzheimer's disease.

And then more recently that has there's been an arm of that which is a trials unit, so we're actually been treating these people, trying to treat them at very early stages of dementia or in fact before it even begins, to see can we prevent the disease.

So I've been really fortunate to come to neuro at a really exciting time where I'm now the principle investors Togeter for the Diane Study at Sydney.

That's one of my major rules.

It sounds pretty exciting moment.

Yeah, it really is, particularly you know, in an intellectual sense or an academic sense, with practical, practical applications.

Absolutely absolutely, and we're starting to see you know, real life impacts, you know, and it is from an academic perspective really exciting.

It's a wonderful time to be in cognitive neurology.

But also it's really special to be part of these family stories.

And I think, you know, that's something which I didn't expect but has been really profinds.

A massive intimacy in that there is that they let you into their brain exactly.

It's not just in their front door, but really actually in their front door, straight inside, right inside.

And you know, we we've you know, we learn about family relationships, dynamics, we've become really meshed and everything that's going on in their lives, and it is it's a privilege, you know when they share, they share things with us that maybe they don't feel comfortable sharing with other people, maybe with other health professionals, because we've developed this sort of deep connection and relationship.

And even just last week actually for the very first time, we organized a family conference for all of the families from Australia and New Zealand to come together to Europe.

And this usually happens every year actually in the US, but our families could never make it there, so there was a big push to do it here on this side of the world.

So we did it and it was amazing.

Just just for when you say cognitive or you're talking about Alzheimer's, but does it include other things like Paginson's or m indeed maneural disease, et cetera.

We're just talking about here just Alzheimer's.

So this was just for Alshem Diane's just Alzheimers.

Diana is just Alzheimer's disease.

But I think it's a great model for us to think, for explore how we think about modern neuron disease, how we think about Parkinson's disease, because you know, in all of these conditions, of course, you know, we want to dig, we want to be able to treat people, but probably where we're going to make the biggest impact is prevention, you know, stopping these disease processes from even starting in the first place.

Or even hopeful they just slow them down.

Or slowing them down exactly because we know take Alzheimer's disease, for example, and I'm using that as a model because that's where we have the most information.

We know that these changes start in our brain twenty to thirty years before symptoms start.

So there's a huge window of opportunity that we can perhaps intervene.

And I think taking this approach that we have in Alzheimer's disease, where we can track people before they develop the symptoms, if we take that approach and we apply that to modern neuron disease, so for example, as a model, as a model and modern neuron disease.

The majority of cases aren't genetics Seemazelszheimer's disease, but there are a number of cases that are.

There's the C nine or seventy two expansion, for example, that explains a lot of genetic forms of modern neuron disease.

And what we're actually trying to do neur and what we have been doing is studying these people as well, with these genetic forms of modern neuron disease, way before they might develop symptoms.

So we can have a similar approach.

We can identify markers of progression, We can work what is the very first step, what happens, what is the very first step to set off the sort of cascade for the development of.

These Usually it's too late, and you have mentioned a few times, excuse me, have mentioned a few times NERA.

Of course, we had your fearless leader, Matt Kenan on there, the CEO of NeuRA, And maybe quickly just to explain to audience, what new is it?

Say, well, it's relatively speaking, quite a new initiative over the last few years.

But what is newer?

Do so newer itself?

The institution where you are now based.

Yes, so ner is a research primarily a research institute, but it has really strong connections with the University, University of New South Wales and importantly with the local health districts, so you know, with the clinics, with the clinical space.

So NeuRA is essentially involved in neuroscience, you know, the science behind neurology in essence, and neuro focuses on three main pillars.

Those are ner degeneration, which we're talking about now, also mental health psychiatry, which is new degeneration and psychiatry actually really quite intricately linked as well, and then another pillar focusing on translation.

And I think that's you know, the key what neur really can do is to as it's taking this science, you know, all of these learnings and then translating it into something meaningful.

And that's ultimately what we want to do.

We want to be able to influence you know, the patient's journey.

We want people to be diagnosed earlier, be diagnosed better, have better treatments.

And that's that's the essence of what NeuRA does.

It's working to really translate that science, how do we make it and how do we take that science into the clinic to change our patients' lives for the better and then how do we influence policy and all of that.

So me, what a great job, but not for everybody.

But so because this is sort of a dense topic, and we'll put it so, I have an opportunity to ask somebody who's an expert in the density of the topic.

When it comes to Alzheimer's slash dementia MND, we probably will spend more time on the former Alzheimer's slash dementia, if that's okay with you.

But because its dense, I've actually had to had a chief science officer write up the questions for me, who happens to be a neuroscientist.

But so I'm going to ask a lot of questions that she is organized for us.

And the reason why I'm doing that is because I want to make sure that I get the right or the most amount of content out of you.

If that's okay, that is relevant to our audience, the sort of things people want to know, if you don't mind.

So some of these questions aren't going to look like a normal podcast, but are normally just having a conversation.

I'm going to have to sort of lean into these questions a little bit and I'll try and explain the question a little bit and then I'll leave the answer obviously over to you.

And the first question that I've had is is the first question I have here is what's around the heading of science and neurodegeneration.

Now we know that there are a number of things that unfortunately one of four things that is ultimately going to get us.

Are they going to be a brain disease or degeneration of the brain neuro degeneration, or it could be a heart which is the most prevalent one around the world.

It could be cancer, which is the second most prevalent around the world, but neuro degeneration is a third, the fourth being metabolic diseases, which were obviously going to talk about.

But when it comes to neuro degeneration and in particular with relation to Alzheimer's slash dementia, and I'll ask you to please split those two up and tell me what the difference between the two is and M and D.

You know what actually is happening to the brain.

Like you know, if I get a skin cancer, I can see it.

I can see it at least it's sort of present, and someone probably can get a microscope and show me what's going on underneath my skin.

But with a brain it's a bit more difficult.

There are definitely no outward signs that I can see.

I can probably hear it, or I can feel it, or I can sense it, but I can't see it.

So what's actually happening in the braining those two diseases And if you wouldn't mind just quickly litting us now.

But the dificitor al's arms and dementia is okay, I'll.

Start with that maybe.

So dementia is a broad term.

It's like the umbrella term.

Basically it means neur degeneration, but it's the outward symptoms of it.

I guess someone who has a neu degenerative disorder and as a result has empowerment in their function, so they can't do they what they normally could do.

And that's just that broad, broad term.

And then underneath that, since the various types of dementia, Alzheimer's disease being the most common.

So that's a form of dementia.

It's a form of dementia similarly from to temporal dementia form of FTD associated with modern neurone disease.

In some cases and tends to affect younger people, younger under the age of sixty five.

And then we've got other forms of dementia like Louis bodied dementia, which is related to Parkinson's disease.

So Parkinson's disease can resulting dementia.

Absolutely, yeah, yeah, and the same and what all of And then we've also got vascular dementia.

Which is because when that's up usually it's like a problem with their arteries.

You basically bloodstops falling.

Up to your brain exactly, very similar to what happens with the schemic heart disease you need to develop angina and heart attacks.

The same process happens in those vessels that supply the brain.

Which is the more common one out of all of those.

I think you just cided four things.

So Alzheimer's disease would be the most common, right, and what each of those, they're distinguished by their symptoms, but primarily by the underlying pathology, as you refer to what's actually happening inside the brain, and that's what defines the differences.

That's how we define them.

And they all have their own sort of unique set of symptoms, but they often overlap, so there can be a little bit of diagnostic difficulty in splitting them out, certainly from a clinical perspective, certainly from just sitting and us just sitting here and talking.

But Alzheimer's disease is the most common, but many people have copathologies.

So they have some of each, have some of h Alzheimer's.

Debrese and vascular dementia are really closely linked and often a lot of the risk factors are similar for both.

Actually, and even the pathology that we see in the Louis body dementia, the Parkinson's disease type, it's called alphas and nucleon and we actually see that quite commonly in Alzheimer's disease as well.

And we used to think that perhaps that was because they're all disorders of aging, and if we look at older people's brains and we see all these pathologies.

But what we've seen from our work in the younger onset dementia, particularly the genetic forms of Alzheimer's disease, is that these people also have that alphasy nuclean pathology in their brains.

What is this pathology?

What do you mean?

What I'm what would you see?

What would you see when you're looking through an MRI or whatever the case may.

Yeah.

Yeah, So, so the pathology refers to the disease like within the within the actual brain structures, and those are usually abnormal proteins.

And these are proteins that are made by the brain and are usually cleared out or sometimes how they're made it can become a bit defective.

But when we look at an MRI scan, we don't see that.

We can't see that protein.

We can't see that as.

So the m I can't pick the protein up.

I can't pick up the protein.

But we do now have different type of imaging called pet scans where we can actually see some of these proteins.

So we put some sort of something in their veins, some sort of color and whatever it is, attaches to that particular protein and light it.

Up exactly take a picture and we can see it.

So that's been a relatively new discovery, but that is transforming, you know, how we diagnose and how we treat these conditions.

And I think it goes back going back to that initial question you asked me about what's happening in the brain in Alzheimer's disease or in dementia, and I think to think about that, we think about, well, how the brain is composed, and the brain is made up of billions of nerve cells, you know called neurons.

They're like eighty six billion nerve cells.

Yeah, yeah, yeah, I've actually looked this up just to confirm recently, because I was talking to my son about it and he was asking me lots of questions, so I had to refresh my memory.

But yes, they're around eighty six billion nerve cells.

But each of those nerve cells are connected to thousands of other nerve cells, so they're all interconnected.

And particularly for cognition, the memory, language, and behavior, those nerve cells are all sort of connected to each other in a network.

So it's not just one specific set of nerve cells neurons there, it's actually a whole connection of nerve cells which subserve those cognitive processes.

So, for example, memory, so your memory predominantly sits in a structure called the hippo campus, which is deep in that temporal lobe here, and the hippo campus is like a seahorse shape structure, and that is where the majority of the sort of memory cells sit.

But that hippocampus is connected through neurons throughout the entirety of the brain right back to the posterior part of the brain and rye around.

So we have this whole network of nerve cells, if you can imagine, and that's what's controlling memory, for example.

And then what happens in these types of conditions is that these nerve cells, one nerve cell, you know, collection of nerve cells dies and that's because an abnormal protein is deposited in it or deposited around it, So that cell does Just if.

I just stop there there, Why does when the protein which our body is producing anyway, but maybe fails our brain fails to clear out for some reason, why does the nerve cell die as a result of that protein Where it is the protein like poisonous or bashes it up or what was happening?

Yeah, I mean it becomes toxic, I guess because there's either too much of it.

So you know, the nerve cell count function, it's metabolism, it's nutrition count function.

If there's too much of this whelmed building, yeah, like getting overwhelmed exactly.

But why do we produce a protein in the first.

Place, So so we produce all of these proteins, and they each have their own potential function within the cell.

So, for example, one of the proteins that are produced in ours Gmer's disease is called TIE TAU, and then we have amyloid and we have TIE.

And TIE actually is really important for the structure of the nerve cells.

It mean, it's like a building block of the nose exactly exactly helps cells sort of regenerate or perhaps have that structure.

That they need, have that structure that they need, and they need that structure in order to process the signals that move along the nerves from one nerve to the next.

So actually that protein is really you know, it's it's a part of the cell.

It's important.

But in Alzheimer's disease, it becomes disrupted and it changes, it changes to a different form of TIE, and that form of TIE is toxic cells and it builds.

Up brain produce this thing that's changed in its structure, molecular structure, with a chemical structure, whatever it is.

To is that like I know.

Why, Yeah, I mean, I think that's that's the mission dollar question.

But I think, you know, one thing to say is that these nerve cells are really extremely powerful, but they're also really fragile.

And you know, we have evolved over time, you know, as a species, I guess to have these really highly evolved and cognitive processes and these nerve cells that can subserve that.

And perhaps there's something about that, there's something about that evolutionary aspect to it that makes these cells particularly vulnerable.

They're too well evolved, perhaps maybe too sensitive, and they and they and as a result of insensitive that they can get damage quite easily.

Yeah, that's interesting, an interesting proposition or hypothesis.

But I guess there are sorts of things you're trying to research and prove up over time with all your collaborations.

So it's it's if I could, if I could just go back a step in relation to the four different types of strands that fit under the umbrella of dementia.

And I think it's a terrible word because they dementia sort of makes that someone's demented, like maybe they can ultimately be their way because they don't know what they're doing and like have a sort of a madness, like in a terrible sort of sort of movie sense.

But it's just a terrible word, dementia.

I just anyway, And I actually understand that for people over sixty miles over sixty is the most research word on the internet.

Okay, yeah, most research word dementia is for men over sixty.

But because it has created a whole lot of concern and worry, like everybody over sixty seeds to be worried about this because they don't want to lose their marbles.

Basically, it's probably not.

That's a very crude way of speaking to a scientist, but yeah, but that's sort of But if I could just look at the four prongs, if I just look at them, liked for the audience purposes, which is sort of my mind to just simplify it.

So probably the only one I can understand, I can't really understand, but I can sort of put a label on this vascular dementia.

And the only reason why I know that one is because one of my uncles had has bascular dementia and I spoke at lengths to Matthi kin And about it.

And basically, like your arteries that feed blood and oxygen and nutrients up to your brain, if they get blocked, brain cells neurons stop getting fed and they can die off.

And if you lose them in the wrong spot.

I guess in relation to say memory in memory area or your speech or whatever the case may be, or just the ability to make decisions, decision making part of your brain.

That is how you get vascular dementia.

Is that correct, sort of in a pcrude way.

In a nutell yes, essentially, And that's often I will explain it to people.

You know, it is that sort of that accelerated edge as such, for or for vassals when we're when we're young, we have these beautiful smooth vessels and the blood flows through it and you know, really lovely mano.

But as we as we age, there was vassels change, you know, as not part of normal aging, but that can be accelerated through that.

But lifestyle can accelerate that too.

So exactly, and Matthew explained to me, is what's good for your heart in relationship vascular dimention, what's good for your heart's good for your brain.

So you know, basically a good healthy lifestyle which made mean you know, you don't have any heart conditions.

What I mean by that is a plaque and clogging up and stuff like that could also be good for to help you at least manage your way through getting vascular dementia, smoking alcohol, crap food, no exercise, et cetera.

So, but wet does into the vascular dimension.

Wetters genetics fit in.

So in other words, you know, like having inherited tendency to have these things, Where does that fit in?

Yeah, well, I agree with all of all of those points that you mean, and I think all the lifestyle factors are extremely important.

But the one thing that we can't change is genetics.

You know, we're born with that.

It's sort of what we're given and then we have to work with it.

Certainly for vascular dementia, I think there's a significant component.

You know this, well, it's not inherited in the way of some of these genes we talk about from modern neurons for example, or for Alzheimer's disease, in that if your parent has it, you know, you have fifty percent chance of developing it.

But I think definitely there are there's lots of evidence there to say that these vascular phenomenon are definitely have a genetic a genetic component to it, and we see that particularly in younger people who are affected by strokes.

Well, for example, you know, you can you can see that clustering of strokes within certain families.

So yeah, I think genetics does play a part in it.

And then it's as understand it for Vescuala Adventure, it's sort of fairly simple to go and get a crowded doppler an ultrasound downe on your when you're crowded arteries.

It takes like, yeah, twenty minute and they can at least sort of tell you listen, he mark you're got.

You know, those arteries are starting to clog up a bit, and we'll maybe ever give you some medication to do something better, or maybe there's some intervention.

Is that correct?

That's correct?

I think yes.

You know, often that can be okay, right now I need to do something.

It can be that sort of defining moment, can't it.

We're right, okay, I'm at that stage and I can see my lifestyle or whatever environmental factors are having it effect on my body and my health.

So often it can be that defining moment to step in and make a change.

Obviously, it would depend on the degree of blockage.

So if you have what will be called a critical stenosis and that it's there, are sufficiently reduced blood flow going through that corotid artery for example, up to the brain, up to the brain, and then in some cases that might require actually a procedure where you can put a stand in there, like you put a stand in the cornary arteries and open them up.

So that's that's a possibility.

Also, it can just tell you, I give you an ex you know, an idea of what your vessels potentially look like.

And also we can do when we do an MRI brain, we can actually see some of the effects of that clogging up of the arteries, not just the corodid arteries, but also the vasculature right within the brain.

Know those you know, as as the arteries move through through the brain, they get smaller and smaller, So any disruption in blood flow can have a significant impact as those vessels get smaller.

But when we look at an MRI in someone who has significant vascular disease, we often see a lot of what we call little white dots, and those are the effect of the vascular disease.

It's it's it's like, I guess, it's like little areas of where the brain has died, cells have died.

They're tiny, tiny.

But you can see it.

We can see it.

Do you have to put some sort of dyeing in the system or just to light it up where you can see it in it just in the right you can see the white dots or whatever it is.

Yeah.

But in the un MRI, they use different sequences to look at different structures or to look at the white matter or the gray matter in more detail.

So there are a number of different sequences that they use an MRI, and some of them make water bright, some of them make fat bright, some of them make tissue bright.

So there's a specific sequence which is part of a typical MRI where you can see quite clearly these sort of chronic we call them chronic microvascular changes.

So if somebody's in their family has an uncle or auntie, whatever mom, d ed, whatever the case may be, who has been diagnosed with vascular dementia or perhaps even passed away, and let's say they're in their thirties, what should they ask the doctor the GP.

So I think that for them, I think they need to be thinking about having a sort of vascular sort of check up with their GP.

One thing they need to talk to their GP about is smoking.

You know, if they smoke.

They should most definitely stop because we know smoking definitely contributes to those white dots.

Checking their blood pressure, having their cholesterol checked, those things are really important, maybe every so often having a test for sort of diabetes or pre diabetes.

So this is there some relationship between diabetes in vestal lit dementia.

Absolutely absolutely, and even between diabetes and an Alzheimer's disease really yeah, So that that I think that speaks sort of metabolic aspect of all of these new degenerative conditions because we talk about abnormal proteins.

Absolutely, this is the pathology, that's what's happening in the brain, but there are lots of other factors involved as well.

What kicks off that pathology, you know, what's what makes why do we have why in Alzheimer's disease?

Can we not clear that amyloid or tow pathology as well as we should do?

So there are other factors involved in sort of kicking those processes off, and that might be neuroinflammation for example, And we know diabetes and metabolic disorders are really intricate in terms of neur inflammation, particularly in relation to neur degeneration, and in fact or maybe I'm jumping on a little bit here, but actually there are some clinical trials happening at the moment using weight loss the g lp one.

Zampi as an example of gop one.

In early Alzheimer's disease.

You mean as an assistance to not getting it or it causes it.

I don't understand.

So the clinical these clinical trials are an early Alzheimer's disease, so people who already have diagnosis.

Yeah, and sort of the build up of the protein.

And the question is can these drugs slow down that process of protein build up or can they clear out?

Can they help clear out some of that amloid and how might they do that?

And I think that is tard because those drugs are also used for diabetes, and I think it's originally exactly exactly, and it's targeting that potential and neuroinflammation and how that interacts with these abnormal proteins in the brain.

So let's now move on to the more complicated for my point of view, at least the more complicated ones.

So let's move on to probably the next popular one that in my mind anyway, Alzheimer's.

What do we You mentioned a build up of tow and build up of amyloids.

And you mentioned that tow is an important protein in the brain.

I guess amyloid is too, for the same reason.

But somehow we're doing it too fast or too much or not clearing it, or what's being produced is a little bit a little bit crazy because they're not quite the right, you know, somehow varied in terms of okay, so and that's happening.

So what does that do?

Is it sort of only stop our memory or because Alzheimer's sort of associated with I can't remember something or I can't remember someone saying because like I'm this person, like you know, I'm not young, but I'm once was like a I can't remember a person's name, though, but I will remember it a bit later on and I remember again, Matthew saying to me, don't worry.

That's more memory loss through like anxiety, brain anxiety, like memory on anxiety, as opposed to because I know so many people say this, my god, I reckon, I'm getting out someone like I just can't remember something.

Rather, it's not that I forgot where my keys are, I can't remember someone's name, or I can't remember that.

Well, sometimes you can't remember a word you're searching in your brain for this word?

When do we start to get worried that we might be getting Alzheimer's disease?

I mean, and I think that's that's really common, and we see a lot of people in the clinic, you know, especially in midlife, I'm starting to worry about you know, those sorts of cognitive symptoms that maybe they've experienced before but haven't put it as much cillions on.

It in midlight being like forty plus sty plus.

Yeah, yeah, I think the definition of midlife is a bit open, but yeah, from forty onwards, and we tend to see that when should we start getting worried about it?

Well, we know in Alzheimer's disease, for example, the very first deficit that we see is in learning, is the ability to learn something something new.

And often that that doesn't usually manifest in people's day to day life, but often we can see people start to struggle at work.

You know, perhaps they've been going along, everything's been fine, and then something new is introduced in work, maybe new software, you know, they have to learn a new curriculum, a new skill exactly, and that's when people start to struggle.

So that can often be one of the very first features is that problem with learning?

So Emmica, don if you just explained what do you mean by learning?

So let's say I'm learning a new I'm learning new software in the business that I'm running or I'm involved in.

I might be an IT guy a girl and they say, look, we've got some new software which we're now going to get ten licenses for for the organization.

It might be something about, you know, how you use AI to build marketing programs or something like that.

How would I know that I can't learn that?

Like, is it like it just becomes a fog or what is it?

What?

What what symptom am I thinking about?

Well, yeah, people do describe it as a fog sometimes, and I think it just becomes more difficult to do it.

It feels more cognitively difficult.

People are really struggling to learn the concept, where before maybe they may might have picked it up really quickly, but people are really struggling to and then to integrate that into their day to day lives so often or into their day to day work life.

So something that might have, you know, taken them a short time with the old software has no taken a really long time to do with this new software, for example.

And do those people present to you guys at in the clinic part of the business.

Yeah, often often who.

Send them there their doctor or do they find you?

How does it work?

I think it's a combination.

You know, people who are very self aware.

People, as you say, are becoming more aware of Alzheimer's disease, off demension in general and their risk.

So people will go out there and try to find information, try to find specialists people who might be able to help them.

But then also you know, GPS know general practitioners and also other specialists.

If there are sort of more complicated cases, particularly people who might have genetic forms young forms of dementia, other specialists might refer them through to us as.

So, and when these people come in, do you put them through a test?

You know, obviously they're giving you some observation that they've observed it.

Do you have a testing program?

We've sort of put them through cognitive tests, you know, ask them to learn a new formata or something, you know, and see how they perform.

Yeah, we have.

Every assessment is slightly different as every person is different and they have you know, different concerns and they might come with family members or by themselves, but essentially a lot of a lot of it is history taken and that's a huge part of what we do as neurologists sit down with the person, take the time to listen to their story, read between the lines as well.

We'll talk to family members as well, usually separately, to give them the opportunity to really explain how life has changed for them.

And then usually we do a variety of bedside assessments.

So, for example, I will often show people a number of different animals, actually little animals, and we ask people to name them.

Some of them are sort of rare animals that you might not necessarily exactly exactly, and then we ask them questions.

We asked different questions, and this is just one example.

But you know, you can actually get a lot of learning from that.

You can actually learn a lot about where the where the person is at.

We can understand, we can learn about language, we can learn about comprehension, we can learn about memory.

There's a whole host of cognitive functions that we can get from those simple sort of bedside tests.

And then we have more standardized and cognitive assessments.

We have screening tools and then we can do more detailed neuropsychological assessments.

So, for example, if it was someone with language impairment, we have this battery of tests that we can really sort of not down on try and get to the bottom of where actually the problem is in language, and then that helps us understand what might be driving it.

Would you then then say, look, we've got to come to this conclusion.

We're going to put you in an row under an emerald.

You shouldn't have a look at your brain.

Yeah, that's and that's usually.

The gold standard at the end of the day.

Yeah, yeah, usually most people.

Often people will come haven't already had an MRI, right, we will.

We like to look at them ourselves.

Were looking for specific patterns of So the MRI looks at the structure of the brain.

Doesn't tell you anything about what the brain's doing, but it tells you what the structure is.

So if for example, we have a patient with front of temporal dementia and when we look at their Brian scams, we see changes, We see what we call atrophy, which is shrinkage in the front and the temporal parts of the brain.

It's around the temporal side.

The front and the temporal around around those regions.

So every each dementia syndrome has its own specific pattern that we see on MRI.

Right, Yeah, I get that.

So do you ask them, for example, when it comes to Alzheimer's, do you ask them, for example, have their head to suffer brain trauma?

Yeah?

We do.

Like, for example, let's say somebody had been a rugby league player, or a rugby union player or a boxer.

Is that important brain injury?

That is important?

I believe that is important.

And I think you know, that opens a whole other box, you know, in terms of research, and you know, we know a little bit about it.

Definitely, we ask people about it.

And I've seen quite a few people come through who have been in the professional sort of realm.

Different contact sports, contact.

Sports come through who now have a diagnosis of dementia or al sign disease.

People often want to know that this cause it.

Right now, we can't tell them that we don't know for definite, but certainly it does seem to be a risk factor, so.

It would appear to be relatable but not necessarily causative.

So in other words, it's in so many percentage of the cases you can maybe able to show that there has been a brain injury for that for so many percentage of cases, but you can't say that that's what's caused those cases.

Yeah, yeah, we can't say for definite the only and that sort of merges then into well, you know, head injury, is that a risk that's a risk factor for the development of Alzheimer's disease and amalloid pathology.

But then we have CTE, you know, and that's a different pathology, but we can't diagnose.

The only way we can tell that pathology there is when we look at the brain under a microscope.

So in life we can't.

We can't, So that's a that's what you only look at it once they passed away.

Yes, when you get you actually get access to the brain.

And that's the way it used to be for Alzheimer's disease.

Really, you know, before we had these methods of identifying the protein.

For example on the pet scans that we talked about earlier.

When we give people a tracer, we take picture a treser for amloid or tie, and we take photos of the brain and we can see the amloid and the tie, or we can take a little sample of the fluid that surrounds the brain and the spinal cord.

So we do a lumber puncture.

I don't know if you've ever had one of those.

Yeah, I know what they are.

Yeah, yeah, people they're pretty freaky.

Yeah.

People don't love them.

They don't enjoy them.

I never the back of the head here, at the back of the.

Neck, bottom of the bottom of the.

Back, bottom of the back.

Yeah.

Yeah.

And you can take some of that and that fluid that you take out, that fluid cushions the brain and the and of course what's really close to the Brian and you can actually measure those proteins and that fluid.

So that way we can we can tell what pathology is in the Brian.

So we can do that for our Seamer's disease, but we can't yet do that for some of the other conditions.

So so Alzheimer's disease is traditionally known as sort of like if I put it into normal pilance, it's like forgetfulness or loss of memory, where people don't don't even know who someone is in the room.

For example, you know, I may have me marriage him my whole life, but one day I don't even know who you are.

I might not even recognize my kids they when they are in this condition.

Do they know that potentially they don't recognize their kids?

These people aware that they might not be were as a particular persons of my child.

But do they think to themselves, maybe that is much and I don't recognize them.

Do they understand?

Can they understand that much?

Or is it just a memory thing that they've lost?

And do they get depressed or feel terrible?

Those are Those are all really interesting and considerations, I think, and something that's important for us to think about as well.

You know, what is what is that person with Alzheimer's disease actually experiencing?

And Alzheimer's disease is more than just memory and as is you know, many of the other types of dementia as well.

You know, it also affects their behavior because I've.

Heard something be quite violent and angry.

Angry, angry and agitated, and that is part of the condition.

And that is because it's the disease itself has changing their brain.

It's changing those connections, it's changing those networks, and it's ultimately making people less tolerant.

But it is it's a actual a part of the disease.

And I think that's really important for people to understand because that can often be quite detrimental to relationships.

You know, people think, oh, they don't they hit me, they don't like me, you know, we've lost or bond and all of those things.

And I think it's really important for people to understand that it's not them, it's not the person themselves, it's the disease, you know, and that's what's driving.

I have a friend who's he's not old, well, he's in his sixties, but unfortunately had to go to a home because he has Alzheimer's disease.

Had to go to a home because he was sort of a very aggressive towards his family but probably doesn't even know it's his family and probably doesn't even really know what he's doing.

And unfortunately it was too dangerous for everybody to be present because and he had to be sort of it's called put in a place where they can manage him.

But like, I got a shock and I heard about it because he was never like that as his whole life.

Not that person, not that person.

Can we maybe we just talk about M and D.

M and D is one close to my mind, because my heart, because my mother passed away from moder neuron disease or ALS.

And actually that's where I meant first met Matthew kin and when he was at the other place, Brand Mind Center.

It's a bit more complex to me.

It seems to me not complex, a little less understood perhaps, But maybe you can just explain what there's a couple of forms of moder neurons.

But maybe you just explained to our audience what mode neurone disease is that where and or otherwise known as MND.

Yeah, well for us, well, I'm sorry to hear it about your mom.

It was.

It's the worst disease to watch someone suffer.

She was, like you, she didn't get until she's eighty six.

I also would like you to include in that the genetic part of it, because it's only accounts for a small percentage as understand it of people who get it, and a lot of people can get it without but without mutations on their genes.

So but maybe you can explain both those.

Yeah, sure of course, So what is modern neuron disease?

Well, and also modern neuron disease has a few a few names also known as ALS.

Als is actually the most common form of modern neuron disease and modern neuron disease is that umbrella term.

And then sitting underneath that, we have a LS amiotrophic lateral sclerosis, which is the most common type, and then we have some other types bulber, which affects the predominantly affects the speech and the swallowing muscles.

And then we have two other variants.

One is PLS, which primary lateral sclerosis, and people with this this is much rarer.

They tend to live longer as well, and that predominantly causes spasticity, an increased tone and people.

I think he had.

A really really he got it quite young.

He did right, and he lived he was you know, that's an exceptional case.

That's not usually the way.

But he's a good example of what I consider the spasticity effect because he could move.

He didn't move, he didn't he couldn't move.

No.

I think in the end he had a tracheostomy.

Yeah, And that's that's a rare form.

And then there's another form p m A, which is primary musculotrophy, and that's that is a weak flacid so as opposed to the sort of stiffness people have a have a flascid weakness, but the most common type is is als and we use that interchangeably with modern neuron disease, and I guess it is what it says.

It predominantly affects the motor neurons.

To come back to all those neurons in the brain there, the neurons themselves specialize in a different ways.

One is into function, and so the motor cells are those that control our ability to what talk, eat, breathe, all of those physical functions.

And in modern neuron disease, we predominantly have a disorder of those modern neurons.

So people it can present in a variety of ways, but generally people present with weakness usually in a limb, or that can be in the speech and the swallow muscles.

And then that progresses over time over a short period of time two to three years.

Finally, it usually affects the breathing muscles.

Can they end up passing away from.

Random usually that's usually the case.

Can I just share with you in the audience on what happened in relation to my mother?

Is interesting enough, you said, because my mother is quite a talktive person and love to have a chat and I would ring her most not some my way home from work, mainly because I would say to Mom, and Mom, I have work, which means she knew she had like forty minutes.

And I would say, I'm home.

I'm going to go to my dinner, which means I could stop the conversation.

God lover.

But one night I remember driving home and my mother didn't drink.

And I was driving home and my dad didn't mind a whisky.

My dad didn't mind a whiskey every them, but Mom didn't drink.

And I said, Hey, Mom, did you have a drink with Dad tonight?

And she said, no, no way, you know, I know, no, dear, I said, but you sound your speech sounds a bit dumb, like you've been drinking.

Hey.

I didn't think much of it.

I thought maybe she didn't want to tell me something.

It's none of my business.

She didn't sound drunk, just like a little bit slurred.

And then that went on for a few weeks, and then I said, I convinced her that she should go, and my brother and sister also were convinced her that she should go to the doctor.

We need to get to see neurologist.

Got down to see a neurologist down here at Saint Vincent's and and then they sent her off to the BMC Brand of Mind Center, and that's she was diagnosed there.

But the process Emma would was at first her speech was slurred.

Then she couldn't really speak, so she used to write everything down.

She's to communicate by writing.

But then she lost the movement of her hands.

She and she couldn't smell properly, she couldn't taste properly.

This is the progression.

Then she couldn't walk.

Her legs sort of gave way on her, but she could hold herself up.

She was sort of quite strong, pretty determined woman.

But then she was on like an a frame type thing, one of those things that we will around.

Then eventually it got to the point where she couldn't control its various things, boughs and things, so that it got to a point where they put it into pallet tip care and then she ultimately passed away from the moment she because everything she taked she couldn't swallow, so it gets into the lungs and then infection occurs and they pass away.

They stop breathing.

And for anybody who's never never experienced out there.

It was the worst thing to experience because their brain is she can think of everything.

Her eyes were perfect, she could read and stuff.

Then she could observe and think like she could never be was like she was trapped a terrible outcoming, and I just want to share that but as a process.

But one of the things I found out at the time, and this may well have changed, was that it's actually quite a prevalent disease amongst in Ireland and amongst people with Celtic backgrounds.

And that I also found out, and maybe this is advanced because it was quite a while ago when she passed away, maybe years now, But one of the things I found out was that you can have the genetic mutation, but you can carry it your whole life and nothing ever happens to you.

But under certain circumstances in lifestyle they can sort of wake the mutation up, for example, alcoholism, exposures to poisons, and or in her case what they said to me, potentially what happened was a severe respiratory disease.

So she got like like one year before she got mand she had a really bad she had the flu in the winter and got really bad, like really bad chest infection and lost a lot of weight as a result of it.

And literally about three months later that's when she started these symptoms started to come on.

In the six months she was gone.

She was eighty six, she was the eighties, but she was quite frail.

But is that Can we just talk about that for a moment, like, because a lot of Australians have Irish background or Celtic background one way, without the Scottish or whatever northern Europe, and let's talk about these mutations because they don't really know which mutations were relevant, or at least they didn't been able to tell me.

They sort of said this category ABC, where there's correlation correlations, in other words, people who've died from this disease had these mutations, you know, on these particular genes, and say fifty percent of those people had this correlation, and then the category aboo was only thirty percent Category C.

Is that because people don't try and get tested.

I did, and I went and try to get tested for this stuff, and I was fine.

I didn't have any The current back five years ago, four years ago, current thinking that maybe new new changes to that now, could you explain that part to us?

Some about mutations, you know, bring then the mutation perhaps been set off later on in life as opposed to early early early disease.

And maybe I've got all that wrong, that's just my memory.

Yeah, no, No, I think that's a super interesting area and it's something I've been particularly interested in throughout my academic career.

And perhaps it is that Irish link as well which has sparked that.

Interest, same as what definitely spoke my interest.

Yeah.

Yeah, And really interesting is that this one particular mutation.

So about ten percent of modern neurone disease cases are probably genetic and the majority aren't.

But this particular mutation is called the C nine or seventy two expansion.

It's actually an expansion in a part of the DNA code, and that has been traced back to a single European founder.

Wow.

Yeah, And actually you can trace you can trace how it's sort of spread throughout Europe if you trace how the Vikings sort of plundered their way throughout Europe.

So we see this specific mutation in Europeans and particularly, but also we see it sort of in areas where the Europeans then spread too, So we don't see it in Asia very much, but certainly we see these strong postures in Europe, particularly in Ireland, which obviously has a strong Celtic heritage, and also in the U.

So that's fascinating.

But you know we're born with it, right, so you know when it's passed, and it's passed on in what's called an autosomal dominant inheritance pattern.

What that means is so you get two genes for everything, basically, get one from your mother and one from your father.

If you inherit this abnormal gene, you just need one copy if they have normal gene in order to be at risk of developing the disease.

So that gives if your parent has it, you have a fifty percent chance of carrying the genus.

If both parents have it, then I'm trying to work for you.

Yeah, you have a seventy five percent risk.

Wow, it's not again, it's not that provo, it's not that prevalent.

I wouldn't expect you'd be very unlucky for two for two parents to carry it.

So so yeah, so that's and that's called this, as I said, the C nine or of seventy two, and that causes more on your own disease but that also causes a related condition called fronto temporal dementia which we do FTD, which we touched on a little bit earlier.

And for a long time before this mutation was discovered, they knew that there were families where there was clustering of both FTD and m and D, and actually there were some people who had both.

And if you had a combination of both both FTD and m and D tended to have a worse prognosis.

Things tended to escalate and deteriorate faster.

So that sort of finding that gene was really instrumental in helping us understand how those two conditions overlap.

So people with more on your own disease, as you say, like your mom, usually their mind is bright.

You know, they don't have any change in behavior.

But in a portion of people they do have some of these features of FTD, and that can actually be really devastating for the families.

In addition, to have an MND, you now have to try and deal with changes in behavior, changes and personality, and that affects how people make decisions and you know, family, the sort of family dynamics and all of that.

So that gene has sort of finding that gene has consolidated that overlap.

I guess also helps us as clinicians make sure that we're asking people the right questions because people don't always volunteer.

But why are some people this never expresses someone till the lady seeks, like in my mum's case.

So yeah, yeah, so you asked me about that.

Yeah, well that's another excellent question.

There's been recent research that says in order for M and D to be sparked off or kicked off, you need six separate steps.

So these sort of six separate things have to happen.

And that could be exposure to your talks and you knew, it could be a stress, it could be a life event.

But if you have a genetic mutation that numbers were just to three, so you're more vulnerable.

Right, we need three events to happen.

Three one or three or all three.

Three, but any three of any any one of the yeah, which and we don't know what they all are, what they all are.

It's not uncommon for people to say that they've had a trauma just before before the onset of modern neuron disease.

I can think of I paid one patient in particular who had fallen and broken their leg, and they had their leg was in a cast, and and and then when the cast came off and they were going through rehabilitation, they had a foot drop, you know, And that was the start of MND.

Wow.

So some people have those stories where it's really clear and you can sort of identify a potential trigger, and other people it's less you know, less obvious, but no doubt, it seems like there are those particular steps to make people too, I guess spark the on.

Set of well, if it's only ten percent, generally speaking, affected by the genetic mutation that they carry through their parents.

They.

What what are the what's the hypothesis now around what causes that?

Is there anything we can avoid or should avoid in order?

Have you found anything that tells you that there's a problem in the way living a lifestyle?

Mark?

Well, the things you're not doing, perhaps you're not exercising enough.

What would we should we be looking at to avoid these things?

Yeah?

You know, And for M and D that sort of flips all of the other lifestyle advice on its head a little, but not completely, but to an extent in that I guess it and what it tells us is maybe everything in moderation because we know that M and D is particularly prevalent in some sort of elite sports.

Wow, yes, yeah, yeah yeah.

So we don't fully really understand this yet and that's another area of research which has been very sort of active recently.

But certainly there are some elite sports partic release soccer players where there is an increased risk of modern your own disease.

So whether that's no, there's it's hard to know.

There's there's two theories to this, whether it's the actual exercise and the level of exercise that's contributing to that, or whether there's something in the genetic makeup of these people who are destined to sort of be you know, elite sports people, whether there's something in that genetic makeup that also makes them more vulnerable modern neuron disease.

We don't know the answer to that yet, but I think you know in that all of these avenues are open up potential routes for better understanding of the disease, diagnosis, and management.

So I think it's really important that we explore all of this.

So if if I, if I go back to as understaid, there's no Q forneron he's at this stage.

But if I go back to dementia, you turn on the TV at home for those who still do that type of thing, and it seems like every week there's a story on the national news about some new development in dealing with dementia is usually what they're talking about, and I presume that they usually talk about Alzheimer's.

I think, where's that up to now in terms of taking a pill or whatever?

There is that the big farmers doing, or you guys are doing, or someone's doing.

Is there some Are there any green shoots that we can now see in relation to dementia, for example Alzheimer's.

Absolutely, this is quite timely, I guess because only in the last few weeks have we had an announcement from recently Yeah, yeah, yeah, Just in the last few weeks we've had an announcement from the TGA, the Therapeutic Kids of Ministry in regulator, yeah, to say that they have now registered the first disease modifying therapy for Alzheimer's disease in Australia.

Wow.

Yeah.

And it's it's therapy as in as in it being a drug.

It's a drug.

Yeah, yeah, Yeah, it's a.

It's called dynanamap.

It's actually an infusion.

You have it every four weeks, likes intravenous infusion every four weeks for eighteen months, is what the trials have done so far.

These are type of drug called monoclonal antibodies.

So that this isn't that the same thing we use for covid monoclona anybodies.

Isn't that the same sort of antiviral that we got for covid, Well that will call it the same thing.

Yeah, Monoclonal antibodies are used for lots of different conditions.

Also use we use them a lot on multiple sclerosis.

Basically, it's trying to harness your own harness sort of the immune system to target these proteins.

That's that's certainly what we're doing in Alzheimer's disease.

These are our drugs that are made in a laboratory.

Obviously, they're called monoclonal antibodies.

So what an antibody is produced when it's when it as part of your immune system, when it's exposed to what's called an antigen or a protein.

So what we're able to do, not me personally, but what they're able to do in the love is actually produce antibodies against this amyloid protein and then they infusion infuse it.

Essentially, what those antibodies do is they bind to the amyloid and they pull it out of the brain.

Wow, and somehow expel it somehow through the bathroom.

Maybe you can just explain.

I don't understand this part, but I've heard about it where only certain types of things can cross the blood brain barrier, because this is there some sort of barrier regard around your brain to stop things from getting into your brain that the brain doesn't want to be dealing with.

How does it work?

Essentially, that's it, because we need to protector.

I think we need to protect our bran.

The brain needs to protect itself from everything else that's going on in the body.

And yeah, that's the term blood brean barrier.

And essentially that can make it that can make it difficult for certain molecules, especially larger molecules, to get into the brain.

And that's protective, but also when we're trying to treat these conditions, it makes it more tricky to how do we deliver these how do we deliver these drugs so they will cross over the blood brein barrier.

So these mono monoclonal antibodies I can't remember the name of that you mentioned to me.

They're obviously able to cross the blood brain barrier the brain and get to these proteins and attach themselves to it and somehow exit them.

How would we normally, just because as I understand that we were all producing these amyloids and tow et cetera all the time, but somehow we manage to get rid of them every clean them out every day or whenever.

How does that work normally?

Yes?

Nor normally?

How we get rid of these amalloid.

Protein so we don't build up excessive amounts.

Yes, there's a few different mechanisms for hobey get more naturally, Yeah, naturally naturally.

Actually, during sleep is when we do a lot of clearing out of the tox and stuff which.

Are part of sleep, because you know we have the light sleep, deep sleep, ram sleep.

I mean, is there is it a part of the Let's say I'm a light sep which I am.

I'm a light sleep and I never really go into too deep a sleep.

And we are trying to do something with you guys at neuro again and has been fantastic to us, like there's such a depth of access and research and you know, like relevancy for this whole project and Ford Australians need to understand.

But certain parts of sleep are really important for us to go into in order, as I understand her, for this clearing process to happen, you know, with the garbage getting cleared out of your brain, if I can put it in vernacular.

And we need to because one of the things I remember my mother, you know, it has never slept.

She used sleep four hours a night for a whole life and often one of whether that was had some sort of part of why she got ill right at the end.

And my father, on the other hand, is used to sleep like eight nine hours every night, no problem to go to bed, took one wake up, didn't even move the whole night.

And and because I'm thinking about myself, you know, because because sleep strategies and sleep systems I think have become more important for Australians to think about than never before.

Not because you just should sleep, but because of the sort of things you're talking about, like clearing the brain out while you're you know, because that's what the brains trying to sort itself out, you know, maybe could explain that a little bit.

Yeah, I've been thinking more about this myself as well.

Actually, the more we think about that process exactly, you know, clear clearing the brain out and how do we stop the build up of these of these proteins.

And actually, for many neuro degenerative conditions, people often have difficulties with sleep many years before the onset of symptoms, so there's definitely a relationship there.

And particularly for Parkinson's disease, abnormal sleep is actually a huge part of the actual syndrome.

But even for Alzheimer's disease, we know that people's sleep is often disrupted for years before.

Now is that does that is that a risk factor?

Is that person sleep contributing to the build up and the lack of clearance that's one question?

Or is it actually a part of the disease.

Yeah, that's the chicken in the you know.

I don't think we know the answer to that to that yet, And I think by one one project that we're really interested in doing is studying these people, these genetic carriers early early on before they develop symptoms, to try and work out when do these sleep patterns emerge and how is it related to these the pathology that we see in the brain, inflammation in the brain, How does how is that all related to help us work out what comes first?

And should we be really targeting sleep?

You know?

Is that something that us is a society, need to think about more.

So many people have per sleep totally, so many.

People, and all we just think it's okay, and and some people just think it's a badge of honor to like particularly too honestly, in your game is a research game because you know a lot of you guys, because I've had some experience with them.

You know, you up to two o'clock in the morning doing your work, and then you might have kids and you're up next morning at six am to get the kids off to school.

And you just think, well, that's normal because that's what everybody in my profession does, and that can equally be applied to people to shift work, people who do run businesses et cetera.

And I know a lot of people think, oh, I can get away sleep in five hours.

Later they're in their thirties, they say I can get away with sleeping five hours a night, And to be honest, I was one of those people.

So as I said, I thought of it as a badge of honor.

Who needs to sleep?

I say stupid things like I will sleep, I will sleep forever one day, so I don't need to waste my time to sleeping.

Now, that was my logic.

The only problem I didn't realize is that can actually beating my forever up, the onset of forever.

I could be speeding that up by making that statement and living that lifestyle.

So sleep is a big, big important thing.

Do you guys have Are you doing much research in the sleep in terms of its contribution to like the things that we just talked about Alzheimer's under the general dementia banner.

Yeah, that's something that we're really starting to look at and trying to build a research program around that.

For example, we can we can look at MRI scans and we can use some of those different sequences to try and understand that what's called the glymphatic system, which is like the system that clears clears the toxin.

So there are there are new protocols that allow us to look at people's MRI scans and determine the maybe the health, let's say, of their glymphatic system.

Do you do that whilst they're as sleep.

Do you do the m R Willers or you can they're awake.

When they're awake?

When when we do that, ideally we would it would be great to do some of those white pick white people are asleep, and that's something we will look to perhaps in the future.

But that's not that easy.

You have to change oern machines before someone's going to go yeah, well exactly, it's too scary.

It's not easy to fall asleep and say no.

If you what's was you wake up and open your eyes and you've got this thing right there and you've got this noise going on, that that that would be they would just scare the But Jesus out of me?

Can I just before wrap and I really appreciate time has been fantastic, very edifying.

Can I just ask one we think you mentioned right at the beginning as part of the Diane program.

You're looking at younger people because most people think of these things as all persons disease and probably they mostly present when people are older anyway, But is there a can you share with us?

Do young people get to me to actually get dimensionally someone in the thirties and forties is that something that happens.

Yeah, unfortunately, yes, wow, yeah, I mean it's rare, thankfully, but it still happens.

We have people in their thirties who have Alzheimer's disease.

We have people in their thirties who have lost all the other members of their family through Alzheimer's disease.

So yes, it definitely does happen, and again that is rare.

But even thinking about you know, front to temporal dementia FTD M and D, I mean that can affect people, you know, very very young, in their thirties and their forties and their fifties, and you know part of that obviously, for the Alzheimer's disease, it's usually genetic, so usually they've sort of been passed down one of those genes from a family member.

But what we're trying to do through the dayan project is workout is there a way that we can prevent Alzheimer's disease and these populations, and then that has brighter implications for the entire new degenittive community, because if we can prevent it and these younger people, perhaps we can prevent it and older people as well.

And it just finally, I think you said that you are looking at not symptoms, but perhaps some sort of signs, whether they're in your blood or in something or other very early that might be telling you that when I might be thirty, but when you're sixty, we know that mark.

When you're sixty, you're going to get on one of these diseases, one of these neurodegenerative diseases.

But we can tell when you're in your thirties because of this, this and this is there some research you're doing now to sort of work out really really early stages someone that has a predisposition to this.

Yes, yeah, that's exactly part of part of what we're doing at neuro and with our sort of international partners is trying to work out can we really pin down what this risk profile is, but also are there any good blood markers or markers in that spinal fluid that we can take an individual And it's all about individualizing it.

You know, what is your own personal risk because we can say your risk is whatever, but that's that's meaningless really unless you can individualize it.

So yeah, that's what really what we're trying to do.

What we really need is sort of objective markers, something that we can measure that and if we repeat it again we get the same result.

And that's really what we're looking.

Towards, or a change like an increase.

An increase or a change exactly what we.

Do with a PC test exactly exactly.

You know that if it's if you're one and a half and somehow the next time we have you tested, you're two and a half, that delta the change, the difference between the two sort of is indicative that that could mean you've got something that's going to happen.

It's going to.

Happen exactly, and maybe we're moving towards that sort of an approach for demanchia.

You know, we're screening.

You know, we do cancer screening, right, you know, are we moving towards a world where we have de mansia screening?

And I think that's that would be ideal, But we need a whole lot of infrastructure, We need a whole lot of change in order to move to that spe.

Perhaps change an attitude too.

I think so, because we tend not to think about these things until we're getting older and someone else in their family's got it.

We don't.

We don't think of brain diseases the same way as we think of cancer or heart disease.

Where do you just finally am where do you see Where does Australia sort of rank them?

I don't mean that in a hard, hard, sort of cool way, but we up there with everybody else, so we as good as everyone else in this research around neurodegenerative diseases, particularly at neuro So like, where do you think you guys are going?

You're happy with where you're at?

Relative speaking?

Where you want more money or what are you after?

Everyone wants more money, more money, everyone's after money to research.

But you know what I'm saying, because EUROS a pretty big institution.

Most people don't even know about it, like it's a big joint.

It's got a beautiful building, ramwek.

You know, David Gonski loves being the Chancellor of the University of South Wales.

He's very proud of it.

But not many may people know about it.

And I know it's doing great work.

Where do you think you guys rank?

You happy with where you're ranking?

I think we're ranking pretty good.

But I think we also have a lot of potential and I think you're going to see a lot of cheat you know, a lot of progress, particularly as we're in this really important fears for dementia, and I think you're as sort of we're ready to take on the challenge and to progress and international stage.

And I definitely think we're already there.

You know, Professor Kiernan recently was a poor international sort of pool looked at all different types of publications and things.

He was ranked number one from Modern your Own Disease Well Research globally.

In terms of publications or his name being on publications.

I'm not sure exactly what the metrics were, but certainly he was.

That's pretty cool.

Yeah, yeah, yeah, So I think we're up there, absolutely, yeah, And we have lots of big ideas.

Yeah, and lots of things to execute on.

And by the way, it's a bigger place and most people get a sense of Most people fortunately don't have to go there.

I've had the privilege of being there.

I didn't have to get the privilege of going there, but my team has, so you know, we should.

And part of to be frank with you, part of Project one hundred is actually to build awareness for programs like what you guys are doing.

It's not just about you parleying to our audience things that they would like to know about the various diseases we been talking about today, new degenerative diseases.

Every time I say that word, I think it's a hard word to say to me.

I just want some some uh.

I feel a sense of mark You're okay because every time I said the word neurodegenerative disease, I have to think about the degenerative past, and I think it's that your brain not working properly or not telling your tongue what to do.

But like, but in terms of that, it's just as important for us to get content and to parlay that out to people, but as it is to showcase what great work Australia is doing in particularly in this regard, and it's been it's quite a privilege to have someone like you come in so and I want to thank neuro for organizing this and you coming along today.

So, doctor Emma, I want to see your name.

I love to know.

My mother would say it, but you're not here.

But doctor Amma Debani, I think that's how your mother would say.

Good on your Thanks very much.

You're welcome, thank you, thank you so much for having me.

You're welcome.