Speaker 1: Professor Matthew kindon Welcome to Project one hundred again made
Speaker 1: and we probably run this on straight Talk as well,
Speaker 1: if you don't mind, because I think there's a lot
Speaker 1: of people who are in the straight talk audience who'd
Speaker 1: like to hear what Project one hundred has got to
Speaker 1: say about this, So appreciate your time.
Speaker 2: No, thanks very much, Mark, and I really appreciate what
Speaker 2: you're doing for the community to raise awareness of brain health.
Speaker 1: Mental health. It's a huge topic and I was shocked
Speaker 1: when I became aware that the broad umbrella of dementia
Speaker 1: today is the number one cause of death in Australia
Speaker 1: and so therefore it's overtaken heart or coronary attacks or
Speaker 1: heart attacks or yeah, heart failure. First question to you
Speaker 1: is is that just simply a result of us living
Speaker 1: longer and therefore if we got through cancer and heart
Speaker 1: problems that eventually our brain's going to get us. Is
Speaker 1: that just that reason or you seeing younger people getting
Speaker 1: it now?
Speaker 2: Well, I think it's a combination of both of those factors.
Speaker 2: But really, you know, as a doctor, when I was
Speaker 2: a junior doctor, cardiovascular health was the key focus and
Speaker 2: you know there was bypass surgery and people having heart attacks,
Speaker 2: and it was the number one and so understandably, you know,
Speaker 2: politicians in the community put a focus on trying to
Speaker 2: understand the condition and treat it. And I think that's
Speaker 2: really the gold standard to understand that, you know, heart
Speaker 2: heart health and heart disease. You have to look after
Speaker 2: vascular health, stop smoking, understand the risk factors cholesterol, blood pressure,
Speaker 2: blood sugar levels. And it was with that understanding and
Speaker 2: then some therapies coming through, and I think, you know,
Speaker 2: everyone would accept that the statin evolution has changed cardiovascular health.
Speaker 2: And then our buyer marker so understanding that we can
Speaker 2: treat against cholesterol, and gradually you started to see cardiovascular
Speaker 2: deaths going down. In my fields. In neurology, stroke was
Speaker 2: always going up every single year, higher and higher and higher.
Speaker 2: And then eventually they did an epidemiological study and they
Speaker 2: saw that stroke was dropping. And the neurologists didn't actually
Speaker 2: believe it, like, how could this be the case? They
Speaker 2: repeated the study and sure enough, stroke was actually dropping.
Speaker 2: And it's because we've learned from the vascular health approaches
Speaker 2: from cardiologists and heart physicians and the same thing has happened.
Speaker 2: So while that's been happening. And then obviously all the
Speaker 2: great advances in cancer because of molecular biology, understanding genetics,
Speaker 2: the human the whole human genome, all of these things
Speaker 2: that are getting well understood, and no one has really
Speaker 2: focused on inverticomus dementia. And I suppose as a community,
Speaker 2: we've often thought that it's an elderly people's condition and
Speaker 2: we didn't really care about it. And you know, okay,
Speaker 2: if we end up a bit demented in a nursing hame,
Speaker 2: that's the cost of living. But really what's happened alarmingly
Speaker 2: is it's really come to the fore and we're seeing
Speaker 2: there's a huge amounts of dementia and neuroady generation. And
Speaker 2: in fact, this geographical region, the Western Pacific, carries three fifths,
Speaker 2: so sixty percent of the world burden. What Yeah, and
Speaker 2: it's going to be a massive cost, you.
Speaker 1: Know about the budget. What is that?
Speaker 2: Well, I think it's it's an unusual sort of racial mix.
Speaker 2: But we've got you know, obviously a lot of Asian populations.
Speaker 2: We've got South Pacific islanders, Obviously we've got the Anglos
Speaker 2: from Western Europe. But it's a huge population. Firstly, and
Speaker 2: they're prone to vascular, particularly related neuro problems, dementia, vascular
Speaker 2: dementia in particular. And also I suppose there's a lot
Speaker 2: of underdeveloped regions. So if we think about our neighboring countries,
Speaker 2: you know, we've been very lucky, and Australia is lucky,
Speaker 2: and there's Japan in Korea, but then it's mixed with
Speaker 2: you know, great poverty. Thailand, Myanmar, Burma, Thaile, you know,
Speaker 2: Indonesia all had huge populations. So the focus globally is
Speaker 2: to try and fix up the Western Pacific and then
Speaker 2: take some of the learnings from the Western Pacific and
Speaker 2: do refinements, particularly in Western Europe and North America. So
Speaker 2: as a neurologist, obviously I'm a bit prejudiced. I'm glad
Speaker 2: there's a focus on brain health because it's really going
Speaker 2: to be an evolution. And in fact, the reason I
Speaker 2: did get into neurology was, you know, George bush Seni,
Speaker 2: you're saying that the nineties were the decade of the brain,
Speaker 2: and the brain has been left behind a little bit,
Speaker 2: and now we're starting to understand these conditions and we're
Speaker 2: going to be like the cardiologists of the nineties. We're
Speaker 2: going to understand risk factors, we're going to be titrading
Speaker 2: blood bier markers, We've got effective therapies and it's going
Speaker 2: to be totally transformational. The joke about neurologists were they're
Speaker 2: really good at making a diagnosis, but they don't do
Speaker 2: any treatment. To go to the neurologists to get your
Speaker 2: diagnosis and prepare you will, that was that's the prejudice
Speaker 2: against us, poor old neurologists. But dare I say it.
Speaker 2: We're going to a therapeutic era and it's really exciting.
Speaker 1: And part of that, of course, is in your role
Speaker 1: as Sea of Newer any Ura at UNSW or across
Speaker 1: the road from the English horse Stable studying whatever it is.
Speaker 1: But now Newer is as I understand it as, or
Speaker 1: re Call is a joint venture between USW and the
Speaker 1: Prince Well' Hospital. Is that right?
Speaker 2: Yeah, so the Southeastern Sydney Local Health District and that
Speaker 2: includes Prince of Wales, Saint George and Sutherlands. So and
Speaker 2: it's a new initiative, but it's pretty big. I mean,
Speaker 2: you've got a big premises of being any premises are
Speaker 2: huge or brand new. How many people've got in your
Speaker 2: ANEW about five hundred and fifty researchers focusing on brain
Speaker 2: health and mental health. It's amazing and encourage everyone to
Speaker 2: come out and visit like you've done, and we're very
Speaker 2: keen to have, you know, really greater community involvement and connection.
Speaker 1: Is that the biggest undertaking in the country. Yeah, I
Speaker 1: would say it is.
Speaker 2: The other sort of big centers around Australia will be
Speaker 2: the Flory in Melbourne, there's the Queensland Brain Institute in Brisbane,
Speaker 2: and there's the Parent Institute in Perth, but I think
Speaker 2: they're the biggest entities, so only.
Speaker 1: The biggest one in Sydney there, yeah, yeah. And does
Speaker 1: government support it.
Speaker 2: Well, of course the government does support it. But times
Speaker 2: are tough and I suppose neuro was established on grand
Speaker 2: funding so National Health and Medical Research Council, so NHMRC
Speaker 2: and AARC Australian Research Council have been very very successful
Speaker 2: in grants.
Speaker 1: Do you have to apply for those grants?
Speaker 2: And at present now the success rate for grants is
Speaker 2: about eight to ten percent and the funding has really
Speaker 2: taken a battering and I was actually pleased in the
Speaker 2: budget to see an extra five hundred and eight million
Speaker 2: coming towards medical research. And that had been driven by
Speaker 2: a campaign through medical research institutes, but also great advocates
Speaker 2: like Monique Ryan who'd been pushing for or to try
Speaker 2: and get the MRFF amount fully released. But now with
Speaker 2: you know, lowering government grants support, researchers have to reach
Speaker 2: out more to the community and what are the best
Speaker 2: what are the most successful ways? Well, the most successful
Speaker 2: way to fund your research program is have an industry partner.
Speaker 2: An industry you know they need to make money. For example, well,
Speaker 2: I need any any farmer company, right. So examples that
Speaker 2: we're working with very closely include Roach Diagnostics based in Switzerland,
Speaker 2: ELI Lily or Lily Farmer the United States. They're they're
Speaker 2: they're key tever are key partners for us to drive
Speaker 2: our research programs. But the beauty about having an industry
Speaker 2: partner is you're more likely to have what we call
Speaker 2: impact and translations. In other words, your discoveries are going
Speaker 2: to make it out to the patient, to the clinic.
Speaker 2: And that's why the health district and the university are
Speaker 2: engaged because they want to see better health outcomes. So
Speaker 2: you're much more likely to get that if you have
Speaker 2: an industry partner. Now, the other key way that Newer
Speaker 2: has been surviving has been the support of the community.
Speaker 2: And we've been very lucky to have fantastic philanthropic support
Speaker 2: and the individuals who funded whole programs and developments of
Speaker 2: the building. Margaret Ainsworth is responsible for the main building
Speaker 2: at Nearer. But I think we're starting to see that
Speaker 2: the community is investing in research with the desire to
Speaker 2: have better health outcomes, and it's really it's great to see.
Speaker 1: So let's just you measure vascular dementia and maybe you
Speaker 1: could explain what is vascular dementia.
Speaker 2: So vascular relates to the blood vessels, and dementia generally
Speaker 2: means problems with memory and cognition. And the brain is
Speaker 2: made up of nerves neurons that have has lining on it,
Speaker 2: and the lining of the myeline is supplied the lining,
Speaker 2: which is called myelin, is built through cholesterol and apo
Speaker 2: lipoproteins and all of those sort of biochemical processes. But
Speaker 2: it needs a vascular supply, It needs a blood. It
Speaker 2: needs a blood.
Speaker 1: So maybe we're just just for audience. Those things that
Speaker 1: you just mentioned, Yeah, they're all fats, they're all flippers.
Speaker 1: Fat's produced by our liver, so we're producing that.
Speaker 2: We're endogenously so inside our body, yes, we are producing it.
Speaker 2: And I think the other thing to say is the
Speaker 2: brain is a network, so all of the brain is working,
Speaker 2: communicating with itself all the time. We used to think that,
Speaker 2: you know, one part of the brain might be memory,
Speaker 2: one part of the brain might be vision. But that
Speaker 2: was because we studied neurology on the basis of a
Speaker 2: deficit like a stroke or an injury. In fact, okay,
Speaker 2: a lot of the neurology understanding came from major wars,
Speaker 2: so particularly World War One, bullet wounds in the back
Speaker 2: of the head, people to understand that's the cerebellum, and
Speaker 2: so it was looking at deficits. And one of the
Speaker 2: great neurologists is a go called Charles Miller Fisher, and
Speaker 2: he's said, you learn neurology stroke by stroke. So you
Speaker 2: see a patient with a stroke, you see what part
Speaker 2: of the brain is affected, and then you see what
Speaker 2: the manifestation is that and then that's your understanding. But
Speaker 2: now we see the brain more as a network. So
Speaker 2: all of these parts of the brain are communicating through
Speaker 2: these nerve fibers, and when the blood supply is affected,
Speaker 2: they start not working as well as they should, so
Speaker 2: the speed of the signal getting through is less. Sometimes
Speaker 2: they die, so little parts of little holes start developing
Speaker 2: small strokes, microstrokes at a very molecular level, So you
Speaker 2: wouldn't see it if you had the brain in front
Speaker 2: of you, but you put it under a microscope, you'd
Speaker 2: see it.
Speaker 1: And you probably can't detect it either while someone's alive.
Speaker 2: Unless there's a certain amount happening, like a volume. It's
Speaker 2: a volume effect, So we start to see it with
Speaker 2: their MARI scans, but by that stage it's more often
Speaker 2: than not more severe. So right at the beginning, and
Speaker 2: that's the trouble, we don't know when this begins, so
Speaker 2: it could be beginning twenty or thirty years before the
Speaker 2: patient manifests any symptoms.
Speaker 1: And what causes this blood supply problem? Like in other words,
Speaker 1: I presume what we talk about is a reduction of
Speaker 1: the blood to blow reduction of blood.
Speaker 2: Supply, and it's really been driven the understanding through vascular researchers,
Speaker 2: so cardiovascular hell, so understanding that the wall of the
Speaker 2: blood vessel gets thicker, the sort of the lumen or
Speaker 2: the hole in the middle gets smaller, less blood gets
Speaker 2: out there. Sometimes the vessel actually breaks apart a little bit,
Speaker 2: a bit of ooze, and you know, blood and proteins
Speaker 2: escape into the brain. That's the process, and if that happens,
Speaker 2: you know in general areas. Interestingly, one of the sort
Speaker 2: of the key problems that you see is people start
Speaker 2: falling over and everyone thinks, oh, falls are normal. No,
Speaker 2: if you have a fall, that's abnormal. I mean, obviously
Speaker 2: you have a fall you're running and your chip on
Speaker 2: a gutter, that's understore. But if you're walking around the
Speaker 2: house and you fall over, you're on the street, you
Speaker 2: fall over, that's abnormal. You legs give away, Yeah, your
Speaker 2: legs give away, or your balance is affected and you
Speaker 2: fall over. That's often the beginning of understanding that someone
Speaker 2: may be suffering from a vascular brain process. So falls
Speaker 2: are very much characteristically linked. The other thing is obviously
Speaker 2: your cognition. So family members notice that maybe you're not
Speaker 2: as sharp as you were. You seem to be forgetting
Speaker 2: things you might be I mean, sometimes, for instance, you
Speaker 2: might drive the car home and you know, hit the
Speaker 2: side of the car and the garage. You might not
Speaker 2: even mention you've done it. You know, another family member
Speaker 2: notices that there's a dent in the car.
Speaker 1: How did that happen? So it's the.
Speaker 2: Behavior and the fine tuning of motor function or brain
Speaker 2: function is being affected. And it's usually often the family members,
Speaker 2: people in the house, children, partners who notice and they
Speaker 2: try and encourage a medical review because.
Speaker 1: I remember when I come saw you just getting a
Speaker 1: check up, and you may be do some physical moments
Speaker 1: like walking and standing on one foot, and then you
Speaker 1: sent me off to get an older center or adoptler.
Speaker 1: I think you caught it on my crodod arteries. So
Speaker 1: why would someone when would a doctor tell someone to
Speaker 1: get that? And why would someone get that? What were those?
Speaker 1: And those especially those tests we want to see my
Speaker 1: old school physician tests. I remember I used to get that.
Speaker 1: My doctor when I was a kid used to do that,
Speaker 1: but doctor since then stopped doing it. What are you
Speaker 1: looking for when you do those very fundamental tests?
Speaker 2: So it's about motor function. So we're seeing how someone walks,
Speaker 2: we're seeing their gate, we're seeing their gate length, and
Speaker 2: then part of that is what we call tandem walking.
Speaker 2: So the police stole our tests. This is a neurology test,
Speaker 2: but doing heel in front of the toe in a
Speaker 2: straight line, and these are markers for things like vascular dementia.
Speaker 2: Also getting someone to stand on the spot and close
Speaker 2: their eyes because if they're having problems with no function
Speaker 2: in their legs in particular, other senses start to take off,
Speaker 2: so they're relying on their eyes. But for instance, at nighttime,
Speaker 2: when they get up in the middle of the night,
Speaker 2: they fall over.
Speaker 1: Yeah, so that's a.
Speaker 2: Way to try and look at that, and coordination testing
Speaker 2: in a general sense. Reflexes are used for us to
Speaker 2: try to determine the level of We use a word
Speaker 2: called lesion. Where is the lesions we're trying to work
Speaker 2: out where the abnormality is, and by tradition we see
Speaker 2: two two. We divide the nervous system up into central,
Speaker 2: which is the brain and the spinal cord we call
Speaker 2: it upper mode in urine or there's the peripheral and
Speaker 2: that's the nerve and muscles in the arms and the legs,
Speaker 2: and reflexes tell us where to go. So in other words,
Speaker 2: if I test someone and they've got very brisk reflexes
Speaker 2: in a territory, so I just tap them or I
Speaker 2: don't even need a tendon hammer. That's suggesting upper mode
Speaker 2: in urine or central problems. If I test their reflexes
Speaker 2: and they've got no reflexes in a region, that would
Speaker 2: suggest that the nerve supply is damage. So that's a
Speaker 2: peripheral abnormality. So we're trying to see is this is
Speaker 2: sense problem like vascular dementia or is it a peripheral
Speaker 2: problem like a diabetic neuropathy.
Speaker 1: Right, So, and then they're crottied Doppler.
Speaker 2: Yeah, So it really depends on what the patient's presenting with.
Speaker 2: But let's say the presentation might be a partners thinks
Speaker 2: that they're not thinking as well as they were, or
Speaker 2: as a family history, and with family history we use
Speaker 2: typically under the age of fifty, so someone has had
Speaker 2: a family members had either a heart attack or stroke
Speaker 2: under fifty that's significant and so as part of my assessment,
Speaker 2: we do investigations and the Doppler study is an ultrasound
Speaker 2: looking at the carotid and vertebraladies. They're the main blood
Speaker 2: vessels that go to the brain, supplying from the heart
Speaker 2: from the heart directly, and if they start to get
Speaker 2: closed off slightly, that can be the app that can
Speaker 2: be the cause of the presentation. It was not a
Speaker 2: blood flo enough blood flowing up and we use again
Speaker 2: about a seventy percent market, so it's less than seventy
Speaker 2: percent and flow. That's significant, right, But now with Doppler,
Speaker 2: with technology, we can actually trace that up. When we
Speaker 2: can go and now look at the blood vessels, the
Speaker 2: middle cerebral artery, posterior cerebral artery, which form a sort
Speaker 2: of circle inside the brain called the circle of Willis.
Speaker 2: So we can study that now through ultrasound, and again
Speaker 2: we can get some marker about blood flow.
Speaker 1: Right, And so what would cause those arteries to do this?
Speaker 1: I mean, obviously smoking is an issue, but yeah, is
Speaker 1: it just high cholesterol, high low density cholesterol.
Speaker 2: All of those factors, But definitely smoking would have been
Speaker 2: probably the most common cause. And I've seen that evolution
Speaker 2: now Like in the nineties we were seeing a lot
Speaker 2: of credit artery. We use the words stenosis. It's less
Speaker 2: common now. People don't smoke as much as they used to,
Speaker 2: Like it's rare that you see smokers. Now you've mentioned
Speaker 2: then cholesterol, so understanding like LDL in particular more than
Speaker 2: about four point five or more more than two but
Speaker 2: the total cholesterol of more than four point five is
Speaker 2: significant blood sugar levels and obviously you know your body
Speaker 2: mass index.
Speaker 1: What about the so called apo b apolipo bread and B,
Speaker 1: I mean, which is their carrier? So of the cholesterol
Speaker 1: most people don't realize cholesterol doesn't get anywhere unless you've
Speaker 1: got something we need to piggyback. Absolutely, And so that's
Speaker 1: a new thing. Is there's a new test.
Speaker 2: Yes, yeah, it's it's a new test. Yeah, And apper
Speaker 2: LiPo protein is one of it. Turns out there's lots
Speaker 2: of different types. There's lots of different forms. You know one, two, three, four, five,
Speaker 2: four is the critical one. But these apper lipoproteins help
Speaker 2: other processes, other nutrients come in and out of cells.
Speaker 2: But the issue about appo LiPo protein E four is
Speaker 2: that it is involved in the removal of amyloid and plaques.
Speaker 2: So if you have higher numbers or manifestations of the
Speaker 2: breakdown of amyloid in the brain is not as good.
Speaker 2: So that makes you more prone to Alzheimer's disease. So
Speaker 2: amyloid and tower proteins in the brain that are linked
Speaker 2: to a specific form of dementia Alzheimer's.
Speaker 1: Disease which forget forget from us basically can't remember stuff. Absolutely, yeah,
Speaker 1: and that happens in one part of the brain more
Speaker 1: prevalent in that hippocampus or the thing is that was
Speaker 1: that right?
Speaker 2: That's the most common and that that's the sort of
Speaker 2: the center of memory function in our human brain. But
Speaker 2: it doesn't have to be there, like it could also
Speaker 2: be some people start losing their visions. It could be
Speaker 2: in the occipital region. It can be lots of different
Speaker 2: parts of the brain. But the more common part, yes,
Speaker 2: is memory.
Speaker 1: And is it fair to say that I don't know
Speaker 1: where I read this, but vision and hearing are quite
Speaker 1: important as early markers for that potentially you might be
Speaker 1: getting dimension, might becoming your way down the track. Yeah,
Speaker 1: why is that? Well?
Speaker 2: I think this is really great work that came out
Speaker 2: from the Lancet Commission, and they discovered fourteen factors which
Speaker 2: could be modified to either prevent or treat dementia, modify
Speaker 2: or prevent and one of those is hearing. And I
Speaker 2: think that you know, I have a colleague as a neurologist,
Speaker 2: and he started developing hearing problems and he noticed that
Speaker 2: when he went to dinner party, he didn't really want
Speaker 2: to engage because he couldn't hear what was going on.
Speaker 2: So people start retreating and that then promotes the brain
Speaker 2: not to function as well as it, you know, normally.
Speaker 1: Retreating from what's social intrational.
Speaker 2: Engagement, and so social engagement is another critical factor that
Speaker 2: was identified by the Lancet Commission. So the more that
Speaker 2: you're engaged in you know, a profession, a work, a environment,
Speaker 2: a community, a sports environment, a rugby league club, the
Speaker 2: better off people go. And if you're isolated the brain,
Speaker 2: the brain doesn't like isolation. So this is all these
Speaker 2: are all modifiable risk factors, and then how could you
Speaker 2: sort of cut off a few of them? Well, firstly
Speaker 2: like if you like exercise, are you involved in a
Speaker 2: in a community approach or as a particular exercise that
Speaker 2: you like doing aerobic type of exercise, but also resistance training,
Speaker 2: and these again are all modifiable risk factors for dementia.
Speaker 2: Another part of that that's only really come out in
Speaker 2: the last few years is an understanding what we're called frailty.
Speaker 2: So you might have said, O, someone looks a bit frail.
Speaker 2: That doesn't really mean anything, but frailty is it's a
Speaker 2: two way process between the body and all of the
Speaker 2: body organs and the brain. So when the brain stops working,
Speaker 2: the organs don't work as well. But if the organs
Speaker 2: don't work as well, the brain stops working as in converse.
Speaker 1: So your dale's you'll get frail.
Speaker 2: How can you prevent yourself from becoming frail? Well, resistance training,
Speaker 2: high protein diets, aerobic training, stay engaged with the community.
Speaker 2: These are the things that are going to help brain health.
Speaker 1: I remember Mark Penny, Professor Mark Pennie M's showing about
Speaker 1: because I was talking about him about his dad, Ron, Yeah,
Speaker 1: who died from dementia, and Ron was like a genius
Speaker 1: skinny fit walked up the stairs to a level of
Speaker 1: whatever it was every day at Sir Vincent's. And I
Speaker 1: said to Mark, are you worried about your genetic predisposition perhaps,
Speaker 1: and would you bother getting a genetic test for dementia?
Speaker 1: And he said no? And I said why? And he
Speaker 1: said to me The reason why, he said, is because
Speaker 1: even if I find out the solution right now, I
Speaker 1: don't have any symptoms. But the solution right now would
Speaker 1: be to do high intensity exercise, he said, So I'm
Speaker 1: mols do it. Anyway, whether I get a diagnosis or not,
Speaker 1: they're only the diagnosis because getting the diagnosis can cause
Speaker 1: a lot of anxiety, and people do retract socially and
Speaker 1: all sorts of things. He said, I'm better probably not knowing,
Speaker 1: but doing the very thing that they would recommend me
Speaker 1: do anyway. And so how does high intensity exercise assist
Speaker 1: in that regard?
Speaker 2: Well, I think obviously he was a visionary, but yeah,
Speaker 2: when you exercise, for instance, blood vessels dilate, so the
Speaker 2: blood vessels dilate, more blood flow starts going through brain,
Speaker 2: in your brain and all over your body, but in
Speaker 2: your muscles. So it's just reflecting what's going on. But
Speaker 2: a number of conditions are also associated with other metabolic
Speaker 2: changes in the brain and the body in a general sense,
Speaker 2: so insulin resistance, metabolic health, mitochondrial function, so all the
Speaker 2: cellular approaches, inflammation, inflammation in the brain, inflammation in the
Speaker 2: organs of the body.
Speaker 1: So all of.
Speaker 2: These are improved through exercise and high intensity exercises. As
Speaker 2: Matt Penny suggested back then, I think the other thing is,
Speaker 2: and I understand what he's saying as well, there's a
Speaker 2: stigma and people don't necessarily want to be associated with
Speaker 2: any of these conditions. But I think what we've got
Speaker 2: to is try and turn that around as a community
Speaker 2: and say, well, we're focusing on brain health. We want
Speaker 2: optimal brain function, and we want to get into it early,
Speaker 2: and we want to maintain it throughout the course of
Speaker 2: your life. So wouldn't it be great if people started
Speaker 2: going to their general practitioners at the age of thirty
Speaker 2: and had a brain health check to prevent dementia and
Speaker 2: erodegeneration in their sixty seventies, eighties, nineties. We don't know
Speaker 2: how long we're going to live for, but it's still
Speaker 2: going upwards. So I think that we can try and
Speaker 2: encourage a more healthy approach to brain health.
Speaker 1: It was funny, you know, today, knowing I was going
Speaker 1: to talk to you, I actually had an appointment, just
Speaker 1: a general point with my GP, who's actually fantastic. I've
Speaker 1: got to give him, I've got to get shower him
Speaker 1: out now. And he's new. He's new, he's a young
Speaker 1: guy I knew, and he and I have all sorts
Speaker 1: of conversations similar to you and I about all sorts
Speaker 1: of things. And I said to him, I wonder whether
Speaker 1: or not I should have say, two days off from
Speaker 1: exercise and go and get a blood test for BDNF
Speaker 1: brain revenue tropic factor. And he said, oh, he said, okay,
Speaker 1: there's not a bad idea, but he can't find any
Speaker 1: where who does that. He's still searching. He hasn't texted yet,
Speaker 1: but he's still searching. And the only reason I was
Speaker 1: saying that was because you know, I'm with things. You know,
Speaker 1: as you know, my mother passed away from a new
Speaker 1: disease or als and I've got a dimension on the
Speaker 1: other side, So you know, I get nervous about these things,
Speaker 1: but not so much that I'm over nervous. I'm not paranoid,
Speaker 1: but but I take the view I'm a contra good
Speaker 1: or something about it. I got to talk to people,
Speaker 1: that's what this whole show's about. And and I thought, well,
Speaker 1: I as I understand it, that particular MOLECULEAR gets produced
Speaker 1: in your brain when you exercise is very good for
Speaker 1: brain health, but no one knows what the level is.
Speaker 1: No one's actually asked me to do a test. And
Speaker 1: I'm assuming he can find he can find someone can
Speaker 1: do it. You probably know the incident anyway, But what
Speaker 1: are some of the things that you think Australians or
Speaker 1: people listening to this show should be asking their doctor
Speaker 1: to get tested, even if it's just baselining you now
Speaker 1: in a relation to brain health, are there things that
Speaker 1: you should be asking apart from the obvious ones, and
Speaker 1: the obvious ones of the heart was good you want, Tommy,
Speaker 1: if it's good for your heart's good for your brain exactly. Yeah,
Speaker 1: But apart from those, you know, ApoB little A E
Speaker 1: and all that stuff. Apart from those ones, are there
Speaker 1: any specific things you should be getting tested when you
Speaker 1: ask for a blood test from your doctor relative to
Speaker 1: your brain health.
Speaker 2: Well, you've already articulated the main ones currently, but this
Speaker 2: is a rapidly evolving landscape. So, for instance, at Neuroscience
Speaker 2: Research Australia have formed a partnership with Roast Diagnostics platform
Speaker 2: and part of the reason for that is to get
Speaker 2: blood bio markers as a Medicare item number, so that
Speaker 2: people can go to their GP and have all of these.
Speaker 1: Get numb for free.
Speaker 2: Yeah, and that's where it's going to be. That's going
Speaker 2: to be in the next five to ten years, right,
Speaker 2: And some of those markers are specifically, you know, identified
Speaker 2: with particular conditions. But there are things called neurofilement, so
Speaker 2: the neurofilament goes up in your blood when there's been
Speaker 2: some nerve damage. There are other markers we call GFAPP.
Speaker 2: These are blood tests that can suggest a particular diagnosis.
Speaker 2: There's been a huge study in the UK and they've
Speaker 2: taken blood and clinical examinations from fifty thousand people and
Speaker 2: they've gone back to the blood bio markers and they're
Speaker 2: show them that if five particular proteins in the blood
Speaker 2: go up about ten years before Alzheimer's disease develops, and
Speaker 2: that's where we're going to be going. So we're going
Speaker 2: to be testing these in healthy individuals and then we
Speaker 2: can start to treat against these blood bio markers to
Speaker 2: try and maximize brain health. It's not here at the present,
Speaker 2: but there's a lot of work going on in your
Speaker 2: hurry right now.
Speaker 1: I can't wait forever. Yeah no, because one of these
Speaker 1: I want to ask you is can you test? Can
Speaker 1: I do a blood test today for amyloids in tower?
Speaker 2: At the moment you can't. But that's exactly so this
Speaker 2: sort of diagnostic pathway is to bittering amyloid and tau
Speaker 2: for Alzheimer's disease, TDP forty three for motor neurone disease,
Speaker 2: in front of temperal dementia, alpha si nucleon for leuis
Speaker 2: body dementia, Parkinson's disease. That's where it's going to be
Speaker 2: and we're going to see what are those levels, but
Speaker 2: we can't really at the moment. We haven't done large
Speaker 2: population studies to know what that range should be.
Speaker 1: It's just people. You don't have a range, So that's
Speaker 1: cutting in. Yeah, So do you think in the next
Speaker 1: five years these are some of these are realistically able
Speaker 1: to be done?
Speaker 2: I'd say with absolute guarantee they will be. And you'll
Speaker 2: be going to the doctor with a blood result like
Speaker 2: you do now with a full blood count hemoglobin and
Speaker 2: they'll say, oh, your neurofilm and is slightly high. This
Speaker 2: is the treatment to bring it down towards roughly normal
Speaker 2: levels or that's really high. We need to do some
Speaker 2: more investigations on that one. We need to lumber Puncher
Speaker 2: and MRIs again. So I think it's going to start
Speaker 2: to deter and the way forward. But then also linked
Speaker 2: to that, we're going to start having treatments and we
Speaker 2: have now two treatments for Alzheimer's, these monoclonal antibodies, and
Speaker 2: there's a lot more on the horizon coming through, so
Speaker 2: it's a very much a therapeutic era.
Speaker 1: Well, so I do want to talk about those monoclone
Speaker 1: antibody treatments in a moment, because I have one. As
Speaker 1: you know, I text you. But I have one friend
Speaker 1: of mine who's in his eighties, and I don't know
Speaker 1: whether it's him or his wife showed him this thing
Speaker 1: and he knows I have this show, and he sent
Speaker 1: me the text, and I said, don't worry. I'm going
Speaker 1: to get Matthew Kin and I'm going to ask him
Speaker 1: the question because he actually is worried at his age
Speaker 1: about dementia. I'm genuinely worried by the way he's in
Speaker 1: great shape. But people do get nervous about the stuff, mate,
Speaker 1: They get really anxious. I mean, I think there's more anxiety.
Speaker 1: Of all the guys I know around my age. The
Speaker 1: one thing that is, particularly the ones who played footy
Speaker 1: or boxed or did anything like that. Had we're in
Speaker 1: contact spoorts, they are all worried about dementia. It's like
Speaker 1: it's a big deal. You'd be seeing as in your religis.
Speaker 1: But it's a big deal.
Speaker 2: Yeah, and I think again industry has taken that on
Speaker 2: board as well. There was recently a superannuation conference and
Speaker 2: all of the key superproviders. You know, imagine you've done
Speaker 2: your whole life, you've worked, you set yourself up, and
Speaker 2: then your cognition goes down. So it's it's incredibly important
Speaker 2: and I can see why people are worried. I'm worried,
Speaker 2: but we don't have a way to identify who is
Speaker 2: at the greatest risk at the moment. And that's why
Speaker 2: the focus on making brain health, you know, the key
Speaker 2: treatment area for our community is critical and that's why
Speaker 2: it's happening. Everyone's worried about it.
Speaker 1: Well, government should be worried about too, because some mean
Speaker 1: their job, is my view, their job is to increase
Speaker 1: their standard of living. Our stand living. That the ultimate
Speaker 1: it's about stand living. And there are lots of measurements
Speaker 1: for that. One measurement that should be how long you
Speaker 1: can live on this planet, how well you live during
Speaker 1: that period. And living with dementia, like when it's full
Speaker 1: blown at least, is not living, you know, like it's
Speaker 1: pretty dreadful on everyone. Else around you, Like if you
Speaker 1: someone said to me today, ail to you or anybody, Look,
Speaker 1: you know, how would you see yourself when you're eighty
Speaker 1: five or ninety. And by the way, medical technology you'll
Speaker 1: get us there now because they can fix the hard thing,
Speaker 1: and replace the hard thing, and fix the guineas and
Speaker 1: fix just better really accept this thing. And if they said,
Speaker 1: if you were to rate your standard living, one thing
Speaker 1: is you probably don't want to be confronted with is
Speaker 1: your kids having to bathe you and not be recognized
Speaker 1: by you, or your kids have having to put you
Speaker 1: in a nursing home because you turn a little bit
Speaker 1: violent because you've got dementia. That would be probably the
Speaker 1: lowest stand of living I can imagine for me. I'd
Speaker 1: tell a lot of people to agree with that. Yeah,
Speaker 1: that's the fear. Absolutely, it's a massive fear.
Speaker 2: Yeah, and it's well founded. I think that the the
Speaker 2: essence of being a human is our brain function, our
Speaker 2: executive function, the fact that we're having this conversation now.
Speaker 2: So when that is affected in any way, it has
Speaker 2: massive implications and it's very hard for individuals and families
Speaker 2: to cope with that.
Speaker 1: So I just had to thought then if Matthew just
Speaker 1: go back to something. When we're talking about high intensity exercise,
Speaker 1: you can do that when you're forty, fifty, sixty, some
Speaker 1: people maybe seventy, but it largely depends on your mobility
Speaker 1: and a lot of other stuff, you know, energy levels,
Speaker 1: et cetera. But when you're eighty does high intensity then? Mean?
Speaker 1: I mean, how do we measure high intensity? Is it
Speaker 1: about my heart as a percentage of maximum heart rate?
Speaker 1: Or is it? And therefore you take one hundred and
Speaker 1: two twenty multiply minus eighty and it gives me one
Speaker 1: forty and I go, try you at eighty five percent
Speaker 1: of that? Or is it? What is it? What is
Speaker 1: high intensity? Well? That is exactly it.
Speaker 2: But I suppose when you're eighty or ninety, are you
Speaker 2: going to suddenly do a high intensity exer's for the
Speaker 2: first time and do it as well as a twenty
Speaker 2: year old. No, so you're going to be doing it
Speaker 2: in your twenties, thirties, forties, fifties, sixty, seventies and eighties.
Speaker 2: And in fact, by doing that, it makes it more
Speaker 2: likely that you are going to be able to do
Speaker 2: it in your eighties, nineties and one hundred. I see
Speaker 2: a lot of people who come in who were in
Speaker 2: fantastic health in their eighties and nineties. So that's the message.
Speaker 2: You don't have to be in bad health, you don't
Speaker 2: have to have you know, disability. But that hasn't come
Speaker 2: out of nowhere. Yeah, So it's like doing homework all day,
Speaker 2: every day for the course of your life.
Speaker 1: Yes, and to that extent. And that's what this shows
Speaker 1: a lot about this is that they you've got to
Speaker 1: take control individuals. We might, but they're not going to
Speaker 1: take control as someone makes them aware and sort of
Speaker 1: give them a bit of an indication of the type
Speaker 1: of life. There's life style of stuff. Yeah, change your life. No,
Speaker 1: don't drink as much, don't drink it all if you
Speaker 1: can help it, garettes at all, eat the right foods,
Speaker 1: don't put on too much weight, exercise properly. Sleep is
Speaker 1: really important. I do want to talk to you about
Speaker 1: something this this APO like APO E. Chris Hemsworth did
Speaker 1: he show on whatever whatever the streaming platform was. He
Speaker 1: talked to Peter a teer Peter Tree blood test on
Speaker 1: you know, one of the most athletic looking people and
Speaker 1: I've ever seen on television. And I say, therefore, is
Speaker 1: it athletic? He's young, And the bad news, as delivered
Speaker 1: by Peter Tear to Hemsworth, was that he had two
Speaker 1: alleles of E four one month from dad. I presume
Speaker 1: he must have been my month for dad and he
Speaker 1: was four E four. One could you comment on is
Speaker 1: are we now testing for this stuff more more more often?
Speaker 1: And two what does it mean?
Speaker 2: Both excellent questions. We are testing for it more often,
Speaker 2: but it's not routine and people often need to ask
Speaker 2: for it. So I think it's important, and that's why
Speaker 2: this show is important to understand that this is part
Speaker 2: of a risk factor for conditions such as dementia. And
Speaker 2: if you have alleles of APO E four, as you mentioned,
Speaker 2: that means that you're less likely to break down the
Speaker 2: proteins that cause dementia in the brain.
Speaker 1: Because if that protein E four ye, or if it's
Speaker 1: E two E three operates more efficiently than ethol. Absolutely,
Speaker 1: that is that the issue. Yeah, And if you've got
Speaker 1: A four, you don't have E two or three or
Speaker 1: two in particular, you're not as likely to break down those,
Speaker 1: so it's not that efficient in getting rid of all
Speaker 1: the debris that's hanging around your brain.
Speaker 2: Yeah, and it's still working, but it's not working as
Speaker 2: well as I suppose the comparison of you know, nineteen seventies,
Speaker 2: you know, Mini with a Tesla or something like that.
Speaker 2: Like it's total different, but it is working to an extent.
Speaker 2: So obviously, if you do have at BOI four like
Speaker 2: Hemsworth's show on his show, that would put you at
Speaker 2: a higher risk. So that would put more emphasis on
Speaker 2: you to focus on all the other modifiable risk factors
Speaker 2: that you can control, the ones that we've already talked about.
Speaker 2: A statistical higher risk.
Speaker 1: Yeah, it doesn't.
Speaker 2: And these are based on and that's a good point.
Speaker 2: These are based on populations. This is population health. However,
Speaker 2: you can extrapulate the population to the best for you.
Speaker 2: But of course an an equals one I e.
Speaker 1: Yourself.
Speaker 2: It's like it's not it's not an exact science.
Speaker 1: Yeah. So, and as I understand it, there is something
Speaker 1: like people who pass away with perhaps Alzheimer's disease or
Speaker 1: some form of dementia, probably heart attacks two, but have
Speaker 1: a ten times more of those people have the genotype
Speaker 1: B four were both they've got both parents. It's a
Speaker 1: ten time factor. So otherwise it's correlation it's not a causation.
Speaker 1: But lets say, look, he looks great, I mean, and
Speaker 1: obviously he's adjusted his lifestyle. And by the way, I
Speaker 1: don't mind telling everyone, I'm me three E four. So
Speaker 1: I got E four from one of my parents. I
Speaker 1: don't know which one, but one of them, And I
Speaker 1: don't know who to blame, so one mum or dad.
Speaker 1: It doesn't really matter because they both passed away. But
Speaker 1: point being is that there's a I don't know, six
Speaker 1: times I don't have ten times chance like some other
Speaker 1: statistical greater chance of having a brain disorder or even
Speaker 1: a hard disorder, because the four actually fixed your heart too,
Speaker 1: like it's a bad for your heart, and as you
Speaker 1: always say, if it's not good for you with your brain,
Speaker 1: E four does that too, and also has effect on
Speaker 1: the kidneys. It's a kidney issue too, by the way,
Speaker 1: because there's the same deal.
Speaker 2: Absolutely the same deal, because as.
Speaker 1: Your kidneys can get the archer can get, the ones
Speaker 1: coming out of the kidney can get damaged because you're hardened,
Speaker 1: and then they don't filter as well, and so you know,
Speaker 1: you start getting early kidney disease. That's exactly. So it's
Speaker 1: a big deal and we should be getting tests of
Speaker 1: this sort of stuff more often. So E. Four just
Speaker 1: explained a little bit more if you don't mind, because
Speaker 1: one of the things that as I understand it, Matthew,
Speaker 1: is that how comes after amyloid accumulation and TAO come
Speaker 1: about as a result of other processes that happened before
Speaker 1: that way before those things start getting produced. And there
Speaker 1: is you know they're talking about, you know, the Crisper
Speaker 1: process projects whereby they can turn some genes off that
Speaker 1: some people have in their brain, whether they've got EPO
Speaker 1: or not, that you can turn off these processes where
Speaker 1: certain molecules are not going to get produced, which ultimately
Speaker 1: end up in producing more amloids in tow Can you
Speaker 1: just talk about your advances in crisper and what crisper is.
Speaker 2: Well, first, I'd say that focusing on a particular gene
Speaker 2: that might do one part of a function, that's great research,
Speaker 2: but it might not necessarily have any impact or translation
Speaker 2: into the humans that we are. So I think that's
Speaker 2: the first thing. You often see these great discoveries, and
Speaker 2: we've been able to model mice. Yeah, it did it on mice,
Speaker 2: and you know, in a lot of the conditions we're
Speaker 2: talking about. All of my studies have been negative because
Speaker 2: how good is that model for the human disease?
Speaker 1: Right?
Speaker 2: And the other thing is we've obviously mentioned amyloid and
Speaker 2: TAW and they're important parts, but they're not the whole
Speaker 2: story either, and so there's a discussion. I remember when
Speaker 2: people we talking about ammeloid they said, well, it's like
Speaker 2: saying if you remove smoke, is at the end of
Speaker 2: the fire.
Speaker 1: No way.
Speaker 2: So there's a whole process going on here. Emoloid and
Speaker 2: TOW are critical parts, and the genes modifying them are
Speaker 2: critical parts. But if we remove all of the amyloid
Speaker 2: out of someone's brain, will they be back to normal? Well, no,
Speaker 2: they're not, because we're doing that now. So we can
Speaker 2: remove the amyloid with the monoclonal antibodies and they don't
Speaker 2: get back to normal, they might either plateau or they
Speaker 2: might might slow down the progression. But then the question
Speaker 2: is can we find tune that when do we start it?
Speaker 2: Do we start these medications at the age of thirty
Speaker 2: when we see four is up and monitoring some other
Speaker 2: parts of the biomus, and that's where we're going. We're
Speaker 2: going to go earlier and earlier and earlier. And it
Speaker 2: might be that one of the medications is related to
Speaker 2: a gene modification in amyloid in a few years time,
Speaker 2: but that's not available at the moment. The other thing
Speaker 2: is when you start knocking out certain genes, you don't
Speaker 2: know what the downstream effects of.
Speaker 1: That effect is. Yeah, exactly. That might be good for
Speaker 1: something else, yeah, and.
Speaker 2: It might be a catastrophe, you know, were there were trials,
Speaker 2: for instance, in Parkinson's disease, putting in stem cells into
Speaker 2: the brain and all sounding great, It was looking good,
Speaker 2: but then the stem cell started to overgrow and cause cancer,
Speaker 2: and so people coming in with you know, overgrowth and
Speaker 2: cancer cells in the brain. So it was a catastrophe.
Speaker 2: So you've got to be able to understand. And that's
Speaker 2: really why human trials are so critical. So a model
Speaker 2: is only as good as a disease. It models, but
Speaker 2: I think we have to get more and more into
Speaker 2: patients and patients with neurological conditions. Of course we need
Speaker 2: basic science and discovery, but we've got to focus on
Speaker 2: the human.
Speaker 1: We are talking. I mean, dementia covers a lot of
Speaker 1: stuff and we've been talking about and Alzheimer is the
Speaker 1: one probably everybody tends to focus on. But loss of memory,
Speaker 1: I guess is probably of describing it. What is the
Speaker 1: general progression? Though? From the moment you and I remember
Speaker 1: asking you this question, I said to you, sometimes I
Speaker 1: just can forget a word, and I just can't remember
Speaker 1: the word, and about two or three minutes that comes
Speaker 1: to me. Or I forget a person's name. I know
Speaker 1: them so well, but I haven't said it maybe for
Speaker 1: a while. And you said to me something like that
Speaker 1: sort of anxiety memory because some of you are said
Speaker 1: to me, oh my god, I can't remember that word.
Speaker 1: And they're older people and they're going and they're just
Speaker 1: marking around, go bloody, early dementia. But what what other
Speaker 1: things could be causing us not to remember that the
Speaker 1: name or the word. What is this anxiety about memory?
Speaker 2: Well, I think once we start focusing on it, we
Speaker 2: all become anxious. Like hearing a story there, I was
Speaker 2: feeling a bit anxious, So that's something natural. But I
Speaker 2: suppose you're worried that you can't recall a name or
Speaker 2: a process, and then a little bit later you do,
Speaker 2: so the function is there, so you haven't lost the function.
Speaker 1: Right, ourzeime's major lost the function.
Speaker 2: It doesn't doesn't come back right. And it's like I
Speaker 2: suppose an onion starts stripping away the very core parts
Speaker 2: of and remain and you might, you know, have memories
Speaker 2: from long standing memories about you know, growing up and
Speaker 2: your parents and so on, but you don't remember that
Speaker 2: you need to go down and get you know, to
Speaker 2: Col's and get dinner for tonight, those sort of things.
Speaker 2: It's so there's a level of what is intrinsic in
Speaker 2: your brain function that's laid down and these these are
Speaker 2: memories that are laid down and reinforced. But it's the
Speaker 2: short term issues that tend to be more problematic. And
Speaker 2: that also means your daily function in your job, in
Speaker 2: your family, in your environment.
Speaker 1: So what is the usual progression? So people start having
Speaker 1: maybe what's something that someone might come to you? And
Speaker 1: obviously I don't want to breach any professional situation here,
Speaker 1: but like maybe someone comes to you and like very
Speaker 1: early stage Alzheimer's, like what would you what would you see?
Speaker 2: Well, part of it can be prolonged word finding difficulties,
Speaker 2: and we might test for it, like you might show
Speaker 2: them a picture of say the Eiffel Tower and anyone.
Speaker 2: So that's the Eiffel Tower, So what's that. That's that
Speaker 2: place that's sort of not here, but it's and it's
Speaker 2: it's made of metal, and they're sort of talking around,
Speaker 2: so it's fluent, it's fluent speech, but they can't say
Speaker 2: Eiffel Tower. They can't say that's a structure in powers
Speaker 2: and Powers is in France. So the connections are all gone.
Speaker 1: There are tests, specific tests later, Yeah, you'll.
Speaker 2: Have them, and so either the neurologists will be involved
Speaker 2: in those tests or there's a neuropsychologist. It's usually a
Speaker 2: multidisciplinary approach and there's testing for word finding difficulties, but
Speaker 2: also then trails, so for instance, doing networks of you know,
Speaker 2: shapes and sizes, doing images of clocks, understanding times. Another
Speaker 2: you know, test is verbal fluency. That's the frontal lobe function.
Speaker 2: So for instance, I don't know if you want to
Speaker 2: do it on the spot, but tell me all the letters,
Speaker 2: all the words that you can think of with the letter.
Speaker 1: M words real, masterclock, I can't even think he got
Speaker 1: me nervous? Can I think of names? No? No, I
Speaker 1: can't think of it. In addiction, money, metal, motor, car Modikaid, Mammoth, Milestone, mightiness, Michaelangelo.
Speaker 1: How's my time going? Perfect?
Speaker 2: You still got abut another ten or twenty seconds, But
Speaker 2: more than more than double figures in a minute is normal?
Speaker 1: Normal? Yeah? And also you're.
Speaker 2: Looking at the words you use there, like like some
Speaker 2: of those were three or four syllables, so they're very
Speaker 2: complex words. So it's totally normal.
Speaker 1: Yeah, but these are this is part of the So
Speaker 1: how would someone know THATTT that they should go and
Speaker 1: see someone? So because you know, like let's say I
Speaker 1: could get to two out like for example, then I'm
Speaker 1: sort of a bit late to the game. Talk to
Speaker 1: a neurologist. Is there some sort of self testing? Is
Speaker 1: there something like can they go to the new website
Speaker 1: and your Your neuro website sort of explains a few
Speaker 1: things to me and maybe it gets me starting to
Speaker 1: think about it. Or I might be talking to my
Speaker 1: brother who's younger than me, but I might have noticed
Speaker 1: something I can say, maybe you just should go and
Speaker 1: see a doctor about this. I mean, how far back
Speaker 1: can we go?
Speaker 2: Well, we have got risk assessment profiles through the neuro website,
Speaker 2: and people can they're they're all free? Is that neuro
Speaker 2: dot com dot you.
Speaker 1: You, and.
Speaker 2: I think it's also just your engagement in life, like
Speaker 2: people like Sudoku's or reading the newspapers or you know,
Speaker 2: looking at the stock market, talking about the the budget.
Speaker 2: All of those sort of things are sort of that
Speaker 2: that they're markers that things are going okay. The tests
Speaker 2: that we're talking about are more buyer markers. Following a
Speaker 2: clinical presentation, so someone has been brought in either on
Speaker 2: their own volition or by by a family member or
Speaker 2: a friend, like you know, Matthew's not not Matthew's not
Speaker 2: the same person that he seemed to be, or there
Speaker 2: seems to be some minor, like high level stuff, and
Speaker 2: then we would go into this sort of cognitive assessment,
Speaker 2: and then that cognitive assessment would suggest what we need
Speaker 2: to do, Like it might say that actually part of
Speaker 2: it as well is assessment of anxiety and mood. So
Speaker 2: I might score badly, but it might be like really
Speaker 2: really down in my in my mood score, and then
Speaker 2: if I can improve my mood score, does the cognitive
Speaker 2: process come out. And that's people use these word pseudo dementia,
Speaker 2: so in other words, it's not really dementia, it's something
Speaker 2: else that's triggering the process. We'd also then you know,
Speaker 2: look at you know, blood test results, vitamin levels, thyroid function,
Speaker 2: these are all markers that will help brain function and
Speaker 2: they could account for the presentation wow.
Speaker 1: And so like this whole an ecosystem around the outcome
Speaker 1: is pretty important. It's not just one thing. It's not
Speaker 1: just going to sit in front of your Olgers and
Speaker 1: he goes, oh, you've got it or you got to
Speaker 1: stage and what's the progress there? So, I mean, where
Speaker 1: would someone end up. Let's say someone starts at seventy
Speaker 1: either got early dementia and you know diagnosed, is it
Speaker 1: ten years or fifteen years? A minute? And then how
Speaker 1: are they at the end of it?
Speaker 2: Well, the beauty is back to the autonomy issue. People
Speaker 2: can have some control of the modifiable risk factor. So
Speaker 2: let's say I was not scoring as well as I
Speaker 2: should be, or I'd been measuring it over the last
Speaker 2: ten years and I'm starting.
Speaker 1: To drop off.
Speaker 2: If I start to adjust some of my lifestyle factors
Speaker 2: and some of the blood results I've got, can I
Speaker 2: either plateau out or start to raise it again. And
Speaker 2: these are things that yes, we can do. So when
Speaker 2: you say is it ten years is at fifteen years. Well, no,
Speaker 2: it's all modifiable. So forty five percent is modifiable. So
Speaker 2: you've got control, right, So as long as you know that, yeah,
Speaker 2: as long as you know so long as you've been
Speaker 2: tested and as well, and part of that as well
Speaker 2: blood pressure. So how often you get blood pressure checked
Speaker 2: by a general practitioner if you're not seeing a general
Speaker 2: practition again see practition to get your blood pressure.
Speaker 1: Gown by one of those omor on things what they're
Speaker 1: called from the chemist. So I go one a home
Speaker 1: just every day. Probably it would be great if because
Speaker 1: somehow I talked to my phone there could be some
Speaker 1: sort of app to it that I could actually you
Speaker 1: probably can get it minds old, but actually I can
Speaker 1: have a record of I can actually see the changes.
Speaker 1: But that's happening. It's a hundred bucks because a hundred
Speaker 1: bucks and the whole family can use it and you
Speaker 1: can use it forever and so but in the end,
Speaker 1: what is a person from dementia die from? Very good question.
Speaker 2: It doesn't kill them, does it? Well, it does, but
Speaker 2: it's back to the brain is the sort of executive
Speaker 2: function controlling all other organs. So usually part of that
Speaker 2: is you're breathing, so you don't necessarily, you know, breathe
Speaker 2: as as quickly and as deeply as normal, so that
Speaker 2: you know the base of the lungs don't fill up
Speaker 2: with air as they normally do. Some fluid might stay
Speaker 2: down there. You might aspirate, so you might swallow your
Speaker 2: food incorrectly. There'll be a chest infection. You die for pneumonia,
Speaker 2: So you die for pneumonia. That's the most common. But alternatively,
Speaker 2: it also does control you know, your heart, your heart rhythm.
Speaker 2: People have heart attacks that they just die in their sleep.
Speaker 2: So the brain is controlling all of these functions. But yeah,
Speaker 2: that's how you die.
Speaker 1: As you know, my mother was went to the other
Speaker 1: place you used to be at Brandon Mind Center when
Speaker 1: she had motor neurone disease, and she died of motor
Speaker 1: neurone disease. And it's a it's a crappy way to die,
Speaker 1: to be honest, it's one of the worst. I've seen
Speaker 1: lots of people pass away and that's the worst thing
Speaker 1: I've ever seen. Motor neurone disease is different to dementia.
Speaker 1: And say, someone like me, who's you know, I've had
Speaker 1: lots of concussions, mini concussions, and major concussions. Is there
Speaker 1: any scientific evidence or statistical evidence about and that correlates
Speaker 1: concussions to als or motori disease.
Speaker 2: Yeah, Well, just to put it into a bit of perspective, So,
Speaker 2: motor neurone disease is a neurodegenerative condition. A neurodegeneration incorporates dimension.
Speaker 2: Dementia is due to say Alzheimer's disease or vascular dimension
Speaker 2: that we've talked about. Modeor neurine disease is due to
Speaker 2: a protein abnormality in the brain as well, called TDP
Speaker 2: forty three. It tends to affect particularly the motor pathway,
Speaker 2: so the cordico spinal tract, which is a tract that
Speaker 2: goes through the brain and spinal col cord and controls
Speaker 2: all of our voluntary muscles. So the motor neurine itself
Speaker 2: is one of the biggest cells in the body. Sometimes
Speaker 2: it's up to one point four meters long and has
Speaker 2: huge metabodys one point one point four meters. It's huge,
Speaker 2: that's massive, massive, but it has high metabolic needs and
Speaker 2: it means what it requires a lot of, you know, protein.
Speaker 2: It's very sensitive to not having things, you know, waste
Speaker 2: cleared out properly, so it needs you know, all the
Speaker 2: things we've talked about healthy sleeping habits are good protein,
Speaker 2: good nutrition, and exercise. But for what for some individuals
Speaker 2: in the community, they're prone to having a disease whereby
Speaker 2: the degeneration occurs in the mode and urine itself, and
Speaker 2: so people start to develop weakness. It's usually focal. So
Speaker 2: in our clinics, I think we give a picture of
Speaker 2: a human and we so where did the disease begin?
Speaker 2: And they can always pinpoint whether it began in my
Speaker 2: right hand, whether it began in my mouth, where it
Speaker 2: began in my.
Speaker 1: Left legatis the patient.
Speaker 2: So it always begins, it seems to begin in one
Speaker 2: area and then it starts to spread and become a
Speaker 2: bit more generalized.
Speaker 1: So just explain where that cell is that one point
Speaker 1: four meter.
Speaker 2: So it starts in the brain and goes all the
Speaker 2: way down through the spinal cord, and then there's what
Speaker 2: we call a sign apse to what we call the
Speaker 2: lower mode in urine, which comes out and goes into
Speaker 2: the nerve for instance, of your arm or your leg,
Speaker 2: or into the tongue.
Speaker 1: So long skinny cellars that must be quite skinny if
Speaker 1: it's going down. Yeah, we'll talk about microscopic. Yeah, microscope,
Speaker 1: but it's always get one point four meters in length
Speaker 1: up to one point four death. Wow.
Speaker 2: But it controls everything you're doing now, like talking, moving
Speaker 2: your hands.
Speaker 1: Your leg. So it's not your brain that does it,
Speaker 1: it's the well.
Speaker 2: The control is through the brain and central the central
Speaker 2: mode of neurine is there in the brain.
Speaker 1: Right, and and that's the thing that controls all your
Speaker 1: motor motor skills what are you want to call it?
Speaker 1: And and so just going back a step on that,
Speaker 1: I remember one of the things they did to my
Speaker 1: mother's they were they did it on the hands. They're
Speaker 1: putting pins in it like I don't know, stimulating her
Speaker 1: hand Yep, that's how she got diagnosed.
Speaker 2: Yeah, So neurophysiology is the critical part of a diagnosis.
Speaker 2: That's that's the investigation. And nerves and muscles are electrically active,
Speaker 2: so the signals going down through the nerve that go
Speaker 2: to the muscle that keeps the muscle live. If the muscle,
Speaker 2: if the nerve is damaged, the muscle starts firing off
Speaker 2: by itself, and a manifestation of that might be muscle twitching.
Speaker 2: But if we put a needle into the muscle and
Speaker 2: it's firing off by itself, so in other words, the
Speaker 2: patient isn't controlling it's going. It's just firing units going
Speaker 2: bang bang bang bang bang. That's a feature of nerve
Speaker 2: damage to that particular muscle.
Speaker 1: Now, if, for.
Speaker 2: Instance, you know you're working as a butcher and you
Speaker 2: accidentally cut the nerve and that muscle was affected, that
Speaker 2: makes sense. But if I start putting needles into lots
Speaker 2: of different areas and getting the same results, it suggesting
Speaker 2: there's a more widespread abnormality of nerve and muscle function,
Speaker 2: and that's what is typically the picture of modeer neurine disease.
Speaker 2: So with your mother, it'll be testing muscles in the
Speaker 2: arms and the legs and the speech muscles, and if
Speaker 2: they're all affected, that's, you know, that's the sign of
Speaker 2: modern neurine disease.
Speaker 1: So her first sign of there being a problem was
Speaker 1: that I used to ring her every night, so I'll
Speaker 1: be going home and my way home from work on
Speaker 1: ring her. My mother loves to speak talk a lot,
Speaker 1: and she's a Orish descent, so Irish people love to
Speaker 1: have a chat, so I would recall the moment I
Speaker 1: got my car, because I knew it was twenty five
Speaker 1: minutes to get home, so I could sort of limit
Speaker 1: the time and say, mom my home, Now I'm going
Speaker 1: to have a dinner. So but I noticed she didn't drink.
Speaker 1: I noticed that she started to sound like she was drunk,
Speaker 1: not drunk, but slurring her words, like a person who
Speaker 1: has been drinking would sound not bad, but just a
Speaker 1: little bit slurring. And she was always very articular. And
Speaker 1: I said to her, are you drinking, like having a
Speaker 1: whisky with dad or something like that, and she said no, no, no,
Speaker 1: And then that's when we decided to get her checked out.
Speaker 1: Does it normally start off in the speech, So.
Speaker 2: There's three areas really were a beginning, So it's usually
Speaker 2: upper limonset is the most common, so in your arms,
Speaker 2: then lower leg so leg weakness is the second, and
Speaker 2: speech is the third, so you call it bulbar onset.
Speaker 2: So it's the tongue muscle, so the tongue has become weak.
Speaker 1: So she would have had those other things before.
Speaker 2: Necessarily, so it can begin in the mouth. And I
Speaker 2: suppose it's interesting that humans are the only ones who
Speaker 2: have a form of communication like speech, and that's also
Speaker 2: an are that that's where mode neurone disease begins. Another
Speaker 2: area where it begins is the pincer grip in the hand,
Speaker 2: and we're the only mammalian species who can do a
Speaker 2: pincer grip. But then when you look at the motors
Speaker 2: strip in the brain, the two biggest areas they have
Speaker 2: massive representation are the bulbar region and the thumb and
Speaker 2: the index finger the bulbarth Yeah, so that's been evolution.
Speaker 2: Our brains have grown in those regions so that we
Speaker 2: can speak, we can do this pincer grip. But as
Speaker 2: a result, it's got huge metabolic demand. And when there's
Speaker 2: a failure of that network, how does it manifest? Speech
Speaker 2: goes off or upper limb function, particularly pincer grip is diminished.
Speaker 1: So has the disease has got something to do with
Speaker 1: the metabolic demand not being satisfied? Yeah, or is it?
Speaker 1: Let's rule genetics out. Is it because the metabolic demand
Speaker 1: is not being met In other words, I'm neither not
Speaker 1: a blood flying there, but no of nutrients getting in there?
Speaker 1: What is it?
Speaker 2: Most likely that is the case, and there's a probably
Speaker 2: a threshold what gets something over a threshold for an abnormality,
Speaker 2: and it's probably cellular failure and that leads to a
Speaker 2: protein abnormality, a folding protein abnormality in this case TDP
Speaker 2: forty three. And that's then that we use the word
Speaker 2: notice it's the origin, and then the origin starts to
Speaker 2: spread out like a fire spreading through the brain or
Speaker 2: through the motor pathways.
Speaker 1: And are there any treatments yet.
Speaker 2: Well, in terms of why individuals get it, we know
Speaker 2: that there's genetic abnormalities and there's been large study has
Speaker 2: been one study that was done here in Australia and
Speaker 2: in Japan and Korea showing that they needed to be
Speaker 2: six things to happen for someone to develop mode of
Speaker 2: neurone disease, six hits and if there is a gene
Speaker 2: in the family that accounts for three of the hits,
Speaker 2: then the other three are at this stage unknown.
Speaker 1: But if there is.
Speaker 2: A genetic abnormality, there is now genetic treatment so to
Speaker 2: first one was approved in May of this year twenty
Speaker 2: twenty six, that's now available to treat superoxide dismutes one
Speaker 2: SOD one genetic forms of als. Then we have neuroprotective therapy.
Speaker 2: So really zola is available and that was through clinical
Speaker 2: trials that we were actually part of in the mid
Speaker 2: nineteen nineties and that was approved in Australia in twenty
Speaker 2: twenty five, two thousand and five. And the second medication
Speaker 2: is a darovone already kava, which is an intravenous infusion,
Speaker 2: and that was approved in twenty twenty five. So the
Speaker 2: other three approved the medications in a space you've got it.
Speaker 1: Yeah, So it's and what's and what's its success rate
Speaker 1: like efficacy in terms.
Speaker 2: Of well, the idea is to keep people in the
Speaker 2: mildiforms for longer and so the patients are living with
Speaker 2: the disease for a longer period of time, less affected.
Speaker 1: Right. So, but you mentioned with some forms of dementia
Speaker 1: that there are lifestyle actors that can improve dementia. Other
Speaker 1: lifestyle actors can improve.
Speaker 2: Well some of the factors that are still relevant. But
Speaker 2: you know, in physical exercise but not too much. And
Speaker 2: there has been, I suppose an understanding that sports people
Speaker 2: are more commonly affected. So for instance, in America, it's
Speaker 2: called Lugerrig's disease. Lugeeric developed als in his thirties and
Speaker 2: obviously we've seen a lot of tennis players, Brad Drewett,
Speaker 2: Peter Dowen, We've seen rugby players have been affected. So
Speaker 2: this AFL Neil Danaher, who's totally Neil Danaher and Fighter
Speaker 2: and D are the third largest unders of modern neurone
Speaker 2: disease research globally, Like, isn't that amazing from Australia And
Speaker 2: who's the other fight M and D which is what
Speaker 2: he established.
Speaker 1: Wow, third biggest in the world. In the world. Yeah,
Speaker 1: it's amazing. That's fantastic. It's fantastic.
Speaker 2: So what are the some of the lifestyle things though,
Speaker 2: Matthew like, well, these are complicated discussions, but certainly we
Speaker 2: know that head injuries form part of that discussion. And
Speaker 2: there was a study that came out a couple of
Speaker 2: years ago showing higher incidences of neurodegenerative diseases, including mode
Speaker 2: neurone disease in contact athletes, particularly professional high level contact.
Speaker 1: Athletes like NFL and stuff like that.
Speaker 2: Yeah, yeah, yeah, And I think that the study came
Speaker 2: I think from the Scottish brain banks, so they've had
Speaker 2: a lot of Scottish rugby union players and they made
Speaker 2: that connection. It's similar here. And I know that the
Speaker 2: Rugby codes are very interested and they're very concerned about it,
Speaker 2: and they're putting a lot of focus on it in
Speaker 2: the AFL and the NRL to try and understand these
Speaker 2: conditions better. But it's a form of research, so we
Speaker 2: still don't have, you know, one hundred percent diagnostic approach
Speaker 2: for chronic traumatic and caphilopathy CTE, and part of that
Speaker 2: is really diagnosed by doing the post mortem examination.
Speaker 1: Maybe you could explain it because a lot of people
Speaker 1: come and say I've been I've heard them, I know them,
Speaker 1: I've been diagnosed with the CTE, And as I understand it,
Speaker 1: you can't do that until you actually get hold of
Speaker 1: their brain once they passed away to do the actual diagnosis.
Speaker 2: That's exactly it, and every approach that's been used up
Speaker 2: till now has been unsuccessful. And in whole groups where
Speaker 2: people said, oh there's a ct and they go and
Speaker 2: to the postmodern examination, there's no neuropathological evidence of ct.
Speaker 1: Maybe you could explain what it looks like. I've seen
Speaker 1: it because I've been to the brain bang at it
Speaker 1: a Brain of Mind center, and in fact I made
Speaker 1: a big donation and then said to them they can
Speaker 1: have my brain when I pass away if they want
Speaker 1: to do evenuevary. But they showed me when it was
Speaker 1: actually like a so here's your brain, like you know,
Speaker 1: that's sort of wrinkly sorting and there was a big
Speaker 1: sort of dent like that is that is that? Am I? Right? So?
Speaker 2: Look there are holes in the brain where fluid passes
Speaker 2: through and they become bigger, and the cell the cell
Speaker 2: processes of the brain becomes smaller, so they shrink, so
Speaker 2: you get shrinkage of different areas. You can also get
Speaker 2: then it's like scar tissue building up in the brain
Speaker 2: and the space has become bigger. That's and then there's
Speaker 2: certain patterns.
Speaker 1: But but why can't you look at that under an
Speaker 1: MRI or a machine.
Speaker 2: Well, there are so many other things that could also
Speaker 2: be affecting the brain, right, I think though that it's
Speaker 2: really interesting that I think we're going to get better
Speaker 2: by using the technology of the day. So AI with
Speaker 2: hundreds of thousands of scans is much better than you
Speaker 2: or I looking at a scan and saying it looks
Speaker 2: normal or it doesn't look normal like that. That's that's
Speaker 2: where're at today. That's all going to be a thing
Speaker 2: of the past.
Speaker 1: Like the guys from Harris and AI, those guys who
Speaker 1: are producing all these AI models to assist the radiologist, yes,
Speaker 1: and the neurologists in your case, in his or her diagnosis.
Speaker 2: And that's a global approach. And at neuro we're hopeful
Speaker 2: of signing up a partnership with IMAD and using the
Speaker 2: sort of the volume of practices they have to use
Speaker 2: AI technology to better diagnose all of the conditions we've
Speaker 2: been talking about, you know, today, and that's going to
Speaker 2: be the reality. But then also can we go earlier
Speaker 2: and at the moment we can't. But let's say we
Speaker 2: did a brain health check of a thirty year old.
Speaker 2: We wouldn't do an MRI scan because what are we
Speaker 2: going to find And what we don't want to do
Speaker 2: is find an incidental finding. Let's say there's a little
Speaker 2: cyst in the brain, what should we do about that?
Speaker 2: And the current understanding of incidental findings is leave them alone?
Speaker 2: Like that just leads to a whole you know, you
Speaker 2: mentioned anxiety, and you imagine the anxiety of the patient,
Speaker 2: of the treating doctor of the family. Do you intervene
Speaker 2: or nind is to not intervene, leave it alone. You
Speaker 2: didn't do the scan to find that that's an incidental finding.
Speaker 1: But maybe you do go back in five years time
Speaker 1: to see if there's been in delta any change. Exactly
Speaker 1: that's your delta. That's good, I don't you said, well,
Speaker 1: but yes, that's exactly it. Yeah, yeah, because as you
Speaker 1: know how to preneuvo. And the only reason I had
Speaker 1: it was not to get well. I did take it
Speaker 1: to you, and I took it to live specially took
Speaker 1: with everybody, but everybody was fine. But the point being
Speaker 1: here is now Prinivas or Australia, I mean I can
Speaker 1: go and get another one, and I presume they've got
Speaker 1: own their own AI systems. Now they could probably look
Speaker 1: at both of them, but I can someone can They
Speaker 1: can say well that has grown. So like one of
Speaker 1: the things you pointed out to me in relation to
Speaker 1: the scan of my brain when I had my whole
Speaker 1: body was I think you said, I think you use
Speaker 1: the word plak be used as normal because for my age,
Speaker 1: but if that was like double in a year or two,
Speaker 1: then you said, well, hang on, let's have a little.
Speaker 2: Bit of that. It's the yeah, and that could be
Speaker 2: getting part the threshold to intervene.
Speaker 1: Yeah, yeah, so I'm actually going to go and get
Speaker 1: another one. But I think down in Melbourne, it's what
Speaker 1: do you think about I mean, I know it's expensive,
Speaker 1: and you know it's easy for me to say, but
Speaker 1: what do you think about those sorts of processes as
Speaker 1: a brain doctor us getting and you can get it
Speaker 1: an your brain much cheaper than a whole reneuvo? But
Speaker 1: what about what do you think about people doing that?
Speaker 1: As a market say at six years of age? Should
Speaker 1: they think about that sort of stuff?
Speaker 2: Well, look, I'm a scientist and I love the brain. Yeah,
Speaker 2: I love all of this sort of stuff.
Speaker 1: You a scientists first or a clinician?
Speaker 2: What do you I'd say clinician your clinician, as in
Speaker 2: you diagnose and examine and prescribe. But we all want
Speaker 2: we all want better outcomes and where's that going to come.
Speaker 2: That's going to come from the science.
Speaker 1: And I think you need to explain that though. I
Speaker 1: think most people don't know the difference between a brain scientist,
Speaker 1: a neuroscientist, and a neurologist. I mean, what are the
Speaker 1: different roles and they know different things? True?
Speaker 2: Well, look I suppose in you're a neurologist is a
Speaker 2: doctor so you do you do medical training. A scientist
Speaker 2: does a science degree and they might focus on neurosciences
Speaker 2: and they might focus on a part of neuroscience, could
Speaker 2: be synapses, it could be on the pure mathematics, it
Speaker 2: could be unstructural.
Speaker 1: But I think.
Speaker 2: It's science unlocks the understanding. And at the beginning we
Speaker 2: talked about brain, you know, being their number one. We're
Speaker 2: careful about saying, you know, you know, cause of death
Speaker 2: in Australia. But to try and turn that around, we
Speaker 2: need people focusing on the science and why has that happened,
Speaker 2: and that could be anything from epidemiology, population studies, what's
Speaker 2: happening in you know, Sydney compared to Perth versus rural Australia.
Speaker 2: That's all science, and then by trying to take that
Speaker 2: forward to try and have a message to try and
Speaker 2: improve outcomes, ideally outcomes for a pop but then also
Speaker 2: outcomes for an individual.
Speaker 1: And they're any exciting maybe a tablet or whatever it
Speaker 1: is exciting things on the you know out there in
Speaker 1: the future that you know of that you guys might
Speaker 1: be looking at, like testing or whatever the case may be,
Speaker 1: for things like dementia. And we'll just leave manual disease
Speaker 1: leave aside, but what about dementia.
Speaker 2: Well, look, I think one of the most exciting things
Speaker 2: that's happened in medicine over the last few years has
Speaker 2: been the GLP one so glucagan like peptides, and these
Speaker 2: have come out of particularly the realm of sugar controlled
Speaker 2: blood sugar diabetes, and they're just so incredibly effective.
Speaker 1: Being ozembic for example, yeah, or mandura or whatever it's called,
Speaker 1: those those things.
Speaker 2: So it actually came from very interesting research showing that
Speaker 2: if you put if you had glucose, either you ingested
Speaker 2: it or injected it, they had different levels in the body.
Speaker 2: So it turns out if you ingested that something was
Speaker 2: released that actually brings the blood sugar levels down much
Speaker 2: better than if you had sugar injected. And it took
Speaker 2: a while that that was called gligan like peptide, so
Speaker 2: GLP GLP one, But GOLP one only survives in the
Speaker 2: body for a few minutes after you eat a meal. Really, yeah,
Speaker 2: so it's not really the stuff you produce. Yeah, it
Speaker 2: turns out there was this endocrinologist and he's working for
Speaker 2: the Veterans Affairs and they said, look, go and you know,
Speaker 2: try and work on this area in general, as they
Speaker 2: just went through virtually like encyclopedias. And he found this
Speaker 2: thing called a Gila monster, and a Gila monster had
Speaker 2: pancreatic overgrowth but also could slow their metabolism down and
Speaker 2: manage blood sugar control. And so he off line. He
Speaker 2: went and found some of the venom of this Gila monster,
Speaker 2: and then he animals it.
Speaker 1: Was a national animal, yeah, g LA.
Speaker 2: And he found a new substance called extendon, and extendon
Speaker 2: looked like glucagan like peptide, and he thought this could
Speaker 2: be the key. So he went back to his bosses
Speaker 2: at Veterans' Affairs and he said, look, I think I
Speaker 2: found something. And I said, look, it's not relevant for us,
Speaker 2: because we're only interested in veterans, more interested in you know,
Speaker 2: blast Day's spinal cord injury. We're not interested in this
Speaker 2: sort of stuff. But he thought he's onto something, so
Speaker 2: he patented himself. He had to put a take a
Speaker 2: loan out on the house, and then basically it was
Speaker 2: becoming very, very expensive. So he then went and presented
Speaker 2: at the American Diabetes Association, and a person from a
Speaker 2: small therapeutics company, Ammelon came along and thought this is fascinating,
Speaker 2: called up his bosses that straight away and they came
Speaker 2: up to a licensing agreement that was eventually then taken
Speaker 2: on with Lily. And that is the whole GLP one.
Speaker 2: So extendon would turn GLP one instead of disappearing within
Speaker 2: a few minutes, could make it last in the body
Speaker 2: for hours four to twenty four hours. And this all
Speaker 2: came from the skill was that a lizard. So I
Speaker 2: suppose that also shows discoveries come from anywhere. But you've
Speaker 2: got to have curiosity, the curiosity like this guy thought, oh,
Speaker 2: this is interesting. There's a lizard that has a big
Speaker 2: pancreas that must be doing something about, you know, blood
Speaker 2: sugar control. And that's where it's all come from.
Speaker 1: And where is GOLP one fit into Brainhill? Now got
Speaker 1: distracted there for a lot now, but it was a
Speaker 1: great story. I love it.
Speaker 2: But what's very interesting is that GP one was used
Speaker 2: for blood sugar control and in the studies that and
Speaker 2: this is all you know. Publishing the best journals of
Speaker 2: the world, New England Journal of Medicine, landst et cetera.
Speaker 2: They're also now seeing that cognitive function is improved in
Speaker 2: diabetics treated with this family of medications.
Speaker 1: So that's established.
Speaker 2: So if you have altered blood sugar control and you
Speaker 2: get treated with these medications, you preserve brain health as
Speaker 2: opposed to not having the treatment. Now the next question is, Okay,
Speaker 2: they're in diabetic patients. What about patients with anonymer disease. Yeah,
Speaker 2: and so that's cutting ENGINEW. So the t I was
Speaker 2: underway in Alzum's disease with GLP one, and I think
Speaker 2: this is where it's really going to start breaking open.
Speaker 2: And again we're going to see the importance of metabolic health,
Speaker 2: brain health, frailty all coming together. But then the individual
Speaker 2: GP is going to be able to unlock all of
Speaker 2: this with the markets coming from the patient. So it's
Speaker 2: going to be fascinating, but I think it's going to
Speaker 2: really improve our outcomes as a community.
Speaker 1: So and GLP one like originally was marketed or is
Speaker 1: that because originally marketed for a bit like a lot
Speaker 1: of people us lose weight and not originally but like
Speaker 1: after that, but when it got into the consumer world,
Speaker 1: the retail world, and how does it stop you from
Speaker 1: putting weight on? What's it make? I thought it'd stop
Speaker 1: your appetitis something.
Speaker 2: It does work on appetite, but it also works on
Speaker 2: emptying of the of your stomach of food. But the
Speaker 2: effects through brain health are also linked to the effects
Speaker 2: on obesity, reducing inflammation, reducing sleep, and when you have
Speaker 2: less sleep, aap near the glymphatic system is working. It's
Speaker 2: clearing up the proteins at night time. So it's all
Speaker 2: We're all a huge ecosystem.
Speaker 1: And that's my final question or my final sort of
Speaker 1: subtopic I wanted to talk about. With sleep. Everyone sleeps,
Speaker 1: we all need different levels of sleep, and of course
Speaker 1: everyone keeps saying you got to sleep from seven eight hours,
Speaker 1: but I mean it's rare that I ever ever do that.
Speaker 1: I might be bed for that long, but I might
Speaker 1: not sleep that whole period. What is the difference between, Well,
Speaker 1: why is it important from a brain health point of
Speaker 1: view to a get overall enough sleep but be consistently
Speaker 1: to do it and c also to have slow wave
Speaker 1: sleep or what they call deep sleep or restored sleep
Speaker 1: not so much round but the other one. What is
Speaker 1: that doing for our brain?
Speaker 2: So this is again an evolving era of side. But
Speaker 2: understanding that there are systems in the brain that switch
Speaker 2: on when we're in sleep and deep sleep, and we
Speaker 2: need that every day to clean out the abnormalities, the
Speaker 2: protein abnormalities. In particular, we've talked about amyloid TAO, but
Speaker 2: presumably TDP forty three ouphas on newclin they've been pushed
Speaker 2: through this sort of cleansing process during us sleep. Now,
Speaker 2: the question I suppose when someone does have a sleep
Speaker 2: abnormality is is it a sleep abnormatic abnormality that's been
Speaker 2: driven by brain function or is it just a lifestyle problem.
Speaker 2: And it's much better to try and address that early on.
Speaker 2: And we all need proper sleep and whatever that hour
Speaker 2: those hours are is everyone's different. Like you said, you know,
Speaker 2: you don't need eight hours, and that's true. Some people
Speaker 2: need five, six, seven. But we all need a certain quality,
Speaker 2: a certain amount of sleep, but also than a deep sleep,
Speaker 2: and this is for preserving brain function.
Speaker 1: And deep sleep. During that deep sleep period or the
Speaker 1: slow wage sleep, the deep sleep, when you're sort of
Speaker 1: basically paralyzed. Yeah, you know, you're not moving, you know
Speaker 1: nothing's going on. Posted when you have your sleep during
Speaker 1: that period, something opens up in your brain and sends
Speaker 1: something out there to flush it. And unless you get
Speaker 1: into that state you don't flush out your brain. Is
Speaker 1: there a general rule as to how many hours per
Speaker 1: night or how much of it as a total percentage
Speaker 1: of your total sleep you should be getting.
Speaker 2: So a rough sleep hours is slight cycle is about
Speaker 2: three hours to two of those, so about six hours
Speaker 2: and probably maybe some break in between. So in and
Speaker 2: around six hours is the perfect. But obviously we're talking
Speaker 2: about adults. The younger you are, the more you need,
Speaker 2: and you know children need more eight ten, et cetera.
Speaker 2: So I think part of it is to try and
Speaker 2: ensure that people are used to looking after themselves, to
Speaker 2: go to sleep, to sleep hygiene.
Speaker 1: Yeah, it's just so easily. Yeah, and whilst you're leaping too.
Speaker 2: Yeah, and that's why again exercise, making sure you get
Speaker 2: a bed when you're fatigued. No booze, no booze, don't
Speaker 2: drink you know, teaen coffe just before beforehand.
Speaker 1: You know, try to stay on down, keep your excitement
Speaker 1: levels down.
Speaker 2: I think you should write a book on all of this,
Speaker 2: because you've got all of the keys.
Speaker 1: Can I can I just ask you one more question?
Speaker 1: Hopefully it's a comment on a lot of people, on
Speaker 1: a lot of guys I know older more, my age more,
Speaker 1: my age category. For many many years have been taking
Speaker 1: enormous and all sorts of those old school of sleeping tablets.
Speaker 1: And some people I know, and one of them are,
Speaker 1: are quite aware and alert when they're sleeping, so they
Speaker 1: don't get into the deep sleep for as long as
Speaker 1: other people do because maybe because they're listening, or they're
Speaker 1: not listening, but sort of instinctively they're listening that any
Speaker 1: little norms wake, come up, any movement, awakem up. They're aware,
Speaker 1: but they're asleep sort of thing. And I'm one of
Speaker 1: those people, and recently I come across these sleeping tables.
Speaker 1: They're not sleeping tablets, the tubblets which actually blocked the
Speaker 1: receptors for arecsen in your brain. And I just wonder
Speaker 1: if there's you might wouldn't get to make comment on
Speaker 1: it enough as area you even looked at. But rection's
Speaker 1: the mullog and ee brain there sort of just for
Speaker 1: the audience that keeps us sort of aware and awakes
Speaker 1: sort of awaking. It's normal. Seemed tables sort of sedate you,
Speaker 1: they said, your whole brain, and you basically feel like
Speaker 1: shit when you wake up because you didn't really sleep.
Speaker 1: They knocked you out. Whereas these things blocked the receptors
Speaker 1: on you on your brain cells that actually look grab
Speaker 1: this RECs and stuff that keep that actually trying to
Speaker 1: keep you awake, So it sort of blocks that that process.
Speaker 1: What do you think about those sorts of tablets and
Speaker 1: you have you have you had much experience with it?
Speaker 2: Well, what I would say is, again we're talking about
Speaker 2: upstream and downstream and lots of other things that happened. So,
Speaker 2: like we've been very interested in erecs and producing cells
Speaker 2: in the hippocampus because they also control our eating behavior
Speaker 2: and they're affected in front of temporal dementia and modeor
Speaker 2: neurine disease. The work that's been done here in Sydney,
Speaker 2: particularly Rebecca are Mad to show on that those cells
Speaker 2: are affected early in front of temporal dementia and modeor
Speaker 2: neurine disease. So although you've taken the approach from the
Speaker 2: erecs and to sleep, it's also important for your eating
Speaker 2: behavior and.
Speaker 1: To have to control the amount of recent or yeah, yeah,
Speaker 1: that's interesting.
Speaker 2: Yeah, and they can degenerate and when they degenerate, that's
Speaker 2: why people start having altered eating behavior. So there's a
Speaker 2: propensity with certain dementias to like sweet foods, and you know,
Speaker 2: to eat chocolates, and patients typically become put on weight
Speaker 2: and become a beast, and to exercise, and that's markers
Speaker 2: that this could be fronto temporal dementias. What I'm saying
Speaker 2: is you focus on erection for sleep, but those erections
Speaker 2: and cells also have other functions. So that's why I'd
Speaker 2: be always careful in doing thing that might alter function
Speaker 2: of cells in the brain.
Speaker 1: Because erection is from the gregwood or rexy, which means
Speaker 1: we say, when we're saying to someone in Greek, it's
Speaker 1: a calix, which means good appetite. And it's funny. So
Speaker 1: now I know why it was fascinating. Now I know
Speaker 1: why they call it a recitent has something to do
Speaker 1: with your appetite, it does and eating behavior. Oh right, yeah,
Speaker 1: So would you expect then if you know, let's say
Speaker 1: the half life of rex and pill was twenty four hours,
Speaker 1: for I say it's probably not the case, but that
Speaker 1: you might lose your hunger, I would say, so, yeah.
Speaker 1: And the other thing is, though I presume that it
Speaker 1: bounces back, because it does have a bounce. There's a
Speaker 1: mad bounce because I've measured it. Uh huh, so I measured.
Speaker 1: I measured a heart rate and HIV. So and I've
Speaker 1: watched it go through my So I look at my
Speaker 1: I go through and I look at my my movements
Speaker 1: of my heart, my art movements. Because it records everything,
Speaker 1: and you sleep deep in the beginning, but there's a
Speaker 1: bounce because the half life actually is five hours. So
Speaker 1: right towards the end of the sleep period, yeah, your
Speaker 1: heart rate shoots up big time and your HIV drops
Speaker 1: big time. Yeah.
Speaker 2: Yeah, well it's right at the core of functions in
Speaker 2: the hypothalamus and then.
Speaker 1: You actually wake up really bright. So to some extent,
Speaker 1: it's a bit of a trap because you think this
Speaker 1: is a sleeping tablet. And when I take the Sleepma tableau,
Speaker 1: wake up and feel really good. I feel really awake,
Speaker 1: Whereas if I take enormous and normal that the usual
Speaker 1: types of sleeping tablets, I wake up and feel like
Speaker 1: shit so immediately that my brain says me, well that's better,
Speaker 1: that's good. But the reason is is because my recxs
Speaker 1: and bounce is back the other direction, and I'm actually
Speaker 1: wide awake and I can actually get away less sleep
Speaker 1: and feel quite away. But it's just a bounce because
Speaker 1: all of a sudden you the receptors are now released
Speaker 1: from they're not blocked, and they grab and everything.
Speaker 2: What's fascinating. So I presume the ancient Greek must have
Speaker 2: known a bit about this.
Speaker 1: They probably did this. Ancient Greek does well. I really
Speaker 1: enjoyed today. I'm got to ask you this one question
Speaker 1: from my friend.
Speaker 2: If you don't monoclonal antibodies, that's what this is.
Speaker 1: Right.
Speaker 2: So monoclonal antibodies are now approved in Australia l kenomabed
Speaker 2: and aanamab, and they're very effective at stripping amyloid from
Speaker 2: the brain. And we know that so when we do
Speaker 2: a PET scan, if we do an amyloid PET scan
Speaker 2: before and after, we can see that the amyloid is
Speaker 2: either cleared or that the volume is right.
Speaker 1: Down post taking the monoclonal. Yeah, anybody.
Speaker 2: But then you may say to me, Okay, that's the case,
Speaker 2: and that protein is the critical driver of Alzheimer's disease.
Speaker 2: The patient should be completely back to normal, but they're
Speaker 2: not so, and that's where research is at. So we're
Speaker 2: clearing amyloid, but the patients aren't necessarily getting better, But
Speaker 2: what's happening is you're slow in the decline. You're turning
Speaker 2: the disease process back perps up to three years, right, okay,
Speaker 2: but cutting edge eries and these are patients who have
Speaker 2: had already manifestations and memory problems, but they're not too
Speaker 2: far affected because it's too late, so they have to
Speaker 2: have a mild effect in their brain function. But the
Speaker 2: cutting edge then is what if we treated people, you know,
Speaker 2: before they developed the condition. So we're looking at now,
Speaker 2: this is research that's being underway at at Neuroscience Research
Speaker 2: Australia and Emma Devenue I think he spoke to as
Speaker 2: one of the key drivers of that. So she's she's
Speaker 2: treating patients who have genetic malformations linked to Alzheimer's disease
Speaker 2: with these monoclonal antibodies in the hope they'll never develop
Speaker 2: the condition. And already we're seeing that if the families
Speaker 2: were developing, say Alzheimer's disease at forty five point fifty,
Speaker 2: they're passing those ages without developing the condition. Oh wow, yeah,
Speaker 2: so it's having an effect. But also these are early
Speaker 2: generation therapies. In other words, that's the first type of approach,
Speaker 2: there'd be more ederations, and there's so many coming through
Speaker 2: right now as we speak.
Speaker 1: So one of those two monoclinal antibodies called it's.
Speaker 2: A nanomab and look Canama, there may be means monoclonal
Speaker 2: antibodies and they're two different companies.
Speaker 1: And they're both are both basically available through neurologies. If
Speaker 1: you're a person in this category.
Speaker 2: There are people being treated here in Sydney now, so
Speaker 2: it's approved by the TGA. It hasn't yet been approved
Speaker 2: by the Pharmaceutical Benefits Advisory Committee, so you get paid
Speaker 2: for it. So yeah, so standard and don't quote me
Speaker 2: on this, but a standard treatment course would be about
Speaker 2: one hundred thousand dollars. But if you if you want
Speaker 2: to preserve your brain function, it's worth it. It's absolutely
Speaker 2: if you afford it, absolutely worth it if you can
Speaker 2: tap into your super and use it.
Speaker 1: And I had one final question for you, just in
Speaker 1: terms of and if I could just go back to
Speaker 1: cholesterol and to these stads, that that's a problem for
Speaker 1: your brain too. And let's say you're and I'd like
Speaker 1: you to comment on this. Let's say yours statin you're
Speaker 1: not able to take saturns. You know, for some reason
Speaker 1: the statins affecture sleep, but whatever the case may be,
Speaker 1: and sleeps critical. So there are now injections you can
Speaker 1: get which actually don't cross the blood brain barrier and
Speaker 1: lake statins do, and it will reduce significantly reduce your LDAL.
Speaker 1: Would you just like to comment on.
Speaker 2: That, Well, we're just talking about monoclonal antibodies. So monoclinal
Speaker 2: antibodies actually came from hematology for cancers. They're very effective
Speaker 2: in melanoma. We're now putting them into the brain for
Speaker 2: Alzheimer's disease. They're also very very effective for cholesterol control.
Speaker 2: So monoclonal antibodies are available for lowering cholesterol. But obviously
Speaker 2: that needs to be under pharmaceutical benefit scheme. There are
Speaker 2: certain people who are entitled to it, are not, and
Speaker 2: there are markers. It's not really my area, but there
Speaker 2: are people who focus on. But if it works, it
Speaker 2: does work. It's very effective.
Speaker 1: And if it's effective, if you can get your cholesterol
Speaker 1: down to the levels where it's like in the right territory, yeah,
Speaker 1: then it's good for your brain.
Speaker 2: It's fantastic for the brain. And again that's going to
Speaker 2: be transformational for our community. That's that's that's an amazing development.
Speaker 1: You know, I'm about to try it, but I'm not
Speaker 1: someone to qualifies under the pharmaceutical benefit scheme. I paid
Speaker 1: for it. Yeah, it's not cheap, but you have to
Speaker 1: go I think two injections a year, and you do
Speaker 1: one where you just do it every week or whatever is.
Speaker 1: But there's another one. We get two injections a year,
Speaker 1: but allegedly at Regicial audio by fifty percent.
Speaker 2: Quite quickly, incredibly effective.
Speaker 1: Yeah, it activates more receptors to grab hold of more
Speaker 1: older right, because there's something in your that turns out
Speaker 1: that blocks these receptors. What they do is they stop that.
Speaker 1: I think it's PCSK or nineteen is the name of
Speaker 1: the you know, the molecule, and that turns it stops that.
Speaker 1: It turns that off and then your receptors are grabbing
Speaker 1: all the elder that can on yourselves and that and
Speaker 1: that's this ingestion just fixes that part, so it goes
Speaker 1: nowhere else just go straight there and sorts it out.
Speaker 1: It's pretty amazing and great science. And again some scientists
Speaker 1: has worked this stuff out. They probably were doing it
Speaker 1: with something using it for something else at some stage,
Speaker 1: and all these things, as you say, you always say,
Speaker 1: and I want everyone to remember this, that what's good
Speaker 1: for your heart is good for your brain. Fantastic going
Speaker 1: to that, Matthew. Thanks very much, Thanks.
Speaker 2: Mark, and and thanks for your support for brain health,
Speaker 2: mental health and and also for neuroscience research Australia. We're
Speaker 2: really grateful, so thank you for most of them.