Panel Discussion Dr Alice Powell, Prof James Burrell, Ms Madelaine Rañola, RN

In this podcast, we delve into the financial implications and logistical challenges associated with new dementia therapies, particularly focusing on treatments such as dananimab and lacanemab. We discuss the estimated cost of these therapies, which can exceed $77,000 over an 18-month treatment period, and the potential out-of-pocket expenses associated with necessary scans and clinical assessments. The lecture emphasizes the high costs of both FDA-approved medications and the required diagnostic imaging, which could price many patients out of receiving these promising therapies. The discussion acknowledges the burden this cost poses on patients and the healthcare system, while also suggesting that the eventual acceptance of this treatment into public funding channels may depend on accumulating evidence of cost-effectiveness from early intervention.

The conversation shifts to the effectiveness of these therapies in improving patient outcomes, with participants debating whether these treatments can restore independent living for individuals with mild dementia. The consensus is that while these drugs may not fully restore cognitive function, they could potentially slow cognitive decline significantly in early-stage patients, leading to better long-term outcomes. The notion of societal perceptions of dementia contrasts sharply with approaches to cancer treatments, thereby reinforcing the need for more appropriate frameworks around funding and support for neurodegenerative diseases, including those with early-stage symptoms.

Addressing the complexities of voluntary assisted dying within the context of dementia care, we explore the legislative barriers that complicate access to these options for patients who may progressively lose decision-making capacity. The nuanced legal frameworks make it challenging for individuals with dementia to qualify for voluntary assisted dying, which raises ethical questions about autonomy and cognitive rights in progressive diseases.

Further segments cover the operational aspects of healthcare funding mechanisms, such as transitioning patients from the NDIS to aged care services upon reaching 65 years of age. Participants outline how existing funding structures will adjust to the new legislation, ensuring no patient should experience a loss of financial support due to age transitions. This segment highlights the legislative evolution aiming to establish a more structured resource allocation for individuals with neurodegenerative conditions.

The diagnosis and identification of conditions such as Creutzfeldt-Jakob Disease (CJD) are thoroughly examined, with a focus on advancements in diagnostic testing and the importance of consensus among specialists for accurate diagnosis. Further points in the discussion address the rarity of certain diseases in Australia, underscoring the need for a broad understanding of variances in symptomology and diagnostic measures unique to neurodegenerative disorders.

The role of dietary interventions and lifestyle choices in dementia prevention receives attention, with participants referencing studies supporting physical activity and social engagement as protective factors against dementia. Despite the popularity of alternative treatments, such as turmeric and curcumin, the emphasis remains on evidence-based practices shown to effectively modify dementia risk.

Lastly, we explore the relationship between cognitive reserve and dementia risk, emphasizing how educational background and occupational complexity correlate with resilience to cognitive decline. The challenges in identifying dementia in patients with high cognitive abilities are discussed, illustrating how some individuals may maintain function longer only to experience a rapid decline once symptoms emerge.

Throughout, the engagement emphasizes the necessity for a comprehensive, informed approach to dementia treatment—advocating for patients' rights while navigating the complexities of healthcare funding, legal frameworks, and evolving treatment paradigms. The session underscores the critical need for ongoing dialogue among healthcare professionals to enhance understanding and develop better care strategies for individuals with dementia and their families.

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Cost. That's the big one, isn't it?

MRI scans, PET scans, CSF scans, monthly injections in rooms,

presumably with the clinical assessment.

Yeah, so, I mean, that's the exact sort of treatment protocol is being established,

but it is very labour-intensive, there's no doubt.

The cost of the drug, let's start with that, over a course of 18 months of treatment

with dananimab, and the number will be similar for lacanimab,

is about $77,000 without any PBS funding at the moment.

There will be a cost associated with infusions, either in an infusion centre

or in private rooms, depending on how people are setting it up.

I'm of the understanding that some private health funds, if patients are insured,

may help cover some of the costs of infusion therapies, but there will be an

out-of-pocket fee, I assume, half a dozen MRI scans.

The exact cost of the scans is not going to be not clear because it depends

how many sequences and how much time in the scanner.

So if we're just doing a quick scan to meet the objectives of the safety assessment,

that might be much more affordable than say a full diagnostic scan.

And then there'll be clinic reviews, not every single infusion,

but probably every time you have an MRI scan or if there are any symptoms or problems.

So we don't know exactly how much it will cost, but the number will price a

lot of people out of therapy I think everybody's aware of that.

My own personal belief is that these therapies are very, very effective and

the evidence is reinforcing their use and that within the next,

and I think this is one of the questions somebody put up,

most expensive therapies, there's a gap between TGA approval and PBS funding

of a year to one to two years.

So I think once that evidence accumulates that we're actually saving the system

money by treating people early, then I think PDS and Medicare funding and things

will come through, but probably not for a year or two.

So back of the envelope, it's about 100k for one year. Yeah.

Amyloid PET scans are about 2,000. So if you're talking two to three of those,

that's also something you need to factor in.

Follow-on question there.

I just want to ask you, these therapies, do they return the patient back to

almost normal so they can live independently?

I know the amyloid plaque and stuff is one thing.

Clearance is one thing. But whether they can go back to their own home,

live independently without any help, that's what I'm asking.

Will they do it? And will they do it long-term?

Yep. So before I answer your question, I just want to, I guess,

point out that I think we're way too nihilistic when it comes to dementia.

So, you know, we spend a huge amount of money on cancer treatments that might

give somebody an extra two or three years of, you know, living well with cancer.

And we don't seem to worry about, you know, the cost of those therapies or the

risk of those therapies.

But with dementia, I think there is this sense that this is an old person's disease.

You know, you can't do anything anyway. What's the point of giving them a therapy

that costs a heap of money.

That's the first thing. The second thing is we're really targeting those patients

that have very few symptoms anyway.

So even somebody with mild dementia is only needing a little bit of support

to live. They're not people in nursing homes. They're not heavily dependent already.

They're mildly dependent or even better.

That's the second point. In terms of your question, the therapies have not been

proven to restore function.

They slow down decline but some

of the studies looking at lecanumab over a four year period

have shown that if you pick that low to

medium tau group the slowing of

decline is so significant that depending on how you measure it it looks like

they get a little better now they're probably not getting better but they're

definitely not getting worse and so if you're picking that very very early group

you might prevent the dementia from happening in the first place so I think

that's where we really need to focus our attention and,

So partially, you know, just echoing your comment that our society sort of delusionally

believes that all cancer is curable and that nothing can be done about neurologic

disease. We need to flip that completely.

Yeah, 100%.

We're going to head off on a tangent. Can you comment on voluntary assisted

dying in dementia? Yeah.

Alice? Sure. I get asked about this quite a lot, actually. Dropping you right in it. Yeah.

So one of the key criteria to access voluntary assisted dying is that you have

capacity to make that decision and that capacity needs to be enduring throughout the process.

So that will exclude, fortunately or unfortunately, whatever your position is,

the majority of people with these conditions because they tend to be slowly

progressive In order to qualify for voluntary assisted dying,

you have to have a likely prognosis of under 12 months with a neurodegenerative disease.

And basically everyone we see with dementia, if they've got that sort of prognosis,

they very likely will have lost capacity to make that decision.

So it's a catch-22. The legislation was written to be a catch-22.

Yeah.

No, no, no, no. No, it can't be. managed in an advanced care directive that

doesn't have... Yeah, that was my question.

Sorry, that was my question. The legislation is different in other countries,

so there are varying... It varies, so I think the Australian legislation is

very clear that you must have decision-making capacity throughout the process.

It might change over time. It's a conservative position, but I guess if you

think it through logically,

let's say I put in my advanced care directive, if I get demented,

I want to have voluntary assisted dying and then I change my mind but I don't

have capacity, what do you do then?

So I think that's the point is that you have to have capacity all the way through.

We could spend the whole day on this. This is really, it's a really squirrelly

thing and the legislation is a very narrow bandwidth.

I've got a question for Mad that's a two-part question.

When the healthcare packages change next month, what happens with people who

are on previous levels? What happens to that funding into the new levels?

And the second one, which is sort of related, is when patients are on the NDIS

and they hit 65, what happens with their funding?

Okay, so the first part, So your patients that are currently on packages in

the current system, they'll automatically, their funding will roll over into the new.

So they will just, they may be recategorised, but the funding that they've got

for the current year will remain.

So there's no concerns, there's no reassessment for people that are currently enrolled.

And then for the people that are actually waiting on packages,

Again, no need for reassessment.

They'll actually be assigned a package within the new eight levels of packages.

And the second question with NDIS as well.

So once people click over to over 65, so they don't lose their funding,

they'll actually continue again with that year's worth of the NDIS.

And then they'll actually change over to an aged care package once.

Yeah, so they won't lose one that they're currently in at the birthday.

They'll get the year's worth of that NDIS funding and then they will change over. Thanks, Matt.

Look, there's just so many fantastic questions. I'm just going to take another

tangent. This one's for Alice. Can you tell us how CJD is diagnosed?

So CJD, we have had some advances in the investigations for CJD.

So there is a very sensitive and specific marker in cerebrospinal fluid,

for example, called RT-QUIC.

So that's something that you send off to Melbourne to the Flory and they will analyse that for you.

And I think turnaround time is a couple of weeks.

There's quite a kind of classic clinical syndrome.

There are quite specific MRI findings so

the cortical ribboning is very specific

and then some also subcortical changes that are characteristic

for CJD so if you write on the request form that that's specifically what you're

looking for then the radiologist can have a very good look and then there's

also findings on EEG which are supportive and I find if you have any concerns

about the diagnosis whether you're correct or not the Flory is a really good resource.

So the professors there who've done decades of work on this,

they will actually for free review the case for you.

So they'll be happy to look at the MRI, look at the EEGs.

I mean, usually a diagnosis made by neurologists with some difficulty, it's fair to say.

But I agree, the Florey Institute, there's a national laboratory that are heavily

invested in CJD research and thankfully there are not that many cases so they're

very excited when there may be a case.

One in a million, correct, at the moment? One in a million incidents?

Something like that, yeah.

There's an add-on question to the CJD? I'm sorry, I should say gold standard

is pathological diagnosis, so looking at the brain.

But you know the sensitivity, specificity of these other tests.

And it is a notifiable disease, so there's a whole heap of repercussions with the diagnosis of CJD.

And if you have a rarer genetic type, then you can also have a blood test diagnosis of it.

Look, are there many diagnosed here? Because I just want to ask,

because you're asking for CJD,

mainly like we get some patients who lived in the UK before 96 or something,

the other ones looked into, whereas an Australian perspective,

that is not too much. and what are the other things we need to do.

And having worked in the UK at that time, so new variant CJD is vanishingly rare.

There have been no proven cases in Australia. It's different pathologically, presents differently.

So the CJD that occurs in Australia is both genetic and sporadic and incredibly low frequency.

So I've had two patients in the last two years at North Shore and I'm on call once a month.

I think I've had maybe five or six in the last 10 years. I mean,

I've got a particular interest in young onset dementia, of course.

But yeah, it's not common.

It's usually, as Dom says, the sporadic, very rarely the genetic form.

And the variant CJD is not really an issue in Australia.

Question for you, James.

Any benefit of turmeric or curcumin in the diet?

It's a teaser. Yeah. I mean, I'm not a chef. No.

Look, I think as a general comment, when you have a disease for which no really

good treatment exists, in other words, a treatment that you can take and it

fixes your problem and you get on with life, people are very interested in looking

at alternative options.

And you know this is an area that in dementia

kind of care that comes up all the time so there's turmeric

there's cumin there's uh you know coconut oil

there's a whole range of different things that people are interested in cbd

oil all of that all of those things you know and it's hard for someone uh you

know when i can't offer an evidence-based therapy it's hard for me to say oh

don't don't don't bother with that, it's rubbish.

I think if something is cheap, unlikely to cause harm, people don't get too

invested in it, then I say go for it.

Cumin and turmeric specifically, I don't think there's a huge amount of evidence

to support its use, but I guess more broadly there is now evidence to support

lifestyle interventions in general.

So there's a big Scandinavian study called the FINGER study,

which I tell all my patients about.

It's the FINGER study because there's five components. The first is intellectual

stimulation, second is social stimulation, third is physical exercise,

fourth is control of vascular the risk factors and the fifth is diet.

And in this one, it was actually a Mediterranean style diet.

You know, they also did a sub study where they added Suvenade,

which you may have heard of as a product available through chemists.

But, you know, using these five interventions, they established that dementia

risk can be modulated by up to 43%.

So that's a dramatic, you know, so that is an evidence-based recommendation,

the components of the So, those are the things that I would be focusing on.

That was not done.

There was a randomized control trial done recently, about a couple of years

ago, because Suvinade is quite expensive. A lot of patients come and ask us.

But I read in one of the medical journals, there was not too much evidence. Yeah.

Okay. This is for Alice. This one is, do people with higher IQ in premorbid

and adolescent period, are they less likely to develop Alzheimer's?

Are there studies of the use of premorbid IQ in predicting dementia?

Interesting question. It can be difficult to tease out high IQ and high levels

of education and high occupational complexity because all of those things kind of go together.

But certainly that is protective.

So those are things that build your cognitive reserve and allow you to be resilient to pathologies.

So yes there is an association between that

and a lower risk of dementia and it's one of the

modifiable risk factors of the 14 that

have been presented by the lancet commission that are responsible

for 45 of modifiable risk of dementia um while it does reduce your chances what

we do find is people who um have a high iq have a high educational level occupational

complexity can still get dementia.

So there is definitely luck into it as well.

And unfortunately, those people will have compensated for a very long time.

By the time they get it, they tend to actually deteriorate quite rapidly.

We call it falling off the cognitive cliff.

You mean symptoms wise because the pathology is happening in the background.

The pathology will have been building up for a very long time.

They're compensating really well and then it all gets saturated and then they

can deteriorate quite quickly.

Here's an interesting question for James.

What's the relationship between amyloidosis and the presence of amyloid in the brain?

So I saw that question and I was worried somebody would actually ask me.

That's why I asked you. Look, I think it depends... What does amyloid mean?

Yeah, it depends what you mean by amyloid. So if you're talking about systemic

amyloidosis, so that could be related to genetic disorders where an excess of

various types of amyloid is produced versus, say.

Amyloidosis related to chronic infection.

We probably don't see that so much in Australia anymore.

Those are systemic disorders which can affect the nervous system,

but they tend not to be associated with Alzheimer's disease.

So they would typically cause cardiac

abnormalities, peripheral nerve abnormalities, those sorts of things.

There's another entity which is probably underlying some of the cerebral microbleeds

and microhemorrhages that we've been talking about this morning,

which is called cerebral amyloid angiopathy.

So this is where there is a form of amyloid that's deposited within blood vessels

and it damages the integrity of the blood vessels.

And that's why patients with this sort of amyloid, cerebral amyloid angiopathy

can have little areas of bleeding detectable only on an MRI scan.

That's a cerebral microbleed. But it's also the pathology that underlies symptomatic

low bar intracranial hemorrhages. So people have had big strokes related to

hemorrhages, often that's related to cerebral amyloid angiopathy.

Um, the relationship between cerebral amyloid angiopathy and Alzheimer's disease,

um, there is an association, but it's, it's not as tight as you might think.

Um, so you can't look at a scan and say, oh, well, there's a few microbleeds.

This person must have Alzheimer's disease.

Um, there is an association, but you know, they, they're sort of separate,

uh, related, but, um, slightly, uh, that's confusing, isn't it?

They're slightly related, but I don't think the presence of one reliably predicts

the other, if that makes sense. Can I make one other comment?

Because amyloidosis is a bit confusing because another way of understanding

amyloidosis is actually people having brain amyloid but not having symptoms.

So that will be a proportion of people. And I think it's over 40% of people

who are over the age of 80 will have amyloidosis, but they might be completely normal cognitively.

So that's, yeah, there's lots of different amyloid.

I asked a question, putting a different way.

Putting it differently, amyloidosis, does blood-brain barrier stop the amyloid

disease to enter the brain?

And when we talk about amyloid plaque, is that the same thing as amyloid getting to the brain?

Amyloid is a physical chemical description of protein deposition.

And it depends. There are many, many different proteins that produce amyloid.

So the amyloid in Alzheimer's disease comes from a different derivation from,

say, transthyretin amyloid that affects people's heart.

So the myeloma characteristically causes amyloid.

So it's actually a microscopic description is amyloid and the protein is the

thing that causes the disease.

Yeah. Fair statement? Yeah, I think that's fair. I think it is confusing.

I agree with you. So, yeah, amyloid just comes from amyla, which is Latin for starch.

This one is a Dorothy Dixer for Alice.

Is MRI reporting fairly standard? No.

Or are some places better? Well, of course, the best place is MMI. But anyhow.

Yeah, interesting question. MRI reporting.

So I think it's, I wouldn't expect everyone to look at the scan,

but I certainly try and look at the brain scan myself because I think there

can be over-reporting and under-reporting.

And certainly a neuroradiologist is very different from a general radiologist.

So a neuroradiologist has a specific interest and training in reporting brain

scans and it's very important in this area that you're looking specifically

for atrophy and you're grading that atrophy and in what brain regions.

So I will very commonly see reports that say normal age-related involutional

change and this might be in a 65-year-old and you look at it and there's frank

atrophies in the sort of temporal and parietal lobes.

But if I ask a friendly neuroradiologist to have a look at that,

they will tell me specifically where it is and then there are certain grading

systems that can be used.

So I think if you are querying a report,

you can pick up the phone to the radiologist, you can ask for another radiologist

to look at it, you can ask for a neurologist's opinion and the other thing that's

becoming more common and can be quite useful is this quantitative analysis.

So you can actually run the volumetric analysis,

brain scans through software, and that will calculate the volumes in the different brain areas.

And you can then compare that with what it should be in a control database for that person's age.

And that's quite useful. Yeah, I think these AI tools are going to help.

I think just to elaborate on what Alice is saying, I think the general standard

of radiology reporting, at least in the setting of neurodegeneration, is actually poor.

And, you know, I have to look at the scans because I don't trust even good neuroradiologists

when it comes to atrophy patterns.

I think, you know, it depends what they're looking for.

They're much better at looking at stroke and hemorrhage and even cerebral microbleeds,

but patterns of atrophy, they're not great.

I think the term involutional change should be A, banned, and B, considered a red flag.

You know, atrophy is associated with advancing age, so you do have to try and

look at the scan in the context of the patient's chronological age,

but there's no such thing as involution, in my view.

Thanks, James. Thanks, Alice. Again, coming back to MAD, this is a really important

point, so we're going to labour this a little bit.

With NDIS, which has a cut-off of 65, can people register before the age of

65 with their neurodegenerative problem and still be supported on the NDIS once they turn 65?

That's a good question. Look, I would encourage people to sign up,

even if they're at 64, to get into the NDIS.

And then it is a matter of sort of negotiating with NDIS and My Aged Care once

they click over the age of 65.

Because 65-year-olds these days, if they're well with their disease,

the NDIS supports are going to be more relevant to them than in my aged care. So just because they...

Age out, if, you know, for lack of a better term, it doesn't mean that the NDIS

supports aren't the better supports for them for their stage of disease.

So I wouldn't count out joining even at the age of 64, just because my aged care starts at 65.

So there's definitely negotiations that can occur.

They can definitely, there are instances where people can continue on the NDIS program,

because it's not as simple as swapping over to my aged care,

because the NDIS funds supports for younger people, so, you know.

Listen, we've got, we're just hitting 10.40, so I'm mindful of time.

We'll just take one more question from the mic up the back, but you know,

there are fantastic questions that we still haven't got to.

So, over the tea break, If your question hasn't been answered, just tackle someone.

But just the last question and then we'll head off to morning tea. Thank you.

I was wanting to query about cognitive testing. There's so many different cognitive testing available.

And we've got so many aging population who are non-speaking.

So do we do a standardized cognitive testing or is it patient specific?

So, the level of caffeination is probably dropping, so I'll try and be brief.

I think first thing I'd like to say more generally is that please do some cognitive

screening. It's very helpful. It gives you a sense of how bad the problem might be.

So, yes, it's a great question. Really important to do some cognitive testing.

The mini mental status examination has largely fallen out of favour, I think, in the field.

Please switch to the Montreal Cognitive Assessment if you can.

I have done the Montreal Cognitive Assessment in Cantonese with an interpreter,

so I can remember the word for daisy.

I'm not going to try and pronounce it because I might make a mess of it, but anyway.

What's that? Yeah, yeah. More generally, though, if you don't have access to

an interpreter, the option might be to use the Roland Universal Dementia Assessment Scale or RUDAS.

All cognitive tests will be affected by language and education background,

but the RUDAS is said to be less affected than some of those other ones.

But sometimes you just have to accept if somebody doesn't speak English as a

first language, they don't have a lot of education, you may struggle to get

an accurate read on their level of cognition.

I think the challenge then is if somebody's always functioned at a certain level,

which is a bit below average, you don't want to over call that and say that they're demented.

So, you know, if you've got people that, you know, have never had a bank account

that, you know, are barely literate, you know, you can't say,

oh, well, because they, you know, they must be demented because their kids need

to pay the bills for them.

You know, that's, you've got to be relative to their optimal performance, if that makes sense.

It just remains for me to thank the three presenters and also thank you all

for your questions. They were fantastic questions. Thank you.

We're going to head to morning tea.