Latest / Dementia Researcher Vodcast / Changing the Course of Dementia: What Will Make the Biggest Difference?

Transcript

Changing the Course of Dementia: What Will Make the Biggest Difference? · Dementia Researcher Vodcast

• 0:00
  - [Announcer] The "Dementia Researcher Podcast,"
• 0:02
  talking careers and research,
• 0:03
  sharing conference highlights, and so much more.
• 0:07
  - Hello and welcome.
• 0:09
  I'm Emma Mead.
• 0:10
  And what you're about to hear was recorded
• 0:12
  at the Alzheimer's Research UK Thames Valley Network
• 0:15
  Dementia Research Day 2026.
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  We spent the day hearing from great speakers,
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  sharing their research,
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  and looking at where science is heading.
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  And we closed with a panel on the question
• 0:28
  that the whole field keeps coming back to:
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  What's actually going to make the biggest difference
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  changing the course of disease?
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  I was joined by four people
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  who come at this from very different angles.
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  Professor Sanjay Manohar,
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  professor Michele Hu, Peter Johnson,
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  and associate professor Laura Winchester.
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  Here's the conversation.
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  (bright music)
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  Hey, good afternoon, everybody,
• 0:59
  and I'd like to extend a warm welcome to everybody
• 1:01
  who's listening on the "Dementia Researcher Podcast"
• 1:04
  this afternoon.
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  Today, we have a panel
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  and we are going to discuss changing the course of dementia
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  and what will make the biggest difference.
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  And I'm delighted to be joined here by an expert panel.
• 1:15
  And I'd like to hand over
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  and allow our panel to introduce themselves.
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  We'll start with Michele at the end, please.
• 1:21
  - Thank you. My name's Michele Hu.
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  I'm a neurology consultant of nearly 20 years,
• 1:26
  over 20 years experience,
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  and I focus on Parkinson's
• 1:30
  and atypical Parkinson's and therapies for this.
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  But I'm also on a dual role
• 1:34
  of professor of clinical neuroscience
• 1:36
  in Oxford University, Nuffield Department.
• 1:40
  - Hello, I'm Peter Johnson.
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  I'm head of service for Dementia Oxfordshire.
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  That's a service delivered by Age UK Oxfordshire.
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  And we support everybody in the community living
• 1:49
  with the dementia diagnosis
• 1:50
  and their families across Oxfordshire.
• 1:53
  - Hi, I'm Laura Winchester.
• 1:55
  I'm based in the Department of Psychiatry at Oxford.
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  My interest is in bioinformatics and looking at data
• 2:02
  to understand Alzheimer's and Parkinson's.
• 2:07
  - Hi, I'm Sanjay Manohar.
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  I'm a computational neuroscientists,
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  but I also run the Cognitive Disorders Clinic
• 2:15
  at the John Radcliffe,
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  which sees a variety of dementia patients.
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  So unlike the psychiatrist who see the older age patients,
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  we see all the younger dementias people with Alzheimer's
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  and slightly unusual dementias as well.
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  And my area of interest is kind of more neuropsychiatric
• 2:34
  and cognitive features of this disease
• 2:37
  and how we explain them.
• 2:39
  - Thank you.
• 2:40
  It's great to have such a range of perspectives here
• 2:42
  on the panel today,
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  so I think we're gonna have a great discussion.
• 2:45
  So before we look ahead,
• 2:47
  to what we think will make the biggest difference
• 2:49
  to people living with dementia,
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  I'd like to kind of take a step back
• 2:52
  and let us think about what the current challenges are
• 2:55
  in the field.
• 2:57
  So I'd maybe like to start with Peter, if I could,
• 2:59
  and hear from your perspective
• 3:01
  from the Dementia Oxfordshire community
• 3:04
  and think about what the people that you interact with
• 3:08
  really see as some of the biggest challenges at the moment.
• 3:12
  - So dealing with the dementia diagnosis is a hard
• 3:15
  and often desperate journey,
• 3:16
  both for the person with the diagnosis and their families.
• 3:20
  And probably one of the biggest challenges they face
• 3:22
  is dealing with the stigma.
• 3:23
  I mean, we've heard it alluded to earlier today
• 3:26
  that you could suffer.
• 3:28
  You get socially isolated very easily
• 3:30
  that some communities have no words for dementia.
• 3:33
  So having the conversation with your community
• 3:35
  can be very difficult
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  and you can be inadvertently isolated and made very lonely.
• 3:41
  And I think that culturally,
• 3:45
  we inadvertently isolate and disempower the people
• 3:49
  by, for instance, if when you get a diagnosis.
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  For the person with the diagnosis,
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  the message sometimes they take out of the room
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  is my life is over.
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  I need to prepare for the end.
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  And for the partner,
• 4:02
  they will go into the room as their spouse
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  and leave as the carer.
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  They're told that they're a carer
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  and they're expected to care
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  for this person they've lived with as a partner
• 4:11
  for 30 years.
• 4:13
  - Yeah, I can see
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  that that could be very distressing and difficult.
• 4:17
  I mean, Michele, is that something that you see
• 4:18
  in the clinical setting as well,
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  or are there any other challenges that you come across?
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  - So yes, so when you're giving somebody a diagnosis
• 4:28
  of early Parkinson's,
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  often what people most fear
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  is what will be my risk of developing future dementia?
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  And also it's increasingly a condition of ageing,
• 4:40
  both dementia and Parkinson's.
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  So because there are populations across the western world
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  are globally increasing
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  in terms of how people are living longer,
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  we are getting really a pandemic
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  of Alzheimer's and Parkinson's.
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  So one of my concerns is, are we gonna have enough people
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  to diagnose these conditions and also to effectively treat
• 5:02
  and support in the community?
• 5:04
  - Yeah, it's really important.
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  Sanjay, maybe from your perspective,
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  it sounds like you interact with younger people
• 5:10
  who are given sort of diagnoses.
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  Do you see similar challenges
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  or are there differences between sort of older populations
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  and younger individuals?
• 5:19
  - Yeah, I think the challenges are very similar.
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  There's a massive shortage
• 5:22
  of community care for these people.
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  And I mean, Dementia Oxfordshire did
• 5:26
  a massively important job in this
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  where the NHS and social services
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  can't quite stretch that far.
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  One thing I'd say about this,
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  this carer business is really critical.
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  And half of the patients with Alzheimer's
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  who we send out of the room
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  promptly forget they've got Alzheimer's.
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  And the other half,
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  you know, they're very distressed by it.
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  But in all cases,
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  the carer is the one who bears the responsibility.
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  There's always a proportion of people who don't have a carer
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  and or are already kind of, you know, being cared for
• 6:01
  in some way.
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  And they're a difficult population too. Yeah.
• 6:06
  - I mean, Peter, maybe, do you have any perspective on that
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  where Sanjay says there are some people
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  that don't have carers, you know?
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  Is that something that you come across often
• 6:14
  in the Dementia Oxfordshire group?
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  - I think it's surprising the number of people
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  that are living alone with dementia,
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  either because they have no family
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  or because their family lives a long way away,
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  often out of county.
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  And that can be very challenging
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  and make it much harder to support that person.
• 6:34
  - Yeah, I can imagine that would be really difficult.
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  And it's good that there are organisations like yourselves
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  to provide that support
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  and groups that can really kind of help people
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  who might be feeling isolated and alone.
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  So it's wonderful to see that.
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  I wondered maybe if we can move a bit
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  towards that more sort of clinical perspective
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  and think about sort of gaps and challenges
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  in terms of how we are treating dementias
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  and other sort of neurogenerative conditions.
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  And maybe, Michele, if I could come to you first,
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  what do you see as the major challenges
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  in the clinical space at the moment?
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  - I think who diagnoses dementia,
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  whether it should be, for example, a neurologist,
• 7:14
  a general physician, or a psychiatrist,
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  is something that we haven't really coordinated very well.
• 7:20
  I personally don't think it matters
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  as long as you actually have a good understanding
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  and a good rapport with the patient.
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  So I think we need to work better
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  with our community services in a more joined up way.
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  So for example,
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  we've recently met with our community psychiatry team.
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  Our older age psychiatrist said,
• 7:39
  and they've actually said,
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  "We think you neurologists are better
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  at diagnosing Parkinson's dementia,
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  but we're better at supporting in the community.
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  So could you do that front aspect and initiate treatment?
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  And we're happy to continue it
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  and provide community support."
• 7:53
  I think that actually is a way going forward
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  that optimistically may make a better use of our resources
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  and be more effective.
• 8:02
  - That's great. Thank you.
• 8:03
  And sort of thinking also about how we understand disease,
• 8:07
  and maybe I'll turn to Laura
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  and ask, you know, what are the main challenges
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  when we think about, you know...
• 8:13
  So bringing together our disease understanding
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  and combining that with our clinical practise,
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  you know, to me, that feels like there's a bit
• 8:19
  of a gap there. I don't know if you have any thoughts
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  about what the challenges are
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  that we can, you know, overcome to address that question.
• 8:26
  - So I think there's lots of gaps there,
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  and I think there's lots of people in the room
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  are probably working on different bits of those gaps.
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  I think there is a lot of work now going
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  into not just looking at maybe cohort,
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  but real-world data as well.
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  So there is people researching both.
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  And I think it's all about what data is available
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  and as people maybe thinking about people coming to clinics
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  and collecting data from those people.
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  So that's available for us to look at
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  in addition to what we are looking at sort of collecting
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  and designing.
• 9:00
  So I think it's joining up those different groups
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  and collecting as much information as possible
• 9:06
  so that we can continue to study that as well.
• 9:09
  - That sounds like a very important step.
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  I mean is that feasible in a clinical setting?
• 9:14
  I don't know if, Sanjay, I can come to you
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  and, you know, think about how we can tie up,
• 9:18
  you know, get collecting the right data
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  for researchers like Laura to use it going forward
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  to address some of these key questions.
• 9:26
  - Yeah, and I think coming to a day like this,
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  you see so much great research,
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  and then maybe something that will surprise
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  quite a few people
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  is that out of, let's say the 500 patients
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  with dementia, you know,
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  several years with Alzheimer's disease,
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  about 10 of them are typical Alzheimer's.
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  The rest all have something else as well.
• 9:53
  We've heard a little bit about copathology
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  and you know, how you might have amyloid,
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  how you might have Lewy body pathology,
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  corticobasal pathology, all these other things.
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  But also they have vascular disease,
• 10:07
  they have epilepsy, they have head injuries,
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  they have, you know, everything else,
• 10:12
  they have comorbidities elsewhere in their body,
• 10:14
  diabetes, and so on.
• 10:16
  So each patient we see
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  has kind of a unique fingerprint profile
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  in a very high dimensional space.
• 10:25
  And each one is unique, right? Each patient.
• 10:29
  That's the key.
• 10:31
  And when you see research
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  that you know, ultimately it's like labels people
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  with having Alzheimer's or not,
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  well, we give Alzheimer's labels on a whim, let's say.
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  The process of diagnosing the disease
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  is partially biological, partially social.
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  It's partly to do with what's important
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  and needed by that patient at the moment.
• 10:55
  And that's a bit old-fashioned, right?
• 10:58
  Because this was conceived in a day
• 11:00
  where we didn't have any disease-modifying therapies.
• 11:04
  Now if you say we're gonna give treatments
• 11:07
  that target a molecule,
• 11:09
  and it becomes so much more important
• 11:11
  to get precision diagnosis
• 11:14
  to fingerprint each patient
• 11:16
  with exactly what's going on biologically.
• 11:17
  And then we've made very early steps into this
• 11:21
  by now having biomarkers
• 11:23
  that we can test promptly and quickly.
• 11:28
  Until a few years ago, until like this year, in fact,
• 11:31
  we had to get cerebral spinal fluid
• 11:34
  with a lumbar puncture on every patient
• 11:36
  if we really wanted to know the biological diagnosis,
• 11:40
  which meant that about 70% of patients we didn't bother
• 11:44
  to get the biological diagnosis, right?
• 11:46
  It's expensive, painful, and inconvenient.
• 11:49
  But I think that is the challenge I would highlight
• 11:53
  is that everyone needs to understand
• 11:56
  the precision with which we know these labels
• 11:59
  and also think of them
• 12:01
  as inhabiting this high-dimensional space.
• 12:02
  And I think that once that challenge is addressed,
• 12:04
  we'll have much better avenues into treating this disease.
• 12:08
  - Yeah, that's so interesting.
• 12:09
  I'd like to maybe pick up at the point you made
• 12:11
  about the different sort of samples
• 12:13
  that we can gather from the clinic now,
• 12:15
  and maybe ask Laura sort of, you know,
• 12:18
  have you got some examples
• 12:19
  of how that, you know, huge amount of data now
• 12:22
  that we can gather from patients clinically can be used?
• 12:26
  You know, are there any examples from the work
• 12:28
  that you're doing for that?
• 12:30
  - So I think, actually, you touched on a couple of things
• 12:33
  that we're thinking about.
• 12:34
  So looking at those datasets and pulling out...
• 12:37
  So there is a biomarker that's working from blood now,
• 12:40
  but that's one, and maybe there are more out there.
• 12:44
  So p-tau is looking for amyloid.
• 12:46
  We might be interested in markers
• 12:47
  for some of the other pathologies that we're thinking about.
• 12:50
  So when you're thinking about dementia,
• 12:53
  it's a complex set of pathologies in there
• 12:56
  and we can use the datasets that we have to perhaps...
• 13:00
  Now we have the bigger datasets,
• 13:01
  you might have power to pull apart these complex problems.
• 13:05
  So thinking about the pathology level,
• 13:07
  but also thinking about at the clinical level
• 13:09
  and looking to see whether there's a lineup there.
• 13:11
  In some cases, there isn't,
• 13:12
  and there's a very interesting question
• 13:14
  with sort of resilience.
• 13:16
  So whether you have a buildup of amyloid,
• 13:18
  but these patients
• 13:19
  are not showing the clinical symptoms yet.
• 13:21
  And so that group are interesting to study.
• 13:23
  And so as we get more data on these patients,
• 13:26
  we'll be able to pull out more information about that.
• 13:29
  And it's about understanding, getting a bigger picture.
• 13:32
  And I think these datasets, as they build,
• 13:33
  become really important.
• 13:35
  - That's really interesting. Thank you.
• 13:37
  And I mean, obviously, to do these analysis,
• 13:40
  we need people to donate samples.
• 13:42
  And maybe, Peter, from your experience, you know,
• 13:46
  is there a great sort of appetite in the dementia research
• 13:48
  or the dementia community to support dementia research?
• 13:52
  And do people really know very much
• 13:54
  about how they can go about donating blood
• 13:58
  or any other sort of samples?
• 14:01
  - I think the reality is that people with carers
• 14:04
  and people with a diagnosis are time-poor.
• 14:07
  So the difficulty is finding a way to engage with people
• 14:10
  that are overwhelmed by caring
• 14:12
  and the condition they're managing.
• 14:13
  So I do think that they do want to engage,
• 14:16
  it's the practicalities of how you engage.
• 14:19
  And you kind of need,
• 14:20
  I mean we've talked about this previously,
• 14:21
  but you kind of need to meet them where they're at.
• 14:23
  So if you engage with them,
• 14:25
  so we have an experts group
• 14:26
  that's often used to engage with people,
• 14:28
  but any of our groups that meet regularly,
• 14:30
  you'll be able to engage in a space
• 14:32
  where they feel comfortable
• 14:33
  and they'll be able to contribute.
• 14:35
  And that kind of works.
• 14:38
  Researchers are very keen to come along
• 14:39
  and just chat to our clients.
• 14:43
  And I don't really understand
• 14:44
  how they use the information they get,
• 14:45
  but clearly they keep coming back, so it has value.
• 14:48
  And I would say from the people
• 14:51
  that are living with a diagnosis and their carers,
• 14:53
  there's a therapeutic value of just being involved.
• 14:57
  It's giving their life meaning. That gives them a purpose.
• 15:00
  And that can make a really big difference.
• 15:02
  It's that sense of what is the point of me.
• 15:04
  It helps them retain that focus of who they are,
• 15:07
  for both the carer and the person with the diagnosis.
• 15:10
  It's a way of them contributing.
• 15:12
  So they are keen to engage,
• 15:14
  but often it's hard for them to do so
• 15:17
  because they're being overwhelmed
• 15:19
  by the rest of their lives.
• 15:20
  - That's really an important point.
• 15:23
  Michele, you had something- - I was saying I've won
• 15:25
  the Oxford Discovery Parkinson's Cohort,
• 15:27
  which has 1,600 individuals now since 2010.
• 15:30
  And people find it really reassuring
• 15:33
  to be in an observational cohort
• 15:35
  because they're seeing often the same staff.
• 15:37
  Perhaps every year or year and a half,
• 15:40
  they're being fed back
• 15:41
  if there's anything that needs clinical care.
• 15:43
  You know, general health improved
• 15:45
  because we're measuring things
• 15:46
  like high blood pressure, et cetera,
• 15:49
  you know, as part of that assessment.
• 15:51
  And we find that people
• 15:54
  are quite willing to do procedural tests
• 15:57
  like a skin biopsy, blood tests, and lumbar puncture.
• 16:00
  And I just wanna take issue.
• 16:02
  It's not painful when we do them, Sanjay.
• 16:04
  (group laughing)
• 16:05
  It's no more painful than when you go to the dentist
• 16:08
  and have a local anaesthetic which stings.
• 16:10
  But after that, and I've just done one about two hours ago,
• 16:13
  so we do them roughly every week
• 16:15
  for about three or four individuals
• 16:17
  and they are often very surprised
• 16:19
  at how straightforward it is.
• 16:22
  And certainly, for Parkinson's,
• 16:23
  it's becoming actually a prerequisite that you have
• 16:27
  the misfolded protein alpha-synuclein identified
• 16:30
  before you're eligible for a trial entry.
• 16:33
  - No, that's really interesting.
• 16:35
  - Thank you. You're absolutely correct.
• 16:37
  (group laughing)
• 16:40
  - Staying with clinical trials perhaps,
• 16:42
  you know, I'm interested to hear,
• 16:44
  we've obviously had quite a few clinical trials,
• 16:47
  clinical successes in the space
• 16:48
  of Alzheimer's disease in particular.
• 16:51
  And you know, we're moving to a place now
• 16:54
  where we're hoping to have more therapies in the clinic.
• 16:58
  But maybe from a clinician's perspective,
• 17:00
  how do you think we can go about improving trial designs
• 17:03
  so that we can more rapidly get the right therapies
• 17:06
  to the right patients at the right time?
• 17:08
  I don't know if, Michele, do you want to answer first?
• 17:10
  - So one way to do it is to use a different,
• 17:14
  more adaptive trial design.
• 17:16
  And in the UK for Parkinson's,
• 17:18
  we now have the Edmund J Safra Accelerating Clinical Trials
• 17:22
  to Parkinson's or the ACT-PD.
• 17:25
  And this uses a model called MAMS, multi-arm, multi-stage.
• 17:29
  And it was adapted originally
• 17:31
  from trials that were done in prostate cancer.
• 17:33
  What's unique about this is you, for example, can have three
• 17:37
  or four different treatment trial arms
• 17:39
  going on simultaneously,
• 17:41
  which in the case of ACT-PD
• 17:44
  will be three oral medications all with different evidence
• 17:48
  for slowing down Parkinson's progression
• 17:50
  and one placebo group.
• 17:52
  So fewer people will need the placebo,
• 17:54
  and you also have much quicker go/no-go decisions
• 17:58
  at 6 to 12 and 18 months
• 17:59
  if you are not seeing any signal of improvement benefit
• 18:03
  within 6 to 12 months.
• 18:05
  So I think this is now also being adopted
• 18:07
  by Michael J. Fox Foundation for their P2P
• 18:10
  or Path to Prevention trial.
• 18:12
  And I think it's gonna be the way forward.
• 18:14
  We also need better ways of mitigating
• 18:18
  against things that can mess up trials.
• 18:21
  For example, placebo effect and expectation bias
• 18:24
  and learning effects.
• 18:25
  So if patients are really desperate
• 18:27
  that they want something to work,
• 18:29
  in fact, in the exenatide trial people,
• 18:31
  the placebo group just got better over time
• 18:34
  over the two years simply by taking part in a trial,
• 18:37
  having something to aim for,
• 18:39
  regular visits with allied health professionals and doctors,
• 18:42
  and just feeling that they were being better cared for.
• 18:45
  - That's really interesting.
• 18:46
  I mean, Peter, is that something that you've come across
• 18:48
  in sort of talking with people with lived experience?
• 18:51
  - I would say giving people hope
• 18:53
  is a very strong therapeutic effect you absolutely see
• 18:57
  in people.
• 18:57
  It is coming back to the point I made before.
• 19:00
  It gives them purpose.
• 19:01
  They've got a reason to focus on something
• 19:03
  in a world that can otherwise feel very dark.
• 19:07
  It's not dissimilar to the importance of socialisation.
• 19:09
  It's keeping your mind active, keeping socially active.
• 19:13
  This all contributes to that
• 19:15
  and that I think that has a big effect.
• 19:17
  - That's really interesting.
• 19:19
  And I mean, thinking about the patients
• 19:20
  that we put onto these trials,
• 19:22
  obviously a really important perspective in drug discovery
• 19:24
  is that we have to have the right patients
• 19:27
  to make sure that we see a clinical effect.
• 19:28
  So I don't know, Laura,
• 19:30
  if you've got any thoughts about that
• 19:31
  from the sort of more biomarker discovery
• 19:34
  and clinical understanding and a cohort understanding.
• 19:38
  - Well, I was sort of thinking about this,
• 19:40
  and I guess, there is, obviously,
• 19:42
  there's an amyloid-targeted treatment.
• 19:45
  And we can now measure amyloid
• 19:46
  and we can point people to that trial or drug.
• 19:52
  And so I guess you are thinking about now
• 19:54
  about picking out cohorts in that same way.
• 19:57
  So making them eligible for something.
• 20:04
  I'm thinking about other therapies.
• 20:05
  Maybe when you're thinking about designing a target,
• 20:07
  you might also think about a biomarker
• 20:09
  that goes alongside it.
• 20:10
  So if you're thinking about tau
• 20:11
  then maybe you want the tau markers.
• 20:13
  If you're thinking about an inflammatory drug,
• 20:15
  then maybe you want to be thinking
• 20:16
  about inflammatory markers
• 20:17
  that go along to check progression
• 20:20
  or to think about end decision points as well.
• 20:22
  And so I think there's probably parallel streams of work
• 20:26
  to be done as you think about the drug targets,
• 20:29
  what else are you thinking about in that particular cohort?
• 20:32
  So yeah, there's a lot with that understanding.
• 20:36
  - That's such an important point.
• 20:37
  I mean, do you have any thoughts
• 20:38
  about how we can create that environment
• 20:41
  to make sure we are pairing up people
• 20:43
  with that sort of expertise
• 20:45
  and understanding what the biomarkers should be
• 20:47
  and how we should go about doing them
• 20:49
  and getting the drug discovery scientists
• 20:51
  having those conversations early?
• 20:53
  - I mean, I think just having these people.
• 20:56
  Panels like this really enable us to chat to each other.
• 20:59
  So I myself as a data science talking to yourself
• 21:02
  as somebody from the Drug Discovery Institute,
• 21:04
  and the clinicians as well.
• 21:05
  So it's just having joined up conversations with people
• 21:08
  who are working in this field
• 21:09
  and making sure that everybody
• 21:10
  is working towards the same thing, I think.
• 21:12
  And so we sort of have the environment.
• 21:14
  We just have to make sure we're using it.
• 21:16
  - Yeah, it's so important.
• 21:17
  And you know, I think that that is really the only way
• 21:19
  we begin to see success, isn't it?
• 21:20
  Making sure that our data scientists,
• 21:22
  our drug discovery scientists,
• 21:23
  and our clinicians are having that good communication
• 21:26
  and obviously making sure we're involving people
• 21:28
  with lived experience
• 21:29
  to know exactly what we should be doing
• 21:31
  to inform our strategy.
• 21:32
  - I think what's really unique about ACT-PD
• 21:35
  is it's had a very active patient engagement group.
• 21:38
  And as a result, we're not doing things
• 21:41
  like asking patients to come in
• 21:43
  following overnight withdrawal of medication
• 21:45
  'cause that's actually really distressing.
• 21:48
  People often get a lot worse,
• 21:49
  particularly if they've had PD for a number of years.
• 21:51
  Also, the main outcomes
• 21:54
  are actually not the ones that are in clinic.
• 21:56
  And there's a heavier reliance on other remote assessments
• 22:01
  that can be done at home
• 22:02
  and digital outcomes,
• 22:03
  which I think will be very important,
• 22:05
  particularly for phase three trials.
• 22:08
  - That sounds really kind of game-changing actually,
• 22:11
  you know, thinking that we can have people
• 22:13
  in the comfort of their own homes
• 22:14
  still kind of reporting on the endpoints of studies.
• 22:17
  I think that that will be fantastic.
• 22:19
  I mean, again, sort of thinking about
• 22:21
  some of the clinical trials that have been ongoing
• 22:23
  and that have been in the clinic
• 22:26
  and have maybe had mixed success.
• 22:27
  And we've had some successes in the Alzheimer's field
• 22:30
  with lecanemab and donanemab,
• 22:32
  and obviously that's a little bit mixed,
• 22:34
  but I would really like first to ask maybe Peter
• 22:38
  and our clinical colleagues,
• 22:40
  you know, what the perspective of those are
• 22:42
  and then think about sort of what's next.
• 22:44
  So Peter, you know, what do the dementia community think
• 22:49
  about the current Alzheimer's therapies
• 22:50
  that are available to some individuals?
• 22:55
  - No, and I think, it's quite a mix
• 22:56
  for people actually living with the condition at the moment.
• 23:01
  I mean it's hope on the horizon,
• 23:02
  but for most of them, it's very difficult for them
• 23:04
  to engage even with trials.
• 23:06
  The criteria are quite strict.
• 23:09
  And it can be challenging
• 23:10
  with the press raising everybody's hopes
• 23:12
  with these big announcements
• 23:13
  and then shooting them down with sensational follow up.
• 23:16
  And they don't know what to think
• 23:18
  and we have to be very careful about what we say.
• 23:25
  The reality is that it requires a relatively early,
• 23:28
  I'll be corrected, but it requires an early diagnosis.
• 23:31
  You've got to manage the side effects,
• 23:32
  which are exclusionary for a lot of people, et cetera.
• 23:35
  So we have to manage expectations
• 23:36
  and say that like you can apply for the trials,
• 23:40
  but it might actually not be good for you to engage.
• 23:43
  - Yeah.
• 23:44
  And it's so difficult
• 23:45
  to manage those expectations, isn't it?
• 23:47
  I think, in a clinical setting I mean.
• 23:49
  Sanjay, you know, in your experience,
• 23:51
  are patients excited about these sorts of developments
• 23:54
  or is it, as Peter mentioned, a bit of a mixed reception?
• 23:58
  - So with most patients who we diagnose with Alzheimer's,
• 24:01
  I would talk to 'em about these therapies,
• 24:05
  mainly because they're in the news
• 24:06
  and everyone has questions about them.
• 24:10
  But in pretty much all the cases,
• 24:13
  now, of course, it depends on what you tell them,
• 24:15
  doesn't it?
• 24:16
  But in most cases,
• 24:18
  when I give an honest description of the findings,
• 24:22
  they all come out thinking,
• 24:23
  "No, it's not ready for consumption yet,"
• 24:27
  particularly when you describe, you know, the profile
• 24:29
  of the care they would need, the effects that could happen.
• 24:33
  And in particular when you tell them that the statistic
• 24:36
  that it prolongs life by four months-
• 24:40
  - But not improving the quality of their life.
• 24:42
  - And this is the thing.
• 24:44
  What patients are most afraid of when they come out clinic
• 24:47
  is being a burden.
• 24:49
  Can you imagine?
• 24:50
  This is actually what a lot of them say to you is that,
• 24:53
  "The other thing I'm most terrified about
• 24:54
  is being a burden,"
• 24:57
  to their partner, to society.
• 25:00
  It must be a terrible feeling to have actually.
• 25:05
  What we need to strive towards is therapies
• 25:08
  that improve the quality of life that people have, right?
• 25:10
  That's what's needed.
• 25:12
  And when a therapy is touted as prolonging life,
• 25:17
  yeah, I think they all know what that means actually.
• 25:21
  - I think you've raised a really important point there
• 25:23
  about improving quality of life.
• 25:25
  And I wonder, you know, we have so many different types
• 25:28
  of therapies now entering the clinic.
• 25:32
  There's been a bit of a focus on disease modifying
• 25:34
  and that being a bit of the sort of the thing
• 25:36
  that everybody's striving for.
• 25:38
  But actually, I wonder if symptomatic treatments
• 25:41
  might be something that patients are, you know,
• 25:45
  have more appetite for.
• 25:46
  Is that sort of your perspective there, Sanjay?
• 25:48
  - That would be my intuition in talking to a lot of them.
• 25:52
  It's something that can make them feel better,
• 25:55
  even if it's short term.
• 25:57
  Exactly of as much benefit, if not more than,
• 26:01
  something that really attracts things on,
• 26:04
  which is, you know, that's how they feel about it.
• 26:06
  Of course, in reality, there will be two months
• 26:08
  of better quality life too.
• 26:10
  And is the, you know, the amount
• 26:12
  of treatment they have worth that?
• 26:15
  That's a second question.
• 26:16
  That's a nice start question, you know?
• 26:18
  That will be addressed and will improve as well.
• 26:21
  - And Michele, what's your thoughts on that?
• 26:24
  Are your patients looking for symptomatic relief
• 26:27
  or disease-modifying therapies?
• 26:29
  I mean there is scope for both, but...
• 26:30
  - Yeah, well, we're quite lucky in Parkinson's
• 26:33
  'cause you know we have a lot more symptomatic drugs
• 26:35
  that are really quite effective.
• 26:37
  We can replace the levodopa.
• 26:39
  We can give dopamine agonists.
• 26:41
  We can use enzymes to make it hang around for longer.
• 26:44
  Then we also have things like deep brain stimulation
• 26:47
  and we can give pump therapies.
• 26:49
  So you know, I think,
• 26:52
  less than 5% of all of our patients with Parkinson's
• 26:55
  will be suitable for these device therapies
• 26:57
  or DBS in any case.
• 26:58
  And I would posit, probably, similar or even less
• 27:01
  will be suitable for the current disease-modifying therapies
• 27:04
  that we have.
• 27:06
  I think there are also lots of other
• 27:08
  potentially more effective, low-cost pragmatic solutions.
• 27:12
  And in Parkinson's,
• 27:13
  the evidence that regular high-intensity exercise
• 27:17
  three times a week,
• 27:18
  and a diet, a change in diet away from processed foods
• 27:22
  to more, you know, less animal-based proteins,
• 27:25
  less fried food,
• 27:26
  sort of African heritage diet,
• 27:28
  really slows down progression.
• 27:30
  But we haven't got enough data to look at it
• 27:32
  beyond 12-month duration.
• 27:34
  And that's one of the studies that I would love to do.
• 27:37
  And I don't see why that wouldn't also be the case actually
• 27:39
  in Alzheimer's or other forms of dementia.
• 27:43
  - That's really interesting,
• 27:44
  and you know, maybe something for the data scientists
• 27:46
  to collaborate with the clinicians on
• 27:48
  to try and understand that.
• 27:50
  I mean, Laura, is there anything
• 27:51
  that you are doing in that field
• 27:52
  to understand sort of prevention versus treatment?
• 27:55
  Or do you know of any research going on around that?
• 27:56
  - So I was immediately drawn.
• 27:58
  There's quite a lot of work done.
• 27:59
  I think there's probably quite a few diets,
• 28:01
  but I know the Mediterranean diet
• 28:02
  is one that people have been working with
• 28:05
  and there's some data there.
• 28:07
  I've been doing a little bit of work with looking at iron
• 28:10
  and looking at whether low or high iron
• 28:12
  might be of interest.
• 28:13
  But there's lots of different things
• 28:15
  that we might be able to do that might be disease-modifying.
• 28:18
  And I think there's a quite a bit of work to be done
• 28:21
  with prevention that might be useful.
• 28:24
  I think Sana was sharing stuff earlier
• 28:27
  about multi-morbidities
• 28:28
  and thinking about maybe not just dementia,
• 28:30
  but thinking about all the other things
• 28:32
  that might be going in parallel.
• 28:33
  And she was using, well, UK Biobank, a very big dataset.
• 28:37
  So there's a lot of work to be done in that area,
• 28:40
  not just with diets,
• 28:41
  but thinking about other things
• 28:42
  that might be prevention as well.
• 28:43
  - UK Biobank have used wrist-worn accelerometers
• 28:47
  and measured continuous sort of home living activity
• 28:50
  and shown that if you've got higher levels,
• 28:52
  you've got a reduced risk of future dementia.
• 28:55
  - That's great. Thank you.
• 28:56
  Peter, maybe just to sort of turn to you
• 28:58
  and ask what the dementia community are looking for
• 29:02
  in terms of treatment.
• 29:03
  Obviously, this might differ
• 29:04
  depending on whether you ask somebody
• 29:06
  with a diagnosis of dementia
• 29:07
  compared to their carer.
• 29:09
  But are patients looking for something
• 29:11
  that's going to, you know, change the course
• 29:13
  of their disease,
• 29:14
  suppress the symptoms,
• 29:15
  or as you know, we've just discussed,
• 29:17
  you know, potentially use a lifestyle intervention
• 29:20
  to slow progression?
• 29:23
  - I mean I think it's very hard
• 29:24
  to give in a generic answer to that
• 29:26
  because there's different types of dementia
• 29:29
  and their personality overlaps with that so much.
• 29:31
  They're all different.
• 29:33
  And you alluded to earlier, Sanjay,
• 29:35
  that you've got to tailor what you say to the individual.
• 29:42
  Some people want to work towards a cure.
• 29:45
  That's just what they desire.
• 29:46
  Other people are much more pragmatic
• 29:48
  and they just might want to,
• 29:49
  "I want to lead a high quality life for as long as I can
• 29:52
  and what can help with that?"
• 29:54
  It's very varied.
• 29:58
  Whether there's a difference
• 29:59
  between the person with the diagnosis and the carer,
• 30:01
  I find it very hard to sort of see the answer to that
• 30:05
  because the reality is as the condition progresses,
• 30:08
  the carer becomes the advocate
• 30:10
  for the person with the diagnosis.
• 30:12
  They're speaking for them
• 30:13
  because they even know that person best
• 30:16
  and they're struggling to articulate the views themselves.
• 30:18
  So I think separating those two things,
• 30:21
  I'm not sure I can give an answer to that.
• 30:23
  - Yeah, I can see it can be very sort of situation
• 30:25
  and patient-dependent and it's, yeah.
• 30:29
  But I can really see a place
• 30:31
  for everything that we've discussed
• 30:32
  in, you know, trying to tackle this really challenging,
• 30:36
  these challenging set of diseases and conditions.
• 30:40
  I would maybe like to sort of go out to the audience
• 30:43
  and ask if there are any questions.
• 30:45
  So we have a few questions on Slido already,
• 30:48
  but please do keep them coming
• 30:49
  if you would like to pose any questions to our panel.
• 30:53
  So the first question is for Sanjay,
• 30:56
  and this is, what role does genetic testing play
• 31:00
  in assessing younger dementia patients?
• 31:02
  And how does this fit with established disease paradigms?
• 31:08
  - So we would tend only to test genetically in clinic
• 31:12
  on the NHS
• 31:13
  if a patient is diagnosed under the age of 50,
• 31:17
  or if they have a first-degree relative,
• 31:22
  and usually, first-degree relative with early onset as well.
• 31:27
  Because it's very common to have a parent with Alzheimer's
• 31:29
  and then have a diagnosed with Alzheimer's just by chance.
• 31:34
  In terms of who wants genetic testing,
• 31:37
  seems to be about 50/50
• 31:39
  if you ask patients whether they want
• 31:40
  to be genetically tested,
• 31:42
  but half of them don't
• 31:44
  'cause of the implications for their family usually.
• 31:49
  And we will do the testing
• 31:54
  on clinically necessary grounds
• 31:56
  when it will provide some kind of diagnostic
• 31:59
  and treatment implication.
• 32:02
  So for, you know, certain types of frontotemporal dementia,
• 32:05
  it's typical we would convince the patient
• 32:08
  that they need that test.
• 32:10
  We can't convince everyone,
• 32:11
  but most of them will agree to having the test.
• 32:14
  But it's not normally done.
• 32:17
  I'm talking about these kind of monogenic genes.
• 32:21
  APOE is not tested on the NHS at the moment.
• 32:24
  Again, this ties
• 32:25
  into the, you know, donanemab, lecanemab question.
• 32:30
  And at some point, it might be.
• 32:33
  But again, the difficulty is what do you tell someone.
• 32:35
  You've got a risk of getting Alzheimer's.
• 32:37
  It's increased by a certain proportion.
• 32:40
  Yeah, so at the moment,
• 32:42
  there's resource limitations as well on genetic tests.
• 32:46
  - Yeah, that's interesting.
• 32:47
  And maybe, actually, just a follow-up question to Laura.
• 32:52
  How useful and how informative do you find
• 32:54
  that kind of the data from genetic testing
• 32:58
  in driving our understanding
• 33:00
  of the mechanisms and append disease?
• 33:01
  - Well, I think APOE is extremely important
• 33:03
  in driving a lot of different parts of disease
• 33:06
  in Alzheimer's.
• 33:09
  It's got an impact.
• 33:11
  In many of the research studies I do,
• 33:13
  I'm always correcting for APOE
• 33:15
  so we consider it wherever we go.
• 33:17
  So yes, that test is very useful to us as data scientists.
• 33:20
  But actually having the whole genome
• 33:23
  is extremely useful as well.
• 33:24
  So to have a look at the other genes,
• 33:26
  we can look at genetic risk scores as well.
• 33:28
  So obviously, there are genes
• 33:30
  that we already know are associated
• 33:31
  to Alzheimer's disease,
• 33:33
  but potentially there are others out there
• 33:34
  that we haven't found yet.
• 33:35
  So I would say that yeah,
• 33:36
  genetics is a very important study of.
• 33:39
  - Yeah, and I guess having that sort of APOE biology
• 33:43
  on the background of all of the other sort of changes
• 33:46
  that occur in the genome is vital
• 33:49
  to aid our understanding.
• 33:50
  Great, thank you.
• 33:52
  So we have a couple of other questions.
• 33:55
  This one is directed to Michele, but also everybody.
• 33:57
  So I'll give Michele the opportunity to answer first.
• 34:01
  What do you think causes the research gap
• 34:04
  in finding biomarkers for earlier and more precise medicine?
• 34:07
  And how can we bridge this gap from basic research?
• 34:10
  - Yeah, so that's something I've thought a lot about
• 34:12
  over the 20 years I've been doing biomarker research.
• 34:15
  I think the basic problem
• 34:16
  is we're dealing with a problem in the brain.
• 34:18
  And you know, we're not dealing with a kidney
• 34:20
  or a liver or skin problem
• 34:21
  where we can easily access diagnostic tissue,
• 34:24
  and we can use that not just for diagnosis,
• 34:26
  for stratification.
• 34:28
  And the second main problem is we have no way
• 34:30
  of direct imaging at alpha-synuclein
• 34:33
  and its deposition in pathological forms,
• 34:35
  both in the brain and in the extra central regions
• 34:39
  where we know it happens.
• 34:40
  For example, the peripheral nervous system,
• 34:42
  the gut, the skin, the heart.
• 34:44
  So those are the two key issues.
• 34:46
  So how do we start to bridge that gap?
• 34:48
  And really there's not much.
• 34:51
  We're starting to think about this,
• 34:53
  I would say, in the last decade.
• 34:54
  So we can measure spinal fluid,
• 34:57
  and within that, we can look at cells
• 34:59
  that have obviously come from areas of the brain
• 35:01
  as well as across the blood-brain barrier from periphery.
• 35:04
  We can then try and link that
• 35:06
  to what's happening in peripheral blood cells, PBMCs.
• 35:09
  We can look at proteomic, epigenomic signatures across both.
• 35:14
  In terms of brain imaging, we can measure dopamine deficit.
• 35:17
  That's helpful, but not that helpful.
• 35:20
  And we can use perhaps more advanced sequences,
• 35:23
  which we're developing and others are,
• 35:25
  to look more at where the pathology is
• 35:27
  in particular the substantia nigra and the locus coeruleus
• 35:30
  and using MRI,
• 35:32
  try and directly correlate the signal change
• 35:35
  to pathological changes at post-mortem brain MRI
• 35:38
  at high resolution.
• 35:39
  So that's another kind of general approach.
• 35:44
  And then we are doing more peripheral skin biopsies
• 35:47
  and tissue biopsies
• 35:48
  to sort of start to understand more
• 35:50
  about things like the gut-brain axis,
• 35:52
  the role of the microbiome,
• 35:55
  and how inflammation might be triggered
• 35:56
  by something totally peripheral,
• 35:58
  but then be weak capitulated in the brain.
• 36:01
  - Yeah, no that's really interesting.
• 36:02
  And you know, going back to something you say
• 36:04
  about the sort of brain region-specific changes,
• 36:06
  something that I often kind of think about
• 36:08
  because you know, pathology
• 36:10
  doesn't happen broadly everywhere, does it?
• 36:12
  And there's a lot of heterogeneity
• 36:14
  in the way that cells respond to the pathology.
• 36:16
  So I think that's such an inclusive point.
• 36:18
  - And lastly, I don't think we've had animal models
• 36:20
  that have particularly weak recapitulated either.
• 36:23
  The clinical phenotype
• 36:25
  are the pathology that we see in humans.
• 36:27
  And some of the human pre-formed fibril models
• 36:31
  of injecting alpha-synuclein into the salivary gland
• 36:35
  where it goes straight up into the brain
• 36:36
  that I've recently seen presented,
• 36:38
  I think, are very exciting.
• 36:39
  - That sounds fascinating.
• 36:42
  - I was just saying that this is very exciting,
• 36:45
  but Alzheimer's disease is quite a long way behind
• 36:48
  in all of this in terms of peripheral markers.
• 36:50
  So we don't have that gut and all these synuclein markers.
• 36:56
  - You've got amyloid and tau PET.
• 36:58
  - We do.
• 36:59
  So the thing is, amyloid and tau PET
• 37:01
  are really difficult to access.
• 37:03
  We don't have it in Oxford.
• 37:04
  We don't have it in Oxford.
• 37:05
  Where do we have it?
• 37:06
  We have to send all our patients to London for this.
• 37:09
  And the ligand's really difficult to make.
• 37:11
  So yeah, we do not have that signature yet
• 37:16
  until we had the blood markers,
• 37:17
  which obviously, looking very promising.
• 37:19
  But I think other types of marker
• 37:23
  are also looking very promising.
• 37:25
  And by that, I mean things like behavioural, cognitive,
• 37:29
  and measures that we can do in clinic,
• 37:34
  looking at how the brain is functioning.
• 37:36
  I always say to the patients
• 37:38
  that we can take pictures of your brain,
• 37:40
  but the problem with your memory
• 37:42
  is not structural necessarily.
• 37:44
  It's to do with the way the brain is working,
• 37:47
  the computations and the neurons firing.
• 37:50
  And if the problem is at that scale,
• 37:51
  and it's certainly early in the disease,
• 37:53
  it's at that scale, right?
• 37:55
  We see atrophy in the hippocampus many years
• 37:58
  into the disease usually.
• 38:00
  So the first biomarker
• 38:02
  is probably going to be a functional-type biomarker
• 38:07
  using behavioural and cognitive probes, I think.
• 38:12
  - Oh, that's, yeah, very, very interesting.
• 38:14
  Laura, I don't know if you want to comment
• 38:16
  about sort of finding biomarkers
• 38:18
  from a more basic research perspective
• 38:21
  or data science perspective.
• 38:21
  - Well, I guess, I was gonna conflict a little bit
• 38:23
  and say that maybe I'm still searching
• 38:26
  for the elusive fluid biomarkers, so.
• 38:29
  CSF when we have it.
• 38:30
  But also I think the idea of finding a blood biomarker
• 38:33
  that enables a clinician to do a blood test
• 38:35
  at the GP level is really useful.
• 38:38
  And we have brilliant progression with that.
• 38:42
  Yeah, with p-tau217.
• 38:44
  I think there are trials going on
• 38:46
  where this would be moved to clinic.
• 38:48
  The question is now actually with this one
• 38:51
  is when do we use it?
• 38:52
  Because of course, you might be able to tell a patient
• 38:55
  that they have the amyloid,
• 38:57
  but what do we do next?
• 38:59
  So I think there is, potentially,
• 39:01
  there is that diagnostic marker with AD,
• 39:04
  but maybe we want to be thinking about other biomarkers
• 39:06
  for tracking maybe progression
• 39:08
  or back again to the drug trial.
• 39:10
  And thinking about whether we can use that
• 39:12
  to tell us more about the disease
• 39:15
  and maybe subtypes of the disease as well.
• 39:17
  - Sounds about nicely to what we were talking about earlier
• 39:19
  about different branches of research
• 39:22
  needing to communicate well with each other.
• 39:24
  - And just in response, if I may.
• 39:25
  (group laughing)
• 39:27
  Actually, you know, we see about 10% of our patients
• 39:30
  who are amyloid-positive either in CSA plasma or in PET,
• 39:37
  they don't progress to get Alzheimer's disease.
• 39:40
  So there's a,
• 39:41
  I don't know if you wanna call that a protective factor
• 39:43
  or some kind of resilience component,
• 39:45
  but yes, you can tell someone they've got the pathology,
• 39:50
  but not have the progressive disease or the dementia.
• 39:53
  And we do do that sometimes,
• 39:55
  for a few patients who we'll tell that to.
• 39:59
  - Thank you.
• 40:00
  So I think we've got time for one more question
• 40:02
  before we sort of close out,
• 40:04
  but I will maybe swipe one from the audience.
• 40:09
  As Sanjay mentioned,
• 40:10
  there's a great variety of Alzheimer's diseases
• 40:13
  and heterogeneity.
• 40:15
  So are current efforts in therapeutic development too broad?
• 40:20
  And how should the community approach this efficiently?
• 40:24
  I'm not sure who wants to take that first.
• 40:26
  - Sanjay.
• 40:27
  (group laughing)
• 40:29
  - I do think that people often talk about
• 40:32
  a lot of researchers working on prognosis
• 40:34
  and what's the value of this?
• 40:37
  Yes, we can tell patients how long they're gonna survive,
• 40:40
  but the real benefit of knowing prognosis
• 40:44
  is in doing clinical trials.
• 40:46
  If you know,
• 40:48
  for a particular person tailored to their genes, biology,
• 40:52
  and other pathologies they have,
• 40:55
  if you know what the trajectory of their disease
• 40:57
  ought to be,
• 40:59
  then that makes all these clinical trials
• 41:01
  much more efficient,
• 41:02
  much, much more efficient.
• 41:03
  I can't really explain how much variability there is
• 41:08
  in this condition.
• 41:08
  There are some patients
• 41:10
  who've gone for 10 years after diagnosis.
• 41:13
  Others for two.
• 41:15
  And if your measure is how long people go on for
• 41:20
  when you give them a treatment,
• 41:22
  you're gonna need an enormous sample size.
• 41:25
  But as soon as we're able to pin them down
• 41:27
  to a particular trajectory
• 41:29
  based on maybe their premorbid MRI,
• 41:31
  their cognitive function,
• 41:33
  their particular profile of deficits,
• 41:35
  and some biomarkers and so on,
• 41:37
  then we can then use this sort of residualized benefit
• 41:43
  in the trial.
• 41:43
  And I think that that's something that is underexplored
• 41:47
  and people don't like putting into trials really very much.
• 41:50
  Right? That's my feeling.
• 41:53
  - Yeah, I think we don't...
• 41:56
  I mean Alzheimer's and Parkinson's,
• 41:58
  they're complex neurodegenerative conditions.
• 42:00
  They progress quite slowly over decades in general.
• 42:04
  And there are these extremes of phenotype and heterogeneity.
• 42:08
  But I think we've been too simplistic thinking
• 42:10
  that we just do a drug trial of one drug versus placebo.
• 42:13
  'Cause for cancer, we never do that.
• 42:16
  Usually you're needing two or three different medications
• 42:19
  and then over a period of time,
• 42:20
  there'll be a repeat staging, scans,
• 42:23
  and different therapeutic regimes.
• 42:25
  I think that's the first thing.
• 42:27
  And I think the individualised trajectory
• 42:30
  can be best achieved
• 42:32
  through assessing the patient in their own home
• 42:35
  and much more frequent granularity of measures over time,
• 42:38
  which we can achieve at low cost with digital data.
• 42:41
  So I think that,
• 42:42
  and maybe having a trial design
• 42:43
  where you have a six-month run in
• 42:46
  where you then establish that patient's baseline
• 42:48
  before then randomising might make a really big difference.
• 42:53
  And you also want to know
• 42:54
  that there is gonna be some patient that respond very well
• 42:56
  and others that don't,
• 42:57
  and how are you gonna then look back
• 42:59
  to see what best predicted that response.
• 43:02
  So target engagement biomarkers I guess.
• 43:05
  - Thank you very much.
• 43:06
  We are coming up to time now,
• 43:08
  and there are still lots of questions,
• 43:10
  so thank you so much to everybody for sending in questions
• 43:13
  and hopefully there can be some more discussion a bit later.
• 43:16
  But I would really like to finish up
• 43:18
  by a little quick fire question to everybody.
• 43:22
  What do you think will create the biggest impact
• 43:24
  in the way we treat and manage dementia?
• 43:26
  So I'd like to go to Peter first.
• 43:30
  - So I'm really interested in what you were saying
• 43:32
  about the digital era
• 43:34
  and the ability to support people in their own home.
• 43:37
  I think that would really make a difference.
• 43:40
  Certainly in terms of like as these disease progresses,
• 43:43
  you've got the issue with any change of routine.
• 43:46
  Anything that's unusual is really distressing
• 43:49
  and can actually have a very negative effect.
• 43:51
  The idea of having digital tracking that monitors them,
• 43:54
  that gives you the ability
• 43:55
  to make some sort of decision about treatment
• 43:59
  without drawing them into hospital,
• 44:01
  drawing them into clinic I think would be very helpful.
• 44:03
  - Thank you very much.
• 44:04
  Laura, we'll turn to you next.
• 44:06
  - It's a really big question.
• 44:07
  I was hoping you would come to me last. (laughs)
• 44:11
  So I don't know.
• 44:13
  I think 'cause we were thinking about trials,
• 44:15
  and I think in terms of just my particular field,
• 44:18
  I think everyone will have their own answer on this.
• 44:20
  And I was thinking about data accessibility.
• 44:24
  And I think there's a really important thing now
• 44:26
  where we are thinking we have these trials,
• 44:28
  we have things ongoing,
• 44:29
  but then the data is locked away afterwards.
• 44:31
  And I think it would be really useful for onward
• 44:33
  if we were able to access
• 44:35
  and work with that data in the community.
• 44:38
  So that's my one thing, but I think there are others.
• 44:40
  - Thank you very much, Laura.
• 44:41
  Sanjay, we'll turn to you.
• 44:42
  - So it's a controversial answer.
• 44:44
  If you break your leg, you can fix it, get a new one.
• 44:47
  Your brain is you. It's your personality.
• 44:50
  And until now, there's been nothing in the universe
• 44:52
  that can do the same thing.
• 44:54
  But now, assistive technology
• 44:58
  and things that can supplant,
• 45:00
  you know, help you with your memory,
• 45:03
  on the horizon with AI.
• 45:05
  And although you can't replace a person, the identity,
• 45:09
  these devices, these algorithms are quite good
• 45:12
  at emulating particular people
• 45:14
  given the amount of training data you give them.
• 45:17
  And there may be ways
• 45:18
  in which AI cannot be a brain replacement,
• 45:22
  but can kind of facilitate thought.
• 45:26
  - Fascinating. Thank you very much.
• 45:27
  Michele.
• 45:28
  - Just very practical.
• 45:29
  I think we may need collaboration,
• 45:32
  real collaboration between hospital care
• 45:35
  and community care and the patient.
• 45:38
  And I think community care could be better streamlined.
• 45:42
  And we would save so many blocked patient bed days
• 45:46
  if we had a way to discharge patients
• 45:48
  that needed it sooner into the community,
• 45:51
  into the appropriate places with support.
• 45:54
  - Wonderful. Thank you so much.
• 45:55
  Lots of different perspectives,
• 45:57
  and it's been wonderful to hear your thoughts and comments.
• 45:59
  So thank you so much.
• 46:00
  And I'd like to thank the audience
• 46:02
  for all the questions that you've submitted,
• 46:05
  and thank everybody on the podcast for listening.
• 46:07
  And please join me in thanking the panel members.
• 46:11
  (audience applauding)
• 46:20
  (bright music)
• 46:27
  That's where we'll leave it.
• 46:28
  My thanks to Sanjay, Michele, Peter, and Laura,
• 46:31
  and to everyone who was there on the day.
• 46:34
  You can find more conversations like this one
• 46:36
  at Dementia Researcher wherever you get your podcasts.
• 46:39
  Thanks for listening.
• 46:41
  - [Announcer] The "Dementia Researcher Podcast"
• 46:43
  was brought to you by University College London
• 46:45
  with generous funding
• 46:46
  from the National Institute for Health and Care Research,
• 46:49
  Alzheimer's Research UK,
• 46:51
  Alzheimer's Society, Alzheimer's Association,
• 46:54
  and Race Against Dementia.
• 46:56
  Dementiaresearcher.nihr.ac.uk
• 47:03
  (upbeat music)