ISTAART PIA Relay Podcast – Joe Kane & Zahinoor Ismail

Voice Over:

Hello and thank you for listening to the second season of the ISTAART PIA Relay Podcast Series brought to you by Dementia Researcher. ISTAART is a professional society and part of the Alzheimer’s Association representing scientists, physicians, and other dementia professionals active in researching and understanding the causes and treatments of Alzheimer’s disease and other dementias.

Voice Over:

In this five-part series, we once again, asked members of the ISTAART professional interest areas to take turns interviewing their colleagues and being interviewed themselves with the interviewee going on to be the next episode’s interviewer. We’ll be releasing one of these podcasts each day in the buildup to the Alzheimer’s Association International Virtual Conference to showcase the work of ISTAART PIAs. Thank you for listening.

Dr Joe Kane:

Hello, everyone and thanks for joining us. I’m Joe Kane and I’m a clinical academic lecturer in old age psychiatry. I work at Queens University, Belfast and I’m communications officer for the Lewy body dementias PIA. Today I’m delighted to be talking with Zahinoor Ismail. Hello, Zahinoor. Can I start by asking you to introduce yourself and tell us which PIA you’re involved with please?

Professor Zahinoor Ismail:

Hi, I’m Zahinoor Ismail and I’m a professor of psychiatry, neurology, epidemiology, and pathology at the University of Calgary affiliated with both the Hotchkiss Brain Institute and the University of Cal and the O’Brien Institute of Public Health. And I’m also affiliated with the University of Exeter and their old age psychiatry program. I am the academic lead of the neuropsychiatric syndromes professional interest area.

Dr Joe Kane:

Perhaps to start with, you could tell us a little bit about your own research. What brought you to dementia research for example?

Professor Zahinoor Ismail:

As a child, I was close to my grandmother and from what I’ve read is that if you have strong relationships with seniors when you’re young, it seems to be more of those folks say in the medical field go on to work in geriatrics and I think I’m fairly textbook that way. I toyed with different fields in medical school, but the brain, I always thought was the most fascinating organ, and so I ended up pursuing old age psychiatry, geriatric psychiatry with then additional subspecialty training in behavioural neurology and neuropsychiatry.

Professor Zahinoor Ismail:

So my work really captures the interface of psychiatry and neurology especially with respect to psychiatric symptomatology observed through a neurological window or framework. Some of what I do is using neuropsychiatric symptoms as early non-cognitive markers of dementia or as prognostic markers of dementia. And a great deal of this comes out of the PIA. The large bulk of my work in my lab involves mild behavioural impairments and the MBI work really evolved from the neuropsychiatric syndromes PIA and it’s work that continues on in the PIA, but it certainly greatly influenced and informed my career.

Professor Zahinoor Ismail:

MBI is characterized by the emergence in later life, so De Novo emergence of neuropsychiatric symptoms that are persistent. So they’re not transient or fluctuating, they persist for a number of months, at least six months. And attendant with the emergence and persistence of those symptoms in older life is a greater risk of incidence cognitive decline and dementia. For some, it’s the index manifestation of dementia and this is pretty novel because we have a cogno-centric paradigm of dementia.

Professor Zahinoor Ismail:

We appreciate cognitive changes. If someone comes into clinic and they complain of memory impairment and they’ve always had memory impairment, then you say, “Okay, well that’s not dementia, we’re looking for change.” But for some reason, that same notion of changes in behavior doesn’t seem to resonate or penetrate. If someone comes into clinic and they’re 67 years old and they’ve never had psychiatric history, we should give them credit for those 67 years, and if they present with new onset psychiatric symptoms, something’s up.

Professor Zahinoor Ismail:

And if we look back at the history of dementia, [inaudible 00:05:11] all those Alzheimer’s patient that we all know and have read about presented the hospital not with cognitive symptoms, but with emotional dysregulation and suspiciousness. So when we look at the epidemiological data in dementia in general, 59% of people present with a neuro-psychiatric symptom before a cognitive diagnosis, and we kind of expect that for FTD with disinhibition and apathy baked right into the construct of FTD and we expect that with Lewy body, with psychosis being such a prominent part, but it’s not really thought of in Alzheimer’s.

Professor Zahinoor Ismail:

And again, when you look at the data, 30% of people who develop AD actually have an initial behavioural prodrome. So if we are looking for earlier markers of the most common type of dementia, then perhaps invoking and including neuropsychiatric symptoms is one way that we can do that. So that’s the work of my lab to a degree of our PIA as well and there are many different projects going on whether it be looking at the cross-sectional brain behaviour correlates, associations with imaging or fluid biomarkers with cognitive status, and then changes in all of those markers over time.

Professor Zahinoor Ismail:

I also do clinical trial work not only in terms of the overall dementia cognitive interventions with novel agents, but also in terms of neuropsychiatric symptoms and have three ongoing studies right now for agitation in dementia. So it’s an area in the dementia field, it’s a neuropsychiatric symptom which I seem to be spending more time with at an intervention level and I’m very interested in teasing out the different domains within the IPA diagnostic criteria for agitation.

Professor Zahinoor Ismail:

I feel that the excessive modal activity, the verbal aggression and the physical aggression while related probably captured different groups and different stages of illness, and we’ve done some work in this area now. We’ve just published a paper in Alzheimer’s and dementia that utilized both the Cohen-Mansfield Agitation Inventory and the Neuropsychiatric Inventory clinician version to derive an abstract measures that capture the three IPA agitation domains and then we validated them, and are exploring that in other data sets including a Canadian study called STAN.

Professor Zahinoor Ismail:

And looking to see if that clinical impression that verbal aggression precedes physical aggression, if that’s the case, isn’t an earlier way to detect agitation and then can intervention rely more on non-pharmacological interventions or more benign or less impactful treatments. What we don’t want to see is when agitation is described or initially captured at a crisis stage when someone punches someone else or pulls a staff’s hair, gouges their eyes, then you’re in a situation where it’s emergent. They might get sent to hospital, they might lose their placement and see psychotics may be necessarily.

Professor Zahinoor Ismail:

We don’t want to do that. So what I really am interested in is capturing the agitation syndrome earlier on in the disease course when it’s less acute, and then cholinesterase inhibitors or synergic drugs in addition to non-pharmacological agents might be more appropriate in order to decrease the burden of anti-psychotics. And again, I think cholinesterase inhibitors are another area in which I’m interested in because we are in this stage where not only are we deprescribing them more often than prescribing them that there’s a clinician nihilism such that when you want to start these medications, and what I see sitting in my nursing home practice for example, is that when cholinesterase inhibitors are discontinued, I see emergent agitation psychosis usually about six or eight weeks.

Professor Zahinoor Ismail:

And the longer-term data as they start to trickle out are showing, hey, wait, these medications may actually treat neuropsychiatric symptoms even though that wasn’t evident in any of the short trials or really nice paper out of the Swedish dementia registry showed that those patients with AD who are prescribed Cholinesterase inhibitors have a lower probability of being prescribed anti-psychotics. To me, that’s really exciting. So if we’re trying to find interventions that are safer, we have medicines already that might be helpful. So that’s something I’m interested in as well in terms of finding optimal pharmacotherapy.

Dr Joe Kane:

You mentioned your work in nursing homes, and of course during COVID, we know that it’s been quite difficult to use some of the non-pharmacological methods that we favour when it comes to behavioural disturbances, and also we know that the environment can be a big factor contributing to MBI and behavioural issues in general. How has COVID influenced your day to day work, your clinical work?

Professor Zahinoor Ismail:

Joe, this is a remarkable thing. We had this global pandemic and it fundamentally changed the nature of our interaction with our patients and their interaction with the world and it was all for the worst. I’ve been in practice 22 years now. And over the last 15 months, I saw more psychosis in that patient population than it ever had before. And strangely enough, Joe, I saw more Parkinsonism as well and that was really odd. And I’ll say in the series of homes I’m working in now, I have about a five year reference range in this last year and they’ve been more agitated, more psychotic, more Parkinsonised.

Professor Zahinoor Ismail:

We’ve always written in grants and studies that non-pharmacological interventions are safe, and I actually wrote in a recent protocol that, well, maybe not as safe as we once thought given the infection risk. And it’s challenging, how do you administer Montessori interventions remotely when the nature and the benefit of that comes from the tactile work from the sensation and the patients using their hands to express say lost verbal skills, it’s extraordinarily challenging.

Professor Zahinoor Ismail:

But my goodness, I found them to be sicker than I’ve ever seen them. Social isolation certainly being a part of that because with the easing of restrictions, for a number of people we’ve seen the agitation decrease a little bit, but you wonder also about the neuro-COVID and the CNS sequelae of direct central consequences of the virus, but more recently studies showing that there’s a CNS inflammatory burden. What is this going to do down the road? Are we going to see dementia pandemic secondary to the COVID pandemic? What is the nature of our relationships with our patients going to look like?

Dr Joe Kane:

Yeah, it’s a big challenge ahead, certainly for anyone working in clinical services. And could I ask you specifically about the work that you’re doing in prodromal DLB and PDMCI regarding behavioral disturbances in your psychiatric symptoms?

Professor Zahinoor Ismail:

Certainly. In the same way that we’ve applied MBI to Alzheimer’s because neuropsychiatric symptoms in preclinical and prodromal AD were underappreciated, we can apply that to other dementias as well. It can be applied to FTD because we know there are robust cohort of symptoms that can emerge beyond just apathy and disinhibition. In DLB, it’s really quite robust especially in psychosis, but also mood anxiety, impulses control, et cetera, with the complicating factor that if they are on dopaminergic agonists, there might be some impulse dyscontrol there.

Professor Zahinoor Ismail:

We looked at PD MCI group through a cohort run by Dr. Oury Monchi Here in Calgary and administered the MBI checklist to this cohort of patients with Parkinson’s and found that those with higher MBI checklist scores had lower MoCA scores, Montreal Cognitive Assessment, and were more likely to be diagnosed with PD MCI as opposed to PD. We also found some middle temporal atrophy in that same group. Subsequent analysis then showed some functional connectivity differences as well. So the story in the alpha-synucleinopathies seems to be thus far similar, such that the neuropsychiatric symptoms measured within the MBI framework.

Professor Zahinoor Ismail:

Because the MBI framework is more specific in that with the emergence and six months persistence of symptoms, some of the transient reactive types of symptoms that might have been captured if you’re measuring neuropsychiatric symptoms traditionally would be excluded so you would get a stronger signal for what are possibly behavioural sequelae of underlying functional dysconnectivity and neurodegeneration. This applies in the synucleinopathies such that it seems that in those who have PD, the MBI burden is associated cross-sectionally with biomarkers and cognitive clinical symptoms that are consistent with say the posterior deficits that are associated with a greater risk for incident of cognitive decline and progression to DLB.

Professor Zahinoor Ismail:

So there is ongoing work into that area, but I think there are certainly parallels with AD in this synucleinopathies.

Dr Joe Kane:

And do you think that there is scope within the MBI checklist that your PIA has worked on for adaptation, for new body disorders or a different threshold, for example?

Professor Zahinoor Ismail:

Certainly. I think the only question is actually the threshold. The MBI checklist again, and this is I think one of the remarkable things that came out of our PIA is turning out to be really a robust rating scale and every analysis seems to really show that it’s capturing things that are very interesting and helpful. It’s divided into five domains consistent with the five MBI domains. So the first is apathy, and there are even specific symptoms for each of the apathy sub domains of decreased interest, decreased initiative and decreased emotional reactivity.

Professor Zahinoor Ismail:

So you can really kind of get granular that way and one would want to probably look at different brain behaviour correlates of the apathy sub domains because I think they are relevant. The second domain is emotional dysregulation and that includes both mood and anxiety symptoms. And based on our work so far, those really seem to be amyloidopathy type symptoms, right. How that plays out in the synucleinopathies is unclear, and knowing that there’s overlap between these proteinopathies and different clinical dementia syndromes.

Professor Zahinoor Ismail:

The third domain is impulse dyscontrol and it’s the broadest domain and it recently really nicely analysed by Tony Sarri from Finland in a network meta analysis, that’s in international psychogeriatrics showing that there are some core symptoms. Argumentative from this, for example is one that’s really important at detecting the overall clinical syndrome, but also connecting to different types of impulses dyscontrol symptoms.

Professor Zahinoor Ismail:

And those can be kind of divided into two parts. One is that sort of agitation, aggression, irritability, impulsivity that we can see again often in Alzheimer’s, but then there is the reward salience and response kind of disinhibition component and part of that is sort of orbital frontal cortex type behaviours that we see and that subdomain within the impulse dyscontrol domain I think is probably quite relevant to to non AD dementias.

Professor Zahinoor Ismail:

The fourth MBI domain is the social cognition domain. Looking at tact and empathy and sympathy and social behaviour and intruding on other people’s activities or speaking to people as if they’re familiar, that probably is mostly FTD type of behavior, but it hasn’t really been measured in a systematic way to see to what extent it really applies in other dimensions as well. And then the fifth domain is psychosis, which includes not only hallucinations, but delusions as well, which we know is certainly relevant to the Lewy body dementias and synucleinopathies.

Professor Zahinoor Ismail:

So to me, and we’re including the MBI checklist in our observational cohorts of Parkinson’s and PMCID LB, I think there’s definitely relevance for not only capturing symptoms, but then using those, those domains to look at kind of endophenotypes or different aspects of the synucleinopathy which might be associated different clinical cognitive biomarker or launched to outcomes.

Dr Joe Kane:

What are the hot topics in your field at the moment?

Professor Zahinoor Ismail:

I think biomarkers is hot everywhere, and it’s certainly hot in neuropsychiatric symptoms whether it be any type of neuro-psychiatric symptom measured anyway, or whether it be mild behavioural impairment as a global construct or domain specific analysis. Understanding the availability, the utility of biomarkers in their relation to these symptoms is really important. But one can look at it two ways, you can frame the measurement of these MBI symptoms or neuropsychiatric symptoms which are very easy to assess with usually a very quick informant rated measure, then that captures a group that may be enriched for biomarker positivity.

Professor Zahinoor Ismail:

Alternatively, the biomarkers, if you look at say, you know Tau PET imaging and where is the Tau or if you look at MR in terms of atrophy, to what extent is that associated with neuropsychiatric symptoms, with MBI domains or global MBI burden and that kind of bi-directional approach isn’t being investigated in a lot of different labs, certainly ours. The most practical is can we get easy to access biomarkers that associate with dementia risk?

Professor Zahinoor Ismail:

So for example, in the NIAAA research framework for Alzheimer’s with the Amyloid, Tau and Neurodegeneration in prodromal disease, when there are objectively measured cognitive symptoms and AD biomarkers, for example, we kind of know a little bit more the role of the neuropsychiatric symptoms in that when you take two groups of people with MCI, those with neuropsychiatric symptoms, and certainly with MBI are more likely to progress.

Professor Zahinoor Ismail:

In the normal cognition group, it’s a lot harder. And it’s a lot harder to aim your PET scan or your lumbar punctured needle at people who are objectively normal in cognition. And I do lumbar punctures and my research ethics board allows me to draw CSF from cognitively normal participants especially if there’s risk but have other collaborators in various parts of Europe and their ethics board won’t allow it.

Professor Zahinoor Ismail:

So finding a blood-based biomarker is obviously a huge research endeavour around the world, because then it allows us to find those preclinical folks. Consistent with your field as well, can we find a marker that’s easily accessible? That’s not part of the ATN traditional framework. Amyloid P-Tau neurofilament light seems to be a marker probably more useful prospectively than cross-sectionally, but can we find markers for different dementias and ones that associate with neuropsychiatric symptoms in advance of cognitive impairment, that would allow us to also help differentiate from general psychiatric phenomenology in older adults?

Professor Zahinoor Ismail:

We know there’s a great degree of specificity conferred from the stipulations in MBI that symptom emergence De Novo and symptom persistence confer in detecting risk, but are there biomarker correlates that even amplify that signal such that then, now you have a real consideration as to whether or not you would engage more detailed measures both clinical cognitive and imaging, but that’s when the primary prevention story starts to come in or secondary prevention in advance of cognitive symptoms as someone in whom you would administer a disease modifying drug.

Professor Zahinoor Ismail:

And I think those are areas where the field is exploring. And then finding better ways to treat these symptoms in those who are suffering from dementia. While the field has moved extensively to capturing preclinical and prodromal disease, we don’t want to forget the majority who are actually experiencing dementia suffering from the various neuropsychiatric symptoms. How can we identify those symptoms, treat them better, find medications and non-pharmacological interventions that are associated with efficacy and safety, COVID included, and ensure that we have optimal quality of life, that we ensure safety, that we can preserve agency and personhood in people with dementia when in the context of neuropsychiatric symptoms, agency and personhood that can be lost or overlooked or ignored.

Professor Zahinoor Ismail:

So really embracing that internal world of someone with dementia to determine to what extent are these symptoms affecting their quality and how can we improve them and how can we engage everyone else to appreciate the importance of these symptoms because maybe they’re not as concrete as cognitive symptoms, but they are important. They are core criteria, they’re fundamental to the disease course and so increasing the profile and the awareness of those.

Professor Zahinoor Ismail:

And I think that’s where syndromic criteria are very important. So I mentioned the IPA agitation criteria, which I think are landmark and really very important in our understanding of agitation. The IPA updated the psychosis criteria in neurocognitive disorders and we included mild neurocognitive disorders, MCI in that group. In harmony with that, our PIA also developed research and biomarker criteria for psychosis in Alzheimer’s and related neurocognitive disorders and these new psychosis criteria allow sort of biomarker research in advance of overt cognitive impairment for associations with psychosis in late life and dementia.

Professor Zahinoor Ismail:

New apathy criteria have just been published. They’re in press or they’re finally published which take the Philippe Robert’s pen diagnostic apathy criteria, and focus them in on neurodegenerative disease and neurocognitive disorders. And with the three domains that are reflected in the NBI checklist and the MBI criteria of decreased interest, decreased initiative and emotional reactivity, where we don’t have good syndromal criteria yet are for social cognition changes and for mood and anxiety disorders.

Professor Zahinoor Ismail:

And that mood and anxiety disorders, mood and anxiety symptoms being probably the most common in dementia, and yet we are still maybe perhaps stuck on a DSM framework for that or an ICU framework, and it doesn’t reflect the underlying neurobiology. So not withstanding the fact that most of every robust treatment trial of antidepressants in dementia has failed, we still recommend treatment of depression. So why is that? And I think our criteria, which is based in psychiatric constructs in early and mid life, a neurodevelopmental model of psychiatric symptoms is different from the presentation of anxiety and depression and those types of symptoms in neurodegenerative disease.

Professor Zahinoor Ismail:

If you think about it, DSM stipulates that the symptoms can not be better accounted for by another medical issue. Would neurodegeneration and the build-up of amyloid tau synuclein vascular burden not be considered a medical condition that would better account for these symptoms? And if so, why are we still using DSM diagnostic criteria? This is the dilemma and our field needs to really embrace nosology better and distinguish between chronic and recurrent psychiatric syndromes and neuro-psychiatric symptoms as sequelae of brain diseases, which also leads them to measurement based care which is another area of great interest for me.

Professor Zahinoor Ismail:

And understanding what is the best source of information. I mentioned agency and personhood. We want to inquire and try to understand the internal world of someone with dementia, but when they have anosognosia and anosognosia can not only be for cognitive deficits, but for functional deficits and for neuropsychiatric symptoms, this really changes care. If someone has anosognosia for neuropsychiatric symptoms and they come into clinic, “How’s your mood?” “Oh, I’m pretty good.” Does that necessarily tell you how they’re doing?

Professor Zahinoor Ismail:

And so we need to be aware of that and proactive such that any assessments of cognition function and behaviour should be assessed incorporating both the patient and an informed caregiver reliable informant. And this actually is in our most recent iteration of Canadian Dementia Guidelines explicitly that self and informant reports of cognition behaviour and function are required for thorough dementia assessments and workup, and I think our field really needs to appreciate that there can be that affective behavioural anosognoia because if someone says, they’re fine, we don’t know that they are. And they can say their cognition is fine and we administer an MMSE or a Rudas, or a MoCA, or an Addenbrooke’s or SLUMS or whatever we want to, and we would see that objective difference.

Professor Zahinoor Ismail:

But if they say they’re not depressed, or they’re not anxious, whereas the objective frame of reference and without that, our clinical work is impaired. So I think we need to explore that more and that’s, again, work, I think, that is important in the field and ongoing.

Dr Joe Kane:

Okay. Gotcha. That’s fascinating. I think the idea that we view several neuropsychiatric syndromes through the lens of neurodevelopmental and working in psychiatry and the idea that we should be embracing a whole different paradigm is pretty challenging and really it makes a lot of sense, and it’s a bit frightening as well as a practitioner.

Professor Zahinoor Ismail:

It is. Again, it comes down to neurology. If you look at DSM criteria, it’s frame of reference is two weeks, have you had these symptoms over two weeks? Sure, but what about the natural history? And to me, the real goods come in the development of the symptoms. And depressive symptoms in an adolescent versus someone who’s 35 years old versus someone who’s 45 versus someone who developed them at the age of 70, as a clinician, as an epidemiologist, those are distinctions that are really, really important. Why do our criteria and our rating scales, why are they silent?

Professor Zahinoor Ismail:

You’re looking at a Beck Anxiety Inventory, a Beck Depression Inventory, they measure across section symptoms over a two week range. The geriatric depression scale over a one-week range. I mean, in older adults, where is the understanding of the evolution of symptoms? And this is a discussion I have with my trainees in the emergency room sometimes at 3:00 AM because someone will come into the emergency room and be 57 years old and have a first episode psychosis and will be presented to me with a diagnosis of schizophrenia and I say, “Okay, is there a past history of this? Is this the first episode? What is the hormonal status? Are they perimenopausal?”

Professor Zahinoor Ismail:

And our clinician trainees are not taught to think of natural history and so they just take cross sectional assessments consistent with our larger nosological frameworks of DSM and ICD and not really inquire about the natural history and the evolution. So to me that’s an area in our field that really requires great work.

Dr Joe Kane:

Could you tell me a little bit about the committee on how your group is organized in the PIA?

Professor Zahinoor Ismail:

Neuropsychiatric Syndromes Committee is co-led by someone from academia and someone from industry, and that’s been a partnership I think going back around in 10 years or so and was developed to foster a partnership and inform drug development and testing to include industry in the conversation as opposed to having a siloed understanding. And so we continue that, and I think it’s very, very helpful because we have insights into clinical trial design and regulatory issues that we might not as a clinician or as a researcher. And at the same time those involved in developing and testing pharmacological interventions have an idea of how clinicians and researchers think out in the field, which can inform study design.

Professor Zahinoor Ismail:

And so the combination of the two is really a nice Petri dish and an idea generator, it works really well. We have 10 members of the executive committee which is diverse and we look at imaging and biomarkers and neurostimulation, but also measurement. We also look at person centred issues like ethics, sex and gender and diversity. And we have members in training and like yourself, communication members and members across the spectrum of experience of fields of expertise. So clinical fields while heavily influenced by psychiatry and old age psychiatry. We have neuropharmacology, neurology, vascular expertise.

Professor Zahinoor Ismail:

We also have a mixture of clinician researchers and the researchers involve clinical trialists and epidemiologists, Imaging experts, measurement based care phenomenology, et cetera. The group is robust and interactive and very friendly and fun. I mean, I really enjoy the time with our PIA and the discussions are interactive and robust and thought provoking, and everyone’s just really nice. It’s a fun group.

Dr Joe Kane:

Speaking of your group, and you mentioned early career researchers, how can I get involved in this fun group?

Professor Zahinoor Ismail:

So we welcome early career researchers and have roles for them and we have a dedicated person to liaise with them and support them and address trainee needs. One of our goals actually in this next year is to develop a more formal mentorship program for junior members knowing that trainees or early career folks have mentorship in their own institution depending on the size of that institution or the busyness of their mentors, we are hoping to provide some sort of lateral mentorship as well for someone from a different institution with a different perspective still appreciating and respecting that existing mentorship that someone may have.

Professor Zahinoor Ismail:

So yeah, over the next year, we’re going to flesh this out more, but embracing junior members is really important to our PIA and I’ll speak to my own experience in that my research career is extensively built on work that came out of the PIA 10 years ago, and I really want to make sure that other people have that incredible opportunity. I come from an institution, especially 10 years ago, where there wasn’t that degree of expertise in their psychiatric symptoms and that neuropsychiatric dementia interface. And having the exposure to thoughts and support and ideas from the PIA at that time was seminal in my career, and I really want to make sure that our PIA continues that because this is how our field grows.

Professor Zahinoor Ismail:

And so embracing junior members is our strength and our senior members are intellectually generous to support and help junior members with research ideas, with constructs, with implementation.

Dr Joe Kane:

What does your PIA have planned on [inaudible 00:40:48] for the coming year? Will they be presenting at the AAIC?

Professor Zahinoor Ismail:

We will be. So we do have an FRS and we submitted two and one was accepted, involves clinical and cognitive outcomes and biomarkers of neuropsychiatric symptoms. Sex differences in [inaudible 00:41:06] and neuro-psychiatric symptoms, we have MBI included in there. Devin is presenting the results from his lithium AD, the lith-AD study, very exciting. And we also have many posters and a few oral presentations as well. Our past chair, Karen Fisher is actually presenting their research and biomarker psychosis criteria and I think that’ll be really interesting and exciting, because as I mentioned, they are in harmony with the IPA criteria and intended to really foster systematic research into biomarkers in the earlier stages.

Professor Zahinoor Ismail:

We have posters across all the topics that I’ve discussed today. My own lab, I think, has about 10 poster presentations. To me that’s one of just the best parts of AAIC is the ability to see what people are doing at a very current level, the fact that there’s so much in neuropsychiatric syndromes and neuropsychiatric symptoms to learn and it’s robust and it’s moving fast and you’ve got all the experts there.

Professor Zahinoor Ismail:

So I think it’s a fantastic learning opportunity where I’m doing some networking as well with junior members and then down the road, we’re going to have some more workshops on various neuropsychiatric symptoms and across the cognitive spectrum from normal cognition through to subjective cognitive decline to MCI through to dementia proper. So we’re trying to capture the spectrum.

Dr Joe Kane:

That sounds great. It definitely sold me on a few of those sessions. Certainly the lithium and AD sounds absolutely unmissable as DFE of the workshops as well so that’s going to be really cool.

Professor Zahinoor Ismail:

As a sneak peak, I mean the abstract is out, but there’s a psychosis effect with lithium. I was very excited when I saw that abstract, again, which is in press in the American Journal of Geriatric Psychiatry, but Dev is going to go into detail and so there’s an agitation effect and psychosis effect, a global effect. Very exciting data and I think warrants a larger study.

Dr Joe Kane:

Thank you very much. It’s actually time to end today’s podcast recording. Before we go, can I have one final question? What advice would you give to any aspiring dementia researchers out there who are thinking of looking into dementia?

Professor Zahinoor Ismail:

My advice would be to not only look at current constructs and paradigms, but also to try turning them on their side and exploring different angles like we discussed. Psychiatric symptoms don’t have to be viewed in a neurodevelopmental framework, they can view through a neurodegenerative one. So bouncing around ideas and with yourself in the shower with other colleagues and friends, with senior clinicians and scientists in PIAs, looking across fields, the inter PIA collaborations are a great way to take ideas from one field and cross-pollinate into another and this certainly happens clinically, but it happens in research as well and sometimes we get into kind of a fixed mindset.

Professor Zahinoor Ismail:

And if we have that kind of growth mindset of exploration and being creative, and I think just not being afraid to ask Lackey questions is to me advice that I would suggest and I can go back. I’ll finish it off with, with Douglas Adams and Hitchhiker’s Guide to the Galaxy and when the heart of darkness was created, it wasn’t because it was an A priority plan as an end point that was defined, it was out of just sheer fun and creativity and research and so to remember that exploration is part zigzagging around and kind of looking at the flowers.

Dr Joe Kane:

I think any podcasts that answer the Douglas Adams reference is going to be a good one. So listen, thank you so much. It has been an absolute privilege to speak to you today. It’s been wonderful getting unrelated psychiatry perspective on the field but anytime anyone asks what we bring to the field, I’m going to hold up you and your work. So thank you so much for speaking with me today.

Professor Zahinoor Ismail:

My pleasure. Thank you.

Dr Joe Kane:

I look forward to seeing some of the PIA’s work at AAIC.

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Thank you for listening. You can find profiles on today’s panellists and information on how to become involved in ISTAART on our website at dementiaresearcher.nihr.ac.uk, and also at alz.org/istaart. We’ll be back tomorrow with the next recording in our ISTAART PIA Relay Podcast Series. Finally, please remember to like, subscribe and leave a review of our podcast. You can do this on our website and in your podcast app. Thank you.

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Brought to you by dementiaresearcher.nihr.ac.uk in association with Alzheimer’s Research UK and Alzheimer’s Society, supporting early career dementia researchers across the world.

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