Under the FTLD Umbrella: A Deep Dive into Frontotemporal Dementia

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Credit Designation Statements

For more information about continuing education credit for this episode, visit the ICEP online learning portal at https://ce.icep.wisc.edu/dementiamatters2025/frontotemporal-dementia

The accreditation for this course expires 8/12/2026. After this date, you will no longer be able to access the course or claim credit.

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Learning Objectives

As a result of participation in this educational activity, members of the healthcare team will:

1. Define frontotemporal lobar degeneration (FTLD) and its causes
2. Describe the symptoms of FTLD and how they may be different from the symptoms of Alzheimer’s disease
3. Discuss the diagnosis process and standard of care for FTLD
4. Describe the different referrals and organizations for those with FTLD
5. Describe current research and major advances in FTLD research, including the ALLFTD research study

References

• AllFTD. ALLFTD. Accessed August 7, 2025. https://www.allftd.org/.
• CurePSP - Home. Accessed August 7, 2025. https://www.psp.org/.
• The Association for Frontotemporal Degeneration. AFTD. September 17, 2024. Accessed August 7, 2025. https://www.theaftd.org/.
• Coleman KK, Berry S, Cummings J, et al. Intranasal oxytocin for apathy in people with frontotemporal dementia (Foxy): A Multicentre, randomised, double-blind, placebo-controlled, adaptive, crossover, phase 2A/2B superiority trial. The Lancet Neurology. 2025;24(2):128-139. doi:10.1016/s1474-4422(24)00456-3
• Staffaroni AM, Quintana M, Wendelberger B, et al. Temporal order of clinical and biomarker changes in familial frontotemporal dementia. Nature Medicine. 2022;28(10):2194-2206. doi:10.1038/s41591-022-01942-9

Transcript

Intro: I'm Dr. Nathaniel Chin, and you're listening to Dementia Matters, a podcast about Alzheimer's disease. Dementia Matters is a production of the Wisconsin Alzheimer's Disease Research Center. Our goal is to educate listeners on the latest news in Alzheimer's disease research and caregiver strategies. Thanks for joining us.

Accreditation Intro: This episode is approved for continuing education credits for physicians, physician assistants, nurses and other members of the healthcare team through the Interprofessional Continuing Education Partnership at UW–Madison. At the time of this recording, Dr. Brad Boeve discloses the following relevant financial relationships with ineligible companies. He is a consultant with Tau Consortium and discloses grants with Cognition Therapeutics, Alector, EIP Pharma, and Transposon Therapeutics. I, Dr. Nathaniel Chin, have the following relevant financial relationships with the ineligible companies as a consultant: NewAmsterdam Pharma and Eli Lilly and Company. Information on how to claim credit will be shared at the end of this episode. Additional continuing education information is provided in the show notes.

Dr. Nathaniel Chin: Welcome back to Dementia Matters. Today I'm joined by Dr. Brad Boeve. Dr. Boeve is a neurologist within Mayo Clinic's Department of Neurology and Center for Sleep Medicine and a professor of neurology in the Division of Behavioral Neurology, as well as the co-director of the Mayo Clinic Alzheimer's Disease Research Center. Boeve is a principal investigator of the ARTFL-LEFFTDS Longitudinal Frontal Temporal Lobar Degeneration, or ALLFTD, research study which aims to further our understanding of frontotemporal lobar degeneration, or FTLD, by collecting data from patients to identify clinical measurements and biomarkers that can be used to follow patients during treatment trials and help predict when someone at risk of FTLD will start experiencing symptoms. Dr. Boeve joins us today to discuss frontotemporal dementia and the clinical evaluation process, as well as his research with the ALLFTD study. Dr. Boeve, welcome to Dementia Matters.

Dr. Brad Boeve: Thanks so much, Nate. I'll define what FTLD is perhaps in a few minutes.

Chin: Okay, and that was a mouthful for me so I appreciate it if you do. Before we discuss the research, though, I'd like to start by tapping into your clinical expertise. Could you share with our listeners what exactly is frontotemporal lobar degeneration, also known as FTLD, and do we know what causes it?

Boeve: Yes. FTLD is an umbrella term that represents basically the third most common constellation of neurodegenerative syndromes with Alzheimer's disease being the most common, Lewy body dementia or Lewy body disease if you include Parkinson's disease under that umbrella too. Then FTLD, which is somewhere in the five to fifteen percent of all neurodegenerative syndromes. Most individuals with FTLD develop symptoms younger than age 65. 65 isn't any specific cutoff but it's largely an early onset group of disorders. In that setting, it's as common as Alzheimer's disease in that age range. In younger folks, it is relatively common to the extent that early onset Alzheimer's disease is relatively relatively common, but I wouldn't say either is common.

Chin: Right. In my practice, of course, as a geriatrician of 65 and older, we just simply don't see that much FTD. In Alzheimer's, of course, we know that amyloid and tau are at least the biological part of the process and we're starting to understand what causes some of those proteins to accumulate. What about with FTLD? Is there a particular cause or gene that's related to this?

Boeve: Yes, and it's quite complicated even for those who do this for a living to be honest. Under the FTLD umbrella, the two most common proteinopathies or the primary protein that's driving the symptoms, it's either tau–and it's a different form of tau but still the basic tau protein–or TDP-43. It's typically either or. Less commonly there's the FET proteins. It gets quite complicated with all of the proteins in the nomenclature. I should also say under the FTLD umbrella there's behavioral variant frontotemporal dementia (bvFTD), FTD with motor neuron disease or with ALS, primary progressive aphasia (PPA), then corticobasal syndrome and progressive supranuclear palsy. Richardson syndrome is also under that umbrella. Depending on the syndrome that reflects the topography of degeneration in the central nervous system. There's certain syndromes that have a predilection for a particular proteinopathy, tau versus TDP-43. As I'm sure we'll talk about, we don't have a perfect ability to detect the underlying protein unless we know a genetic cause. The genetic cause is somewhere in the 20 to 40 percent of all individuals with an FTLD spectrum disorder will have a genetic contribution. Under that, a large percentage of them have a single mutation in a pathogenic gene. It's much more genetically driven than Alzheimer's disease. APOE, we know quite a bit about that in Alzheimer's disease but the pathogenic mutations are that much more of an issue in FTLD.

Chin: Wow, that does sound really complicated, Brad. Genes are important, and it can even be a single mutation, but then there's TDP-43, which is a protein. There's tau, which is different than the tau we think of with Alzheimer's disease but still part of that tau protein complex. Then there's multiple different syndromes within it. I'm emphasizing this to our listeners because I'm going to ask you the next question and you might have to give me a couple of answers so that each syndrome gets a little bit of attention. That's because really what are the symptoms of FTLD? Maybe you have to break it by the syndrome. How are they different than Alzheimer's, because sometimes the language part can overlap?

Boeve: Yeah, and this underscores the challenges that we have as clinicians. We really need biomarkers and we're still not quite where we want to be for biomarkers in the FTLD area, but we expect that to change quite a bit over the next few years. In behavioral variant FTD, the symptoms are largely personality or behavioral change, executive dysfunction, language dysfunction. In the classic sense, memory is relatively preserved but, as we're seeing more and more people with bvFTD, they do have some degree of memory impairment. It really underscores the challenges differentiating between Alzheimer's disease. In bvFTD, roughly half will have a primary tau disorder. Roughly half will have TDP-43. Those are probably more on the order of 45 percent each and then five to ten percent even rarer proteins. In primary progressive aphasia, there's three variants. Some would argue more than three, but the three main variants–semantic variant, primary progressive aphasia, primarily affects the anterior temporal lobe in the dominant hemisphere. There's especially dysnomia, difficulty coming up with names of people or things. This is very common in the population. A lot of people are worried about this because so many of us are in a social setting, “Oh, what is that person's name?” This is a consistent dysnomia. That's largely a TDP-43 disorder. Contrast that with the non-fluent agrammatic variant of PPA, where speech hesitancy, agrammatism, the fluency is affected, and that's more often a tau-related disorder. Not always, but largely a tau disorder. The so-called logopenic variant–it's kind of complicated to describe, but there's a lot of working memory issues as well as language. That's often atypical Alzheimer's disease, underlying logopenic variant PPA. Corticobasal syndrome–we used to use the term corticobasal degeneration, but we know about half of the people with corticobasal syndrome don't have corticobasal degeneration as the cause. That's why we use the syndromic term. Many of them have a primary tauopathy, but some can have atypical Alzheimer's disease even though cognition is largely preserved, at least early on, and it seems to be more of a motor phenotype. The classic progressive supranuclear palsy or Richardson syndrome, that's usually a tau-related disorder.

Chin: Brad, I can't imagine being at one of your conferences and meetings and communicating among the experts. You have to be very clear about what you're talking about when you're describing this umbrella and all the different syndromes.

Boeve: It is. And the same in manuscripts. Imagine, it's challenging for those who do this for a living or other health care professionals. Imagine if you're a patient or family member trying to decipher this. It really is a challenge.

Chin: One thing I'm not going to ask you to talk about is the LATE–limbic predominant age-related TDP-43 encephalopathy–because one of your colleagues, our colleague, Dr. Wolk, has already done that on the podcast. We'll put that episode in the show notes. I won't ask you to speak to that TDP-43 issue. When it comes to FTLD, can you diagnose this in that stage of mild cognitive impairment, or is this usually a condition that's diagnosed in the dementia stage?

Boeve: Yeah. With sporadic bvFTD, it's almost always by the time that a person is recognized to have FTD, they have a mild dementia syndrome. That's getting better with the circle of clinicians across the country, if not the world. We are getting better at identifying people early, but we call this the diagnostic odyssey of FTD. It can take one to four years before a person is diagnosed. It's understandable; somebody is in their 30s or 40s, atypical depression or late-life schizophrenia for lack of a better term, or midlife crisis, or bipolar disorder. These are appropriate considerations based on a lot of the symptoms that are happening. It's only when they don't respond to treatment or some other things are, “Oh boy, this is way out of character for this individual.” Then usually an imaging study, an MRI or an FDG PET, a glucose PET scan. Sometimes an MRI can look more normal than that, and an FDG PET is usually abnormal but not always. It, again, underscores the challenges with establishing a diagnosis. We still don't have good blood or CSF markers and we still don't have good molecular PET imaging studies. Although we anticipate the next five years that's going to change for a more specific four-repeat tau, maybe even a three-repeat tau, ligand and then a TDP ligand.

Chin: How about the language version of FTLD? You can diagnose that in MCI?

Boeve: Yes. Again, if it's the clinician who can identify individuals. This sometimes gets a little bit hairy in terms of is this MCI of the language type or is this very early PPA. That is a little bit semantics, even in semantic PPA to be honest. The main point is it's a language disorder, whether it's more fluent or non-fluent, to use the classic basic terms in aphasia. We often will hear about, well, somebody was told that they had a stroke, but we can't see it on the MRI scan. That obviously doesn't make sense. There's either a stroke or there isn't. That's pretty common when it evolves insidiously and progressively worsens, not acutely. It sounds degenerative.

Chin: Do people with FTLD progress faster than those with Alzheimer's or Lewy body or vascular dementia?

Boeve: You always hate this answer, it depends, but it really does. Anyone with any of these syndromes along with coexisting ALS, then as one would expect the rate of progression is unfortunately fairly fast, but that's relatively uncommon. There are some with bvFTD that from onset until death it could be two to three years. I know of some–and I'm still following some–either sporadic or familial, and they can have symptoms 30 or 40 years, very slowly progressive, amazingly slowly progressive. That's less the case with corticobasal and PSP. Those syndromes, it's usually five to ten years. PPA and some variants of bvFTD can be extremely slow.

Chin: I'll just ask you for those two, the behavioral variant bvFTD and the semantic version. How does a clinician diagnose those? When we refer to you as a specialist, what process do you go through or what would you recommend primary care doctors be thinking about and patients be thinking about? You already mentioned this, but there's just no biomarkers other than FDG PET. Is there anything else you use in a neurology clinic to help?

Boeve: So much like everything in clinical medicine, medicine is the history. The exam is important too, but the history, and especially in bvFTD, it's the off-color, it's the clear change in behavior. That's really the clue that somebody, for example, is at a funeral and making a few jokes or saying people based on their appearance, how they look, when that's just not appropriate in a social setting. This can begin just with a few off-color comments and then months seem to be relatively normal and then a few more. It can smolder along. With the language, just because humans are so much more reliant on language for functioning, it's a bit more apparent that I can't get my words out. It's like my tongue is tied or I just cannot come up with a name of a person or a thing. Often it's “that person” or “that thing” is used in place of the appropriate nouns.

Chin: Yeah. You were saying, and my limited experience with behavioral variant, is it true that the person just doesn't have the insight into recognizing these changes? When families report this, they feel like there's some, “No, you're wrong for observing this. I feel totally fine?”

Boeve: Yeah, that is the prototype and that is largely true. As we're seeing more and more people early in the illness, for a lot, including in bvFTD, insight is, I wouldn't say it's completely preserved, but it's more preserved than not. As the illness progresses, then anasognosia, or insight, is clearly more affected. The genetic forms too, especially if they know there's a mutation in the family. I've met many many individuals that, I just know I'm different. I'm like my sister. I'm like my father. I otherwise feel okay, but I just, I can't come up with words or I'm just more emotionally detached with my spouse or with my kids or comments along those lines.

Chin: I'm sure you get this question a lot when you're out in public. I don't want to worry our listeners who are experiencing word finding or difficulty naming something. I'm going to ask you the question of, what do you say to the person who comes up to you and says, well, I'm struggling to find words here and there. Should I be evaluated for FTD?

Boeve: I guess the best term in terms of the red flag, so to speak, if something's happening and it's relatively consistent. It may not happen all the time, but being in a social setting and not coming up with a name or being with family and wondering, “What's that person's name?” When it's more consistent than that. And then a behavioral change, it's more that just family members or friends say, this is different than this person. It's not a one-off. It's more than one or two or three comments.

Chin: Okay. Now I want to look at after a diagnosis. What does the standard of care look like? Are there medications specific to the disease or are there referrals that a person should make as a clinician or a patient should go to?

Boeve: Yeah. This is where an early accurate diagnosis can be very helpful. Unfortunately, we still do not have any FDA-approved agents for FTD, for any of the FTD syndromes. We're not including ALS under that umbrella. A lot of this is first recognition and then non-pharmacologic things–education, empowerment, how do we maximize quality of life. From a pharmacologic standpoint, there was a recent trial published, one of the first trials, called the FOXY trial. This was intranasal oxytocin for improving apathy in people with bvFTD. That's not easily available, but now there's evidence supporting its use. The standard of care from any treatment perspective is the SSRI or SNRI class, just because it often will help with anxiety or mood or there can be a tendency to overeat or apathy can be prominent. It is a bit of a trial and error approach. There is data from a trial that was done several years ago using trazodone, which we use quite often for insomnia, but this was used at a much higher dose for people with bvFTD. It was shown to be effective but without good FDA guidance; a lot of this is clinical experience. Also, and this is kind of controversial, the standard is not to use a cholinesterase inhibitor like donepezil, rivastigmine or galantamine. I think most people in the field agree that, one, they're not that helpful, and two, sometimes, almost paradoxically, symptoms can get worse. An occasional person might have some lift of the apathy. In my experience, that's the one symptom that sometimes can improve with a cholinesterase inhibitor. Memantine has been studied in a large trial and it was unfortunately not shown to be efficacious. Still, memantine is often used but there's no evidence supporting it. So much of this is symptom-based as opposed to disease-based.

Chin: Do you have any referrals that people commonly will go to? With Alzheimer's, of course, we do a lot of occupational therapy or speech therapy, counseling. Is there anything in particular with FTLD that's been beneficial?

Boeve: Yeah, great question. PPA, absolutely, involvement with a speech therapist. Sometimes working with a speech therapist who does have knowledge in the PPA area. The approach as part of the speech therapy plan, it's largely based on the stroke experience but there are some adaptations that are done because it's rare to get a stroke in the anterior temporal lobe and therefore the semantic variant to PPA, you don't see that often clinically in vascular disorders. Absolutely, speech therapy can be quite helpful. Then in those who have motor impairment, involving occupational therapy and physical therapy. In the bvFTD, a psychiatrist can be invariably helpful. There can be some challenges sometimes requiring hospitalization. As a neurologist or geriatrician, it's often hard how to hospitalize and what's the most appropriate service that's going to be most helpful for this individual. Involving a psychiatrist early on is often a good idea too.

Chin: Brad, you know that in Alzheimer's we do a lot of referrals to the Alzheimer's Association or the Alzheimer's Foundation of America. I'm involved in both of those. Is there an organization in this world that you make a referral to or you connect people to?

Boeve: An excellent question. The Association for Frontotemporal Degeneration, or AFTD. Every individual that we meet with any of these syndromes we have been talking about, AFTD. They have an excellent website, theaftd.org, and a strong referral network. That's the organization, basically the equivalent of the Alzheimer's Association. Then depending on other things, for example, corticobasal syndrome or PSP, the CurePSP organization is an excellent website. It's curepsp.org. They have a lot of resources also for CBS, PSP and other motor phenotypes in the FTLD. Those are the two most common and they're both excellent.

Chin: Another important referral in care is usually to clinical research, particularly in our field. I suspect that the same is true for FTLD. Can you start by giving us the 30,000 foot view on where we are FTLD research and then the major advances in the past decade or so?

Boeve: Yeah. FTD research was for many, many years embedded in the Alzheimer’s research networks, especially across the Alzheimer's disease research centers. That still continues, but an offshoot of that is the ARTFL-LEFFTDS Consortium. Just to explain this, and it's a little bit of a long story, but years ago there was one research proposal–Advancement of Research and Treatment in Frontotemporal Lobar Degeneration. That's ARTFL. That was focused on sporadic FTLD and to some extent familial FTLD. At the same time, a related group submitted a grant for familial FTD and that was LEFFTDS–Longitudinal Evaluation of Familial Frontotemporal Lobar Degeneration Subjects. Then the NIH thought, well, these are largely overlapping. Why not just make the infrastructure the same, which was a very good idea. It was combined into ARTFL-LEFFTDS and that's proceeded for a good five years. Then the next phase was ALLFTD–ARTFL LEFFTDS Longitudinal Frontotemporal Lobar Degeneration, so ALLFTD. And so, and hopefully the next phase of ALLFTD, hopefully that will be funded and will begin as early as the fall. That's what we're hoping for, but through that course, we've learned an enormous amount. One is it's important to build the infrastructure. This started with eight sites with one grant, 15 in another. Now our ALLFTD is 28 sites in North America, two Canadian sites and the others in the U.S. We meet regularly and it's really built into very similar to the ADRC network with 35, 36 centers across the US. The key thing is coalescing on how do we characterize and follow individuals, early and accurate diagnosis, collection of biofluid–so blood and spinal fluid in those who are willing–longitudinal MRI scans, which are going to be the core and have been the core for clinical trials, and PET scans. This is where, again, we desperately need a ligand that is specific for the forms of tau and for TDP-43. That's what we anticipate is a major breakthrough over the next five years is these ligands. We have over 3,000 people we've seen over ARTFL-LEFFTDS over the course of 10 years. We have about 1,600 people who are active. It's quite a large cohort of individuals. We don't have a blood test yet, really working hard on it. In the spinal fluid, there are some signals in spinal fluid, not there yet to be like we can diagnose Alzheimer's disease with very high accuracy based on spinal fluid or molecular PETs. Those are the breakthroughs that we really anticipate over the next three to five years. Just like in Alzheimer's disease, as those breakthroughs happen, that's going to really accelerate therapeutics and trials. We've had many trials. We're going to hear the result of a phase three trial in a particular genetic form, progranulin, later this year. There are several other phase two trials in progranulin. There are several focused on tau mutation carriers being planned. Same thing for the C9orf72 gene. There have been some that occurred and more being planned. The clinical trial landscape, even though these are relatively uncommon, there's a lot of interest by pharma, fortunately, largely because the biology, it's not fully understood, but in many ways understood, at least to the point where we can identify the target and there's a means to intervene in the target.

Chin: Why is it so important to have this network of sites working to build this cohort of individuals? Because it seems like ALLFTD, like you said, is similar to our Alzheimer's Disease Research Center network. Collectively, you have, you just said, 3,000 participants. Why is that so critical?

Boeve: One is there are–this sounds kind of trite– there are so many individuals that have similar symptoms and therefore diagnosis is relatively straightforward. We're learning a lot. A lot of people have atypical features and findings. We're finding genetic variants in seemingly sporadic individuals. That can impact clinical care, so whether it's a suspected or known genetic alteration in a family or we find a spontaneous mutation in an individual, that opens up potential avenues for clinical trials but it obviously has implications for biologic relatives. Having 28 sites for all the trials that have been happening and that are being planned, you want a trial network so they know what to do, what measures are done, the scans, the way that a standard clinical trial is done. Without that infrastructure, it'd be very laborious and expensive for our industry partners to just design and conduct one trial, but there's multiple going on and, again, several more planned.

Chin: What have you learned so far from the ALLFTD study? I know there's a lot of scientific papers that come out of this group, so if there's just a couple that you wanted to mention for our listeners who might be interested in either participating or just looking further into the study.

Boeve: Yeah, we've had the good fortune with so many experts in the field. There's been over 500 publications that are directly or indirectly related to ARTFL-LEFFTDS, ALLFTD. One of the most notable scientifically, I think a lot would agree, is the families with a mutation in either tau or progranulin or the C9orf72–we often abbreviate to C9. The data from those families in ALLFTD and also the data in the sister study in Europe called GENFI. GENFI has been going on longer than ARTFL-LEFFTDS, ALLFTD, and they're a fantastic group and a really large cohort too. The global effort is called the Frontotemporal Dementia Prevention Initiative, FPI, but this was pretty complicated. It was taking all the clinical data, available MRI data and some biofluid markers to develop a disease progression model using Bayesian statistics. This gets quite complicated, but we've been able to put together models of what tends to happen among those with a MAPT or tau mutation. Overlaps to some extent but is different in important ways for progranulin. Same is true for C9. That's been done on disease modeling using available data, and the true test of any model is obviously testing it prospectively. Trying to do this with many, many more individuals, but pharma has really jumped on to these models and they're using this intellectual background as they design trials. It's not too hard to see, and it's not to the point of AI applications, but it's kind of a rudimentary AI approach to a complex and relatively uncommon group of disorders.

Chin: I mean, one of the things that seems very clear, Brad, in talking to you is we ultimately want to get to treatment. We want to get to ways of helping people. In order to do that, we have to understand the disease. We have to understand what's causing it, what the course looks like, what you just referred to, and so that just takes a lot of people and a lot of data and then ideally AI to help us craft it.

Boeve: Yeah, and that is true. This has been part of the challenge. Many of our patients and families–and I hear this often, and all of us completely understand–number one priority, we need the urgency for treatments including prevention for those who have a mutation but don't have any symptoms. Absolutely, that's priority number one. In order to get there, you have to understand the natural history of the illness, collect this data to know with biomarkers. This makes sense when you think about it. If, for example, a person in their thirties, they have a mutation and it may or may not be 100 percent penetrant, meaning they may or may not eventually develop an illness. If they use the therapy as a prevention, how do you prove that you're delaying or preventing the illness? That's where the biomarkers come in. You have to find something that's tracking in the asymptomatic phase impacted by an intervention. That's good evidence. Okay, we're affecting the underlying disease process and thereby preventing or at least delaying the onset. That's the big challenge, but there's so many families that are very involved and this isn't fun to do all these tests periodically. It's pretty anxiety-provoking, but we know how to get there. It's just a matter of having the funding, which as we know that's a whole other story right now, but the acceleration of treatment, that's the goal.

Chin: Well, speaking of which, though, a part of your mission, though, is setting the stage for proper clinical trials. That's what ALLFTD is helping do. You mentioned a couple already. There are some treatment trials underway. What types of specific medications do you think are going to be possible in the next 10 years with your understanding of the disease progression?

Boeve: Yeah. First, again coming to the example of a bvFTD, roughly half have a primary tau problem, roughly half have a TDP. This sounds so basic, but if we have a tau-active treatment, we don't necessarily want to use a tau-active treatment in somebody who has a TDP disorder, especially if there's toxicity. Getting better biomarkers to know who has a tau problem versus TDP–that's going to be key from a treatment standpoint, so the biomarker development, those focused on tau, those focused on TDP and associated downstream or perhaps even upstream effects. We also know inflammation is part of the degenerative process in almost all of these. There's actually one trial going on in semantic variant PPA with an anti-inflammatory agent to see could that impact, but some medicines don't cross the blood-brain barrier very well. You have to use it at a dose that doesn't cause any bad systemic side effects, but those, it just makes sense. Just like lecanemab and donanemab now for amyloid in Alzheimer's disease, the Tau Platform trial being developed for the tau angle of Alzheimer's disease. I just heard over the weekend, the PSP Tau Platform (PTP) trial, that's going forward. A spectrum of tau agents is going to be designed for PTP, for PSP. What we're learning in PSP and in Alzheimer's disease that relates to tau will have direct implications for tau in FTD also.

Chin: To end today, Brad, what brings you the most hope when you think about the research and the clinical care for those with or at risk of developing FTD?

Boeve: It's these treatments. I've been around for a few decades. I remember when I started off thinking, we'll probably have a truly disease-modifying treatment within the next five, 10 years. It took, you know, over 20 years, at least over my career. We've got a long ways to go in Alzheimer's disease. To see all that hard work, and then the treatment on amyloid and what we've learned and what we know we still need to do to impact Alzheimer's disease. We're earlier in that same course in FTD. I think we've learned a lot, good and you know not so good, of what agents and how not to do trials and not to be critical of the history, but you know everybody's doing their best and you learn from those experiences, okay, well, This is not how to do a trial going forward. That's the excitement, to know that we're going to have treatments for tau, TDP, all of these genetic forms in the future, and I mean this with all sincerity, I think the future really does look far more optimistic now than even two, three years ago.

Chin: Well, I want to end on that high note, Brad. Thank you for being on Dementia Matters today, and certainly I hope to have you on in the future.

Boeve: Great. Thank you so much, Nate. I appreciate the opportunity.

Accreditation Outro: As a reminder, continuing education credit is available for this episode through the Interprofessional Continuing Education Partnership at University of Wisconsin–Madison. To claim credit, you can text this code: KOYHUN at this number 608-260-7097. Again the number is 608-260-7097 and text this code: KOYHUN. Your feedback is important to us. To complete an evaluation form for this episode, see the show notes.

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