Name:
Description:
Thumbnail URL:
https://cadmoremediastorage.blob.core.windows.net/4f887d56-65b7-4f58-aa7e-d34452b35e1a/videoscrubberimages/Scrubber_10.jpg
Duration:
Embed URL:
https://stream.cadmore.media/player/4f887d56-65b7-4f58-aa7e-d34452b35e1a
Content URL:
https://asa1cadmoremedia.blob.core.windows.net/asset-4f15696f-180e-4986-991d-74fd1ea55085/Randall Bateman - Interview V3.mp4
Upload Date:
2022-12-04T12:46:31.2009778Z
Transcript:
Language: EN.
Segment:1 Please could you introduce yourself and tell us about your current research focuses?.
RANDALL BATEMAN: I'm a professor of neurology at Washington University (MO, USA) and my official title is the Charles F. and Joanne Knight Distinguished Professor of Neurology. I do quite a bit of research in Alzheimer's disease and this includes both lab-based research, as well as clinical and translational research.
Segment:2 What primary prevention trials are ongoing for Alzheimer's disease and what are they telling us so far?.
RANDALL BATEMAN: Well, there's a distinction we make in the prevention trials. There's primary prevention, which some of us use the term primary to mean before there's any pathology.
RANDALL BATEMAN: And then there's secondary prevention, which is once someone begins to have the pathology of Alzheimer's disease, but they have not yet manifested the disease with memory loss, forgetfulness, or dementia, we would call that secondary prevention. And then there's symptomatic trials. And the vast majority of trials today are in symptomatic phases of Alzheimer's disease. However, there are ongoing secondary prevention trials, which is usually about up to 15 years before the symptom onset.
RANDALL BATEMAN: So people who either have amyloid plaques or by genetic risk factor have a genetic risk of getting Alzheimer's disease get enrolled into these prevention trials. And there's a number of these trials ongoing. For example, I helped lead one called the Dominantly Inherited Alzheimer's Network Trials Unit (DIAN-TU). And in this platform where we study families that carry mutations that cause early onset Alzheimer's disease, we have two different drugs currently active for therapeutic testing.
RANDALL BATEMAN: And the platform is preparing to launch additional drugs to be tested. These kinds of secondary prevention trials that are underway will be read out over the next 5 years, starting in 2020 for our trial and then later for other trials to read out the effects of prevention in Alzheimer's disease, and to tell us if these drugs that are currently being tested or previously tested for symptomatic Alzheimer's disease, whether those drugs can actually slow or prevent the onset of the disease in the prevention mode.
Segment:3 There has been a lot of traction around whether the amyloid hypothesis should still be the way forward when considering primary prevention treatment. In your opinion, should researchers be exploring alternative avenues to amyloid-β? .
RANDALL BATEMAN: Oh, absolutely. And we are. For example, the DIAN-TU is preparing a launch, drugs targeting tau, an important pathology of Alzheimer's disease. And there are also other drug trials that are starting up targeting inflammation, immunomodulatory-- many other mechanisms are being tested.
RANDALL BATEMAN: And in general and in a field like this where we don't know the relative contributions of each of these targets to either the prevention leading up to the disease or after clinical onset, that progression that occurs afterwards, it is important to have a multifaceted approach and a diversified approach to targeting this. Now getting back to primary prevention, Eric McDade at Washington University is leading a primary prevention initiative to treat these family members even before they have pathology and to try to prevent them from getting one of the first pathologies that appears in these people who get early onset Alzheimer's disease.
RANDALL BATEMAN: And that's the amyloid plaques. So for primary prevention, it makes a lot more sense to me to stay targeted and focused on amyloid and amyloid beta as the pathogenic cause of their disease and try to prevent that from being established in the first place. And this perhaps is the strongest test of what is called the amyloid hypothesis, that if you prevent the amyloid pathologies, the plaques, the higher-order aggregates from accumulating, you should be able to prevent the entire disease from coming on in those individuals.
RANDALL BATEMAN: Whereas otherwise, they would normally get the disease at a 100% penetrance.
Segment:4 What are the main challenges surrounding primary prevention trials for Alzheimer’s?.
RANDALL BATEMAN: Prevention trials in Alzheimer's disease, one of the challenges is to identify who to treat. And it's the reason that we had started the prevention trials in these mutation carriers. Because we know ahead of time who's going to get the disease, and we can predict about when they're going to get it. But for the rest of the population, which accounts for more than 99% of the people who would get Alzheimer's disease, it's a much harder thing to be able to tell who's going to get the disease and when they'll get it.
RANDALL BATEMAN: But an enormous amount of clinical research over the past 20 years has led to an understanding that people who develop the pathologies of Alzheimer's disease plaques and especially tau tangles, that these are the people that manifest the disease clinically. And so by following those group of individuals with biomarkers, initially PET scans and cerebrospinal fluid, but now in the blood we can detect plaques and tangles.
RANDALL BATEMAN: We can begin to identify those people who we think are at risk of getting Alzheimer's disease and enroll them in prevention trials, trying to prevent them from getting the onset of the clinical disease.
Segment:5 Looking forward, where do you anticipate the field will be in 5–10 years’ time? .
RANDALL BATEMAN: So I expect that by 5 years, we will have fully established and validated biomarkers, blood biomarkers that will tell us not just who's at risk of getting Alzheimer's disease, but about when they'll get it.
RANDALL BATEMAN: We'll be able to have some prognostic ability of the range of when people will get the disease. We may have some of the first prevention treatments and/or some of the first therapeutic treatments for people who are already sick for Alzheimer's disease, being successful in their clinical trials and potentially approved for clinical use by the medical community. By 10 years, I fully expect us to have treatments which will have been tested in prevention and in symptomatic disease which will have a large effect on the disease course.
RANDALL BATEMAN: This is one of the things we're looking to do, is to have a big impact on how the disease progresses, not just a small, marginal effect on disease progression, but really being able to hold it off and potentially save millions of people from getting the disease. And I think we are within reach, that within 10 years there's the good possibility that we'll be able to do that. [MUSIC PLAYING]
Form Title Download
Form Title Bookmark
Form Title Share
Form Title Cite
