So this is a work that has been led by a colleague of mine, Niklas Mattsson-Carlgren, but I was presenting on his behalf at CTAD. So the main idea behind it is can we really assess better preclinical Alzheimer’s disease using plasma biomarkers. So the idea of this presentation was twofold. First, to assess whether we can select individuals that at the moment don’t have amyloid pathology in their brains, but they will likely accumulate it in the following years...
So this is a work that has been led by a colleague of mine, Niklas Mattsson-Carlgren, but I was presenting on his behalf at CTAD. So the main idea behind it is can we really assess better preclinical Alzheimer’s disease using plasma biomarkers. So the idea of this presentation was twofold. First, to assess whether we can select individuals that at the moment don’t have amyloid pathology in their brains, but they will likely accumulate it in the following years. And these are mainly some people that will be interesting for clinical trials and treatments in the future when we go earlier and earlier with the disease treatments. And the other idea was to see whether with these plasma biomarkers we can really assess amyloid status using, instead of one single plasma biomarker, to use follow-up over time. So going to the first objective, that was to assess who is likely to become amyloid positive or to accumulate amyloid pathology in the following years, what we found is that different plasma biomarkers, in this case P-Tau217, but also amyloid beta 42 to 40 ratio, was already somehow abnormal when we look in this particular set of individuals. And what we see is that the ABETA42/40, that seems to be a very sensitive biomarker, is already completely abnormal, similar to those that are already amyloid positive. Whereas P-Tau217, that is a very sensitive marker as well, but maybe a little bit later in the disease progression, seems to be somehow elevated compared to the individuals that don’t have pathology and will not have pathology in the following years, but still doesn’t reach the levels of those participants that are positive. So combining these two biomarkers is likely a good alternative to really detect this early, very incipient pathology, that there are people that are not positive, but will accumulate in the following years. And therefore, we could maybe use, select these individuals to really prevent the accumulation of amyloid before it starts accumulating. And the second objective, what we found is that using two different P-Tau217 measurements, meaning one at baseline and another at a follow-up, those that really increase in time are the ones that are more likely to be amyloid positive, being like a very sensitive way of selecting these individuals instead of doing a more invasive test such as CSF or PET.
This transcript is AI-generated. While we strive for accuracy, please verify this copy with the video.
