We now have one class of disease-modifying treatment for Alzheimer’s disease, the amyloid-targeted treatments. And data demonstrates that individuals who receive this have a slower rate of cognitive decline. However, they still decline. And so it’s clear that there’s other pathologies that are present that need to be addressed. And amyloid-targeted treatments by themselves are not enough to prevent further progression of the disease...
We now have one class of disease-modifying treatment for Alzheimer’s disease, the amyloid-targeted treatments. And data demonstrates that individuals who receive this have a slower rate of cognitive decline. However, they still decline. And so it’s clear that there’s other pathologies that are present that need to be addressed. And amyloid-targeted treatments by themselves are not enough to prevent further progression of the disease. So with combination therapies, one of the key questions is how do we augment amyloid-targeted treatments? It’s quite obvious that a key target is tau, which of course is another key pathology in Alzheimer’s disease and strongly correlates with cognitive impairment. So there’s a great interest in combining anti-tau treatments with amyloid-targeted treatments. However, there’s a lot of questions about how to do this, when to do this. We now have many patients already receiving amyloid-targeted treatments. And so do we start tau-targeted treatments at the same time? Do we clear amyloid first and then add tau-targeted treatments? There are many questions, but one way, one tool that we need to help us get answers are really biomarkers. And biomarkers can tell us about whether certain pathologies are present and the severity of that pathology. So perhaps for individuals who just have mostly amyloid pathology, a little bit of tau pathology, maybe for them, we just want to initially start them with amyloid-targeted treatments and then perhaps later start with tau-targeted treatments. However, if they already have quite significant tau pathology, maybe that should be the primary modality. So there’s a lot of unknowns. We don’t know the answer to these questions, but certainly having biomarkers for these pathologies can be helpful. Of course, Alzheimer’s disease frequently has copathologies associated with it, including alpha-synuclein, TDP-43, cerebral vascular disease. We do have some biomarkers of this, but they need to get better. Inflammation is a huge area of interest, but is extremely complicated. And simple biomarkers like GFAP and TREM2 just really don’t capture its complexity. So we need to develop these biomarkers. And ideally, they should be blood-based biomarkers because that’s the biomarkers that are most accessible in a clinical space. To do this, we really need reference standards for the pathologies that we want to capture. We can use imaging scans to see the extent of pathology throughout life. So those tend to be very helpful to us as we’re trying to develop fluid-based biomarkers, especially blood biomarkers. Clinical symptoms are very important and interesting. However, sometimes they are affected by many different factors, including multiple pathologies. So we really need more than just the presence or absence of symptoms and severity of symptoms. So we really have made a lot of progress, especially on developing quite outstanding biomarkers of amyloid and tau. So we’re trying to translate everything that we’ve learned from that to these other pathologies. With the eventual goal of a more precision medicine approach, where we are looking at all of these pathologies and deciding which treatments are best for which patients at which time. So that’s the eventual goal. We do have a ways to go to get there, but it’s amazing how fast the developments are occurring in this space.
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