Well, in the cerebrospinal fluid, it’s possible to measure proteins. And the levels of these proteins in the CSF, they reflect ongoing physiological processes in the brain. And so we know that we can measure amyloid and tau, and when it’s abnormal that there’s Alzheimer’s pathology but we can measure thousands of other proteins. And those levels also tell us something about the mechanisms that go beyond amyloid and tau...
Well, in the cerebrospinal fluid, it’s possible to measure proteins. And the levels of these proteins in the CSF, they reflect ongoing physiological processes in the brain. And so we know that we can measure amyloid and tau, and when it’s abnormal that there’s Alzheimer’s pathology but we can measure thousands of other proteins. And those levels also tell us something about the mechanisms that go beyond amyloid and tau. And so what we found and others as well is that it seems that there’s biological differences between people, and we can pick that up with the CSF proteomic measurements. Well, currently, more than 70% of the Alzheimer’s disease drug pipeline, they target mechanisms that go beyond amyloid and tau. But at this point, most of these drugs are tested in every patient. But we see that all those molecular processes, well, we can pick them up in the CSF, but they’re not disrupted in every patient. We see that they are disrupted in distinct subtypes only. So if you have all these different biological processes that a treatment may target and Alzheimer’s disease is not one biological disease then why would that work equally well for everyone so I think we need to start testing the right drug on the right patients and to get there, molecular tools to improve the molecular diagnosis of Alzheimer’s so that’s beyond amyloid and tau that’s the core but we need additional markers to understand what the precise biological subtype is of a person. And then we can match the right targets to the right patients and increase the chances that if it works, that we can actually measure that it works.
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