Well, what we know of sporadic Alzheimer’s disease is that amyloid aggregates into plaques in the brain and tau into tangles, but the sequence of molecular events leading to these aggregations and then how the brain further reacts to that, so what is a consequence of that, that’s poorly understood. And that’s because it’s very difficult for sporadic Alzheimer’s disease to place a person in their individual disease timelines...
Well, what we know of sporadic Alzheimer’s disease is that amyloid aggregates into plaques in the brain and tau into tangles, but the sequence of molecular events leading to these aggregations and then how the brain further reacts to that, so what is a consequence of that, that’s poorly understood. And that’s because it’s very difficult for sporadic Alzheimer’s disease to place a person in their individual disease timelines. Based on cross-sectional data, it’s difficult to understand where a person is in their disease timeline. So we know that there’s preclinical Alzheimer’s disease, that you have normal cognition and abnormal amyloid. But then people vary a lot in how they progress. And another limitation is that we need to follow people over time and have repeated molecular measurements. And this is also something that’s not simple to do. And I think the only way to have a very detailed molecular window into the brain is by measuring proteomics in the cerebrospinal fluid.
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