
August 6, 2026
@michaelokun
Can we predict Alzheimer's disease by measuring when biomarkers change, instead of simply measuring how much is there? Biomarkers are measurable biological signals, such as blood proteins or brain imaging findings, that help track disease processes before symptoms become obvious. Pelkmans, Bikou, and Salvadó describe in a new Brain commentary how modeling the timing of biomarker changes may move us closer to predicting an individual's risk of future cognitive decline rather than simply describing where they are today. Key points: - The commentary highlights new work showing that the timing of changes in plasma p-tau217, amyloid PET, tau PET, and cognition may be more informative than simply comparing biomarker levels at one point in time. - Strong coupling between biomarker timing and cognitive decline was observed in the Alzheimer's Disease Neuroimaging Initiative (ADNI), while weaker coupling in the population-based Mayo Clinic Study of Aging suggests aging is influenced by multiple interacting pathologies. - The authors argue that future prediction models should integrate Alzheimer's biomarkers w/ vascular disease, inflammation, α-synuclein, TDP-43, resilience, and other biological factors to better predict who will experience cognitive decline. My take: This commentary captures an important shift in Alzheimer's disease research. We are moving beyond asking whether a biomarker is abnormal and beginning to ask when it becomes abnormal. Timing may ultimately prove just as important as the biomarker itself. The future will likely require integrating multiple biological pathways rather than relying on a single test to predict cognitive decline. Here are 3 points that resonated w/ me: 1- Alzheimer's disease does not unfold the same way in every person, and understanding individual timing may improve prediction and personalize care. 2- Blood biomarkers such as plasma p-tau217 continue to emerge as powerful tools that may help identify disease years before symptoms become disabling. 3- Aging brains frequently contain more than one disease process, so cognitive decline cannot always be explained by Alzheimer's pathology alone.
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