Abstract:BackgroundWe previously identified three CSF proteomic Alzheimer’s disease (AD) subtypes: one with increased amyloid metabolism and aberrant neuronal plasticity, one with innate immune activation and one with blood‐brain barrier dysfunction. We studied their replicability in another cohort, and whether increasing the number of proteins (from 556 to 1059) would enable detecting more subtypes.MethodWe selected 419 AD individuals with abnormal CSF abeta42 and 187 controls (normal cognition and normal AD biomarker… Show more
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