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Three major biomarkers: beta-amyloid (A), pathologic tau (T), andneurodegeneration (N), are recognized as valid proxies for neuropathologicchanges of Alzheimer's disease. While there are extensive studies oncerebrospinal fluids biomarkers (amyloid, tau), the spatial propagation patternacross brain is missing and their interactive mechanisms with neurodegenerationare still unclear. To this end, we aim to analyze the spatiotemporalassociations between ATN biomarkers using large-scale neuroimaging data. Wefirst investigate the temporal appearances of amyloid plaques, tau tangles, andneuronal loss by modeling the longitudinal transition trajectories. Second, wepropose linear mixed-effects models to quantify the pathological interactionsand propagation of ATN biomarkers at each brain region. Our analysis of thecurrent data shows that there exists a temporal latency in the build-up ofamyloid to the onset of tau pathology and neurodegeneration. The propagationpattern of amyloid can be characterized by its diffusion along the topologicalbrain network. Our models provide sufficient evidence that the progression ofpathological tau and neurodegeneration share a strong regional association,which is different from amyloid.

Analyzing the Spatiotemporal Interaction and Propagation of ATN Biomarkers in Alzheimer's Disease using Longitudinal Neuroimaging Data