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A deeper understanding of the spatial relationships of β-amyloid (Aβ), tau, and neurodegeneration in Alzheimer’s disease (AD) could provide insight into pathogenesis and clinical trial design. We included 81 amyloid-positive patients (age 64.4 ± 9.5) diagnosed with AD dementia or mild cognitive impairment due to AD and available  11 C-PiB (PIB),  18 F-Flortaucipir (FTP), 18 F-FDG-PET, and 3T-MRI, and 31 amyloid-positive, cognitively normal participants (age 77.3 ± 6.5, no FDG-PET). W-score voxel-wise deviation maps were created and binarized for each imaging-modality ( W  &gt; 1.64,  P  &lt; 0.05) adjusting for age, sex, and total intracranial volume (sMRI-only) using amyloid-negative cognitively normal adults. For symptomatic patients, FDG-PET and atrophy W-maps were combined into neurodegeneration maps (ND). Aβ-pathology showed the greatest proportion of cortical gray matter suprathreshold voxels (spatial extent) for both symptomatic and asymptomatic participants (median 94–55%, respectively), followed by tau (79–11%) and neurodegeneration (41–3%). Amyloid &gt; tau &gt; neurodegeneration was the most frequent hierarchy for both groups (79–77%, respectively), followed by tau &gt; amyloid &gt; neurodegeneration (13–10%) and amyloid &gt; neurodegeneration &gt; tau (6–13%). For symptomatic participants, most abnormal voxels were PIB+/FTP+/ND− (median 35%), and the great majority of ND+ voxels (91%) colocalized with molecular pathology. Amyloid spatially exceeded tau and neurodegeneration, with individual heterogeneities. Molecular pathology and neurodegeneration showed a progressive overlap along AD course, indicating shared vulnerabilities or synergistic toxic mechanisms.

Spatial Relationships between Molecular Pathology and Neurodegeneration in the Alzheimer’s Disease Continuum