Characterisation of Posterior Predominant Amyloid PET Binding Across Multiple Cohorts
Giorgio, J.; Blazhenets, G.; Landau, S.; Pezzoli, S.; Yokoyama, J. S.; Soleimani-Meigooni, D.; Carrillo, M.; Grinberg, L.; Seeley, W. W. T.; Spina, S.; Nudelman, K.; Apostolova, L.; Dickerson, B.; Jagust, W. J.; Rabinovici, G.; La Joie, R.
Show abstract
The standard approach to quantify amyloid (A{beta}) PET averages uptake within a single cortical mask that assumes no clinically relevant spatial heterogeneity in uptake patterns. Here, in a sample of 12,379 clinically impaired participants taken from four phenotypically diverse cohorts we use data-driven approaches to discover heterogeneous patterns of A{beta}-PET binding, uncovering a reproducible and clinically relevant pattern of posterior predominant A{beta}-PET binding. In particular, A{beta}-PET positive participants who have posterior predominant binding are less likely to be APOE-{varepsilon}4 carriers, more severely impaired, have thinner cortex in posterior regions, and greater posterior tau PET burden. Furthermore, in a subsample of participants with neuropathological assessment, participants with posterior predominant A{beta} binding have a higher likelihood of having cerebral amyloid angiopathy at autopsy. These findings suggest that A{beta}-PET accumulates along two orthogonal axes with biological and clinical relevance, indicating that the standard approach to assess A{beta}-PET is insufficient to capture meaningful signal from A{beta}-PET imaging. This work has implications for the diagnosis and treatment of Alzheimers disease and extends our understanding of the mechanisms governing variable A{beta}-PET distribution and its downstream effects.
Matching journals
The top 5 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Amyloid-associated increases in soluble tau is a key driver in accumulation of tau aggregates and cognitive decline in early Alzheimer 98%
- Hemispheric Asymmetry of Tau Pathology is Related to Asymmetric Amyloid Deposition in Alzheimer's Disease 98%
- AI-driven fusion of neurological work-up for assessment of biological Alzheimer’s disease 96%
Similar papers in this journal
- Glucose metabolism reflects local atrophy and tau pathology in symptomatic Alzheimer’s disease 98%
- Default mode network tau predicts future clinical decline in atypical early Alzheimer’s disease 98%
- Tau-first subtype of Alzheimer's disease consistently identified across in vivo and post mortem studies 98%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.