Abstract
The abnormal accumulation of amyloid-β and tau targets specific spatial networks in Alzheimer's disease. However, the relationship between these networks across different disease stages and their association with brain connectivity has not been explored. In this study, we applied a joint independent component analysis to 18F- Flutemetamol (amyloid-β) and 18F-Flortaucipir (tau) PET images to identify amyloid-β and tau networks across different stages of Alzheimer's disease. We then assessed whether these patterns were associated with resting-state functional networks and white matter tracts. Our analyses revealed nine patterns that were linked across tau and amyloid-β data. The amyloid-β and tau patterns showed a fair to moderate overlap with distinct functional networks but only tau was associated with white matter integrity loss and multiple cognitive functions. These findings show that amyloid-β and tau have different spatial affinities, which can be used to understand how they accumulate in the brain and potentially damage the brain's connections.
Highlights
The accumulation of amyloid-b and tau deposits has been implicated in the genesis of Alzheimer’s disease (Jack et al, 2010; Jack et al, 2013; Jack et al, 2018; Jack and Holtzman, 2013)
There were no significant differences in cognition between amyloid-b negative and amyloid-b positive controls, but patients with mild cognitive impairment and Alzheimer’s disease dementia showed worse scores in several cognitive tests
We identified these different spatial patterns in vivo and assessed how they relate to functional and anatomical brain connectivity
Summary
The accumulation of amyloid-b and tau deposits has been implicated in the genesis of Alzheimer’s disease (Jack et al, 2010; Jack et al, 2013; Jack et al, 2018; Jack and Holtzman, 2013) These deposits appear and spread in the brain according to a characteristic spatial pattern: whereas amyloid-b deposits appear first in neocortical regions and spread to limbic and subcortical areas (Thal et al, 2002); tau deposits appear in the transentorhinal cortex and spread to paralimbic and neocortical areas (Braak and Braak, 1991). Tau PET studies found that tau deposition occurs mainly in medial and inferior temporal areas, with
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