In Alzheimer's disease (AD), amyloid-? (A?) pathology and intrinsic functional connectivity (iFC) interact. Across stages of AD, we expected individual spatial correspondence of A? and iFC to reveal both A? accumulation and its detrimental effects on iFC. We used resting-state functional magnetic imaging and A? imaging in a cross-sectional sample of 90 subjects across stages of AD and healthy older adults. Global and local correspondence of A? and iFC were assessed within the posterior default mode network (pDMN) by within-subject voxel-wise correlations. Beginning at preclinical stages, global A?-iFC correspondence was positive for the whole pDMN, showing that A? accumulates in areas of high connectivity, and reached a plateau at prodromal stages. Starting at preclinical stages, local correspondence was negative in network centers, indicating that A? reduces connectivity of the pDMN as a function of local plaque concentration, and peaked at prodromal stages. Positive global correspondence suggests that A? accumulation progresses along iFC, with this effect starting in preclinical stages, and being constant along clinical periods. Negative local correspondence suggests detrimental effects of A? on iFC in network centers, starting at preclinical stages, and peaking when first symptoms appear. Data reveal a complex trajectory of A? and iFC correspondence, affecting both A? accumulation and iFC impairments.     «

In Alzheimer's disease (AD), amyloid-? (A?) pathology and intrinsic functional connectivity (iFC) interact. Across stages of AD, we expected individual spatial correspondence of A? and iFC to reveal both A? accumulation and its detrimental effects on iFC. We used resting-state functional magnetic imaging and A? imaging in a cross-sectional sample of 90 subjects across stages of AD and healthy older adults. Global and local correspondence of A? and iFC were assessed within the posterior default m...     »