Relationships between Beta-Amyloid and Functional Connectivity in Different Components of the Default Mode Network in Aging

Beta-amyloid deposition, a hallmark of Alzheimer's disease, is also common in cognitively normal older adults. Using Pittsburgh compound-B PET imaging, the study found that greater beta-amyloid burden in normal controls is associated with altered functional connectivity within the default mode network during rest. Connectivity decreased in regions critical for episodic memory, including posteromedial cortex, ventral medial prefrontal cortex, and angular gyrus, while increases appeared in dorsal and anterior medial prefrontal and lateral temporal cortices. The decreases align with known vulnerability of memory-related areas in Alzheimer's disease, and the increases may reflect compensatory mechanisms.

Study at a glance

Abstract

Although beta-amyloid (Aβ) deposition is a characteristic feature of Alzheimer's disease (AD), this pathology is commonly found in elderly normal controls (NC). The pattern of Aβ deposition as detected with Pittsburgh compound-B positron emission tomography (PIB-PET) imaging shows substantial spatial overlap with the default mode network (DMN), a group of brain regions that typically deactivates during externally driven cognitive tasks. In this study, we show that DMN functional connectivity (FC) during rest is altered with increasing levels of PIB uptake in NC. Specifically, FC decreases were identified in regions implicated in episodic memory (EM) processing (posteromedial cortex, ventral medial prefrontal cortex, and angular gyrus), whereas connectivity increases were detected in dorsal and anterior medial prefrontal and lateral temporal cortices. This pattern of decreases is consistent with previous studies that suggest heightened vulnerability of EM-related brain regions in AD, whereas the observed increases in FC may reflect a compensatory response.