Abstract
A functional brain network, termed the parietal memory network (PMN), has been shown to reflect the familiarity of stimuli in both memory encoding and retrieval. The function of this network has been separated from the commonly investigated default mode network (DMN) in both resting-state fMRI and task-activations. This study examined the deficit of the PMN in Alzheimer’s disease (AD) patients using resting-state fMRI and independent component analysis (ICA) and investigated its diagnostic value in identifying AD patients. The DMN was also examined as a reference network. In addition, the robustness of the findings was examined using different types of analysis methods and parameters. Our results showed that the integrity as an intrinsic connectivity network for the PMN was significantly decreased in AD and this feature showed at least equivalent predictive ability to that for the DMN. These findings were robust to varied methods and parameters. Our findings suggest that the intrinsic connectivity of the PMN is disrupted in AD and further call for considering the PMN and the DMN separately in clinical neuroimaging studies.
Highlights
The default mode network (DMN) is the most frequently investigated functional brain network in Alzheimer’s disease (AD), and the intrinsic connectivity of DMN has been reported disrupted in a variety of resting-state fMRI studies (Greicius et al, 2004; Jones et al, 2011, 2016; Petrella et al, 2011)
We examined the above hypothesis by comparing the integrity of the parietal memory network (PMN) between AD patients and healthy controls (HCs) using independent component analysis (ICA)
We found that the PMN had significant lower network integrity in AD, compared with HCs
Summary
The default mode network (DMN) is the most frequently investigated functional brain network in Alzheimer’s disease (AD), and the intrinsic connectivity of DMN has been reported disrupted in a variety of resting-state fMRI studies (Greicius et al, 2004; Jones et al, 2011, 2016; Petrella et al, 2011). The DMN connectivity disruption has been identified in populations at risks for AD, such as elderly people, mild cognitive impairment (MCI) patients, and APOE-ε4 allele carriers (Sorg et al, 2007; Damoiseaux et al, 2008; Filippini et al, 2009; Petrella et al, 2011; Binnewijzend et al, 2012). AD first targets recent memory function, impairing the ability to remember recently acquired information, while DMN has been named after its characteristics of showing deactivation in attention-demanding tasks, and its functions have been demonstrated in vast cognitive domains (Andrews-Hanna et al, 2010; Raichle, 2015). The posterior part of DMN (i.e., posterior cingulate/precuneus and bilateral parietal cortex) are often linked to memory processing (Andrews-Hanna et al, 2010; Sestieri et al, 2011; Raichle, 2015), but the parietal regions are functionally inhomogeneous and memory functions are not unique to the DMN regions (Cavanna and Trimble, 2006; Cauda et al, 2010; Sestieri et al, 2017).
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