Table 3.

Summary of functional connectivity changes of the default mode and saliency networks in Alzheimer's disease and Parkinson's disease.

Functional connectivity changes in AD and PD
AD	DMN	Reduced DMN connectivity during resting state in early stage MCI to late stage AD and in asymptomatic patients at genetic risk for AD (Seeley et al., 2007; Zhou et al., 2010; Machulda et al., 2011; Thomas et al., 2014; Wang et al., 2015)
		Reduced DMN connectivity in AD correlates with disease severity as measured by the Clinical Dementia Rating (Gour et al., 2011; Disbrow et al., 2014; Zhao Q. et al., 2017)
	SAN	Abnormal SAN connectivity across disease spectrum and those at genetic risk of AD (van Eimeren et al., 2009; Zhou et al., 2010)
		Anterior insular cortex, a key hub of the SAN, demonstrates hyperconnectivity to the SAN in AD (Delaveau et al., 2010)
PD	DMN	The most consistent connectivity change in PD involves a region of the R posterior IPC, which is part of the DMN (Rademacher et al., 1999) and altered IPC connectivity is more prominent in PD patients with cognitive impairment (Martin et al., 2008; Martin, 2009)
		Slower processing speeds in PD are associated with decreased DMN connectivity at rest, specifically between the posterior cingulate, medial prefrontal and inferior parietal nodes (Bzdok et al., 2015)
	SAN	Reduced anti-correlation between the SAN and DMN is associated with worse performance on tests of executive functioning, psychomotor speed and verbal memory (Wu et al., 2012)

AD, Alzheimer's disease; PD, Parkinson's disease; DMN, default mode network; MCI, mild cognitive impairment; SAN, salience network; R posterior IPC, right posterior inferior parietal cortex.