Although previous studies demonstrated decreased functional connectivity in the default mode network in the cognitively normal older adults with amyloid burden, effects of amyloid burden in the other large-scale intrinsic connectivity networks are not yet clear. The aim of this study was to investigate the distinctive association pattern of amyloid-β deposition on the three large-scale intrinsic connectivity networks (the default mode network, salience network and central executive network) in older adults with normal cognition. Fifty-six older adults with normal cognition underwent functional magnetic resonance imaging and were dichotomized using 11C-labelled Pittsburgh compound B positron emission tomography imaging into subjects with (PiB+; n=27) and without (PiB-; n=29) detectable amyloid burden. We found that the functional connectivities of (i) the default mode network were greater; (ii) the salience network were not different; and (iii) the central executive network were lower in the Pittsburgh compound B positive group, compared with the Pittsburgh compound B negative group. Anterior cingulate cortex Pittsburgh compound B retention was negatively correlated with the functional connectivities of the posterior default mode network, and positively correlated with fronto-parietal functional connectivity (within the central executive network) in the Pittsburgh compound B positive group. The anti-correlation strength between the default mode network and the central executive network was negatively correlated with the anterior cingulate cortex Pittsburgh compound B levels. Additionally, significant group × episodic memory interactions with functional connectivities in the posterior default mode network, and the frontal default mode network were observed. Our results of aberrant default mode network functional connectivity and distinctive correlation patterns between the Pittsburgh compound B retention in the anterior cingulate cortex and functional connectivities in the default mode network and central executive network in the Pittsburgh compound B positive group might reflect a detrimental effect of amyloid retention on functional changes in the course of Alzheimer's disease progression.

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Previous studies have shown an association between late-onset depression (LOD) and cognitive impairment in older adults. However, the neural correlates of this relationship are not yet clear. The aim of this study was to investigate the differences in both cortical thickness and subcortical volumes between drug-naive LOD patients and healthy controls and explore the relationship between LOD and cognitive impairments. A total of 48 elderly, drug-naive patients with LOD and 47 group-matched healthy control subjects underwent 3T MRI scanning, and the cortical thickness was compared between the groups in multiple locations, across the continuous cortical surface. The subcortical volumes were also compared on a structure-by-structure basis. Subjects with LOD exhibited significantly decreased cortical thickness in the rostral anterior cingulate cortex, the medial orbitofrontal cortex, dorsolateral prefrontal cortex, the superior and middle temporal cortex, and the posterior cingulate cortex when compared with healthy subjects (all p<0.05, false discovery rate corrected). Reduced volumes of the right hippocampus was also observed in LOD patients when compared with healthy controls (p<0.001). There were significant correlations between memory functions and cortical thickness of medial temporal, isthmus cingulate, and precuneus (p<0.001). This study was the first study to explore the relationships between the cortical thickness/subcortical volumes and cognitive impairments of drug-naive patients with LOD. These structural changes might explain the neurobiological mechanism of LOD as a risk factor of dementia.

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