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Default mode network (DMN) is vulnerable to the effects of APOE genotype. Given the reduced brain volumes and APOE ε 4-related brain changes in elderly carriers, it is less known that whether these changes would influence the functional connectivity and to what extent. This study aimed to examine the functional connectivity within DMN, and its diagnostic value with age-related morphometric alterations considered.
Whole brain and seed-based resting-state functional connectivity (RSFC) analysis were conducted in cognitively normal APOE ε 4 carriers and matched non-carriers (N=38). The absolute values of mean correlation coefficients (z-values) were used as a measure of functional connectivity strength (FCS) between DMN subregions, which were also used to estimate their diagnostic value by receiver-operating characteristic (ROC) curves.
APOE ε 4 carriers demonstrated decreased interhemispheric FCS, particularly between right hippocampal formation (R.HF) and left inferior parietal lobular (L.IPL) (t=3.487, p<0.001). ROC analysis showed that the FCS of R.HF and L.IPL could differentiate APOE ε 4 carriers from healthy counterparts (AUC value=0.734, p=0.025). Moreover, after adjusting the impact of morphometry, the differentiated value of FCS of R.HF and L.IPL was markedly improved (AUC value=0.828, p=0.002).
Our findings suggest that APOE ε 4 allele affects the functional connectivity within posterior DMN, particularly the atrophy-corrected interhemispheric FCS before the clinical expression of neurodegenerative disease.
This chapter discusses imaging studies in insomnia and in association with insomnia complaints in people not diagnosed with insomnia. This review includes studies applying structural and functional MRI, magnetic resonance spectroscopy (MRS), high-density electroencephalography, and transcranial magnetic stimulation (TMS). The studies reviewed have reported almost exclusively on regions of the temporal lobe, frontal lobe, and parietal lobe. These cortical regions are of interest because of their key involvement in the cognitive domains that are most affected in insomnia and after sleep deprivation. For each lobe, the chapter systematically addresses differences between insomniacs and controls and correlations of insomnia symptom severity with brain changes in both insomniacs and people not diagnosed with insomnia. Subsequently, the findings are summarized and interpreted with respect to functional relevance, pitfalls, and conclusions on cause, risk factor, or consequence. Neuroimaging has a high promise to reveal insights into the causes and consequences of insomnia.