Intrinsic functional connectivity of the default mode and cognitive control networks relate to change in behavioral performance over two years

Cortex ◽  
2020 ◽  
Vol 132 ◽  
pp. 180-190
Author(s):  
Isabella A. Breukelaar ◽  
Kristi R. Griffiths ◽  
Anthony Harris ◽  
Sheryl L. Foster ◽  
Leanne M. Williams ◽  
...  
2020 ◽  
pp. 089198872096827
Author(s):  
Abhishek Jaywant ◽  
Larissa DelPonte ◽  
Dora Kanellopoulos ◽  
Michael W. O’Dell ◽  
Faith M. Gunning

Post-stroke depression and executive dysfunction co-occur and are highly debilitating. Few treatments alleviate both depression and executive dysfunction after stroke. Understanding the brain network changes underlying post-stroke depression with executive dysfunction can inform the development of targeted and efficacious treatment. In this review, we synthesize neuroimaging findings in post-stroke depression and post-stroke executive dysfunction and highlight the network commonalities that may underlie this comorbidity. Structural and functional alterations in the cognitive control network, salience network, and default mode network are associated with depression and executive dysfunction after stroke. Specifically, post-stroke depression and executive dysfunction are both linked to changes in intrinsic functional connectivity within resting state networks, functional over-connectivity between the default mode and salience/cognitive control networks, and reduced cross-hemispheric frontoparietal functional connectivity. Cognitive training and noninvasive brain stimulation targeted at these brain network abnormalities and specific clinical phenotypes may help advance treatment for post-stroke depression with executive dysfunction.


2017 ◽  
Vol 81 (10) ◽  
pp. S378-S379
Author(s):  
Amy Peters ◽  
Lisanne Jenkins ◽  
Jonathan Stange ◽  
Katie Bessette ◽  
Kristy Skerrett ◽  
...  

2021 ◽  
Vol 15 ◽  
Author(s):  
Katherine G. Warthen ◽  
Robert C. Welsh ◽  
Benjamin Sanford ◽  
Vincent Koppelmans ◽  
Margit Burmeister ◽  
...  

Neuropeptide Y (NPY) is a neurotransmitter that has been implicated in the development of anxiety and mood disorders. Low levels of NPY have been associated with risk for these disorders, and high levels with resilience. Anxiety and depression are associated with altered intrinsic functional connectivity of brain networks, but the effect of NPY on functional connectivity is not known. Here, we test the hypothesis that individual differences in NPY expression affect resting functional connectivity of the default mode and salience networks. We evaluated static connectivity using graph theoretical techniques and dynamic connectivity with Leading Eigenvector Dynamics Analysis (LEiDA). To increase our power of detecting NPY effects, we genotyped 221 individuals and identified 29 healthy subjects at the extremes of genetically predicted NPY expression (12 high, 17 low). Static connectivity analysis revealed that lower levels of NPY were associated with shorter path lengths, higher global efficiency, higher clustering, higher small-worldness, and average higher node strength within the salience network, whereas subjects with high NPY expression displayed higher modularity and node eccentricity within the salience network. Dynamic connectivity analysis showed that the salience network of low-NPY subjects spent more time in a highly coordinated state relative to high-NPY subjects, and the salience network of high-NPY subjects switched between states more frequently. No group differences were found for static or dynamic connectivity of the default mode network. These findings suggest that genetically driven individual differences in NPY expression influence risk of mood and anxiety disorders by altering the intrinsic functional connectivity of the salience network.


2006 ◽  
Vol 14 (7S_Part_16) ◽  
pp. P907-P907
Author(s):  
Gloria Benson ◽  
Andrea Hildebrandt ◽  
Catharina Lange ◽  
Theresa Köbe ◽  
Claudia Schwarz ◽  
...  

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A442-A442
Author(s):  
A C Raikes ◽  
N S Dailey ◽  
J R Vanuk ◽  
A Alkozei ◽  
M A Grandner ◽  
...  

Abstract Introduction Light exposure, particularly blue wavelength light, has consistent positive effects on daytime sleepiness following mild traumatic brain injuries (mTBIs). While self-perceived improvements in daytime sleepiness are well-documented, the neurobiological underpinnings are not well understood. The purpose of this study was to localize changes in functional connectivity after daily morning blue light therapy (BLT) and to associate these changes with improvements in post-mTBI daytime sleepiness. Methods 29 individuals with a history of mTBI were randomized to receive either BLT (n=13) or placebo amber light (ALT; n=16). All participants self-reported daytime sleepiness (Epworth Sleepiness Scale (ESS); lower is better) and underwent resting-state functional magnetic resonance imaging at pre- and post-treatment. Whole-brain functional connectivity (FC) was estimated as the correlations between 400 cortical regions of interest (ROIs) assigned to 7 resting-state networks. A two-sample T-test for post-treatment ROI-to-ROI FC identified target connections (FDR corrected p<0.01). Post-treatment ESS scores and FC for these connections were correlated for treatment-related brain-behavior associations (uncorrected p<0.05). Results Lower FC after BLT in 4 ROI-to-ROI connections linking the default mode and visual networks was associated with lower ESS scores. Higher FC after BLT in 9 ROI-to-ROI connections linking attention, cognitive control, and visual networks was also associated with lower ESS scores. Conclusion BLT resulted in decreased self-reported daytime sleepiness, which was associated with decoupling of the default mode and visual networks as well as increased connectivity between and within attention and cognitive control networks, suggesting potentially improved attention to relevant stimuli and cognitive processes and less internal mentation. These associations may contribute to improved alertness, attention, and cognitive performance following a mTBI. Further work is needed to identify the optimal timing and dosage of BLT to maximize these outcomes. Support This study was funded by an award to Dr. Killgore from the US Army Medical Research and Materiel Command (USAMRMC; award number: W81XWH-14-1-0571).


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