Spatial Disassociation of Disrupted Functional Connectivity for the Default Mode Network in Patients with End-Stage Renal Disease

To investigate the aberrant functional connectivity of the default mode network (DMN) in patients with end-stage renal disease (ESRD) and their clinical relevance

Opening or closing eyes at rest modulates the functional connectivity of V1 with default and salience networks

Current evidence suggests that volitional opening or closing of the eyes modulates brain activity and connectivity. However, how the eye state influences the functional connectivity of the primary visual cortex has been poorly investigated. Using the same scanner, fMRI data from two groups of participants similar in age, sex and educational level were acquired. One group (n = 105) performed a resting state with eyes closed, and the other group (n = 63) performed a resting state with eyes open. Seed-based voxel-wise functional connectivity whole-brain analyses were performed to study differences in the connectivity of the primary visual cortex. This region showed higher connectivity with the default mode and sensorimotor networks in the eyes closed group, but higher connectivity with the salience network in the eyes open group. All these findings were replicated using an open source shared dataset. These results suggest that opening or closing the eyes may set brain functional connectivity in an interoceptive or exteroceptive state

Resting State Functional Connectivity of the Rat Claustrum

The claustrum is structurally connected with many cortical areas.A major hurdle standing in the way of understanding claustrum function is the difficulty in assessing the global functional connectivity (FC) of this structure. The primary issues lie in the inability to isolate claustrum signal from the adjacent insular cortex (Ins), caudate/putamen (CPu), and endopiriform nucleus (Endo). To address this issue, we used (7T) fMRI in the rat and describe a novel analytic method to study claustrum without signal contamination from the surrounding structures. Using this approach, we acquired claustrum signal distinct from Ins, CPu, and Endo, and used this claustrum signal to determine whole brain resting state functional connectivity (RSFC). Claustrum RSFC was distinct from the adjacent structures and displayed extensive connections with sensory cortices and the cingulate cortex, consistent with known structural connectivity of the claustrum. These results suggest fMRI and improved analysis can be combined to accurately assay claustrum function

Altered frontal and insular functional connectivity as pivotal mechanisms for apathy in Alzheimer’s disease

Background: Apathy is a common and early symptom in Alzheimer’s disease (AD) and is linked to poorer prognosis. Theoretical interpretations of apathy implicate alterations of connections amongst fronto-striatal and limbic regions. Objective: To test the association between presence of apathy and patterns of brain functional connectivity in patients with clinically-established AD. Methods: Seventy AD patients were included. Thirty-five patients experienced apathy as defined by the screening question of the Neuropsychiatric Inventory, and thirty-five did not. All patients agreed to undergo an MRI protocol inclusive of resting-state acquisitions. The hemodynamic-dependent signal was extracted bilaterally from five regions of interest: ventromedial prefrontal cortices, anterior cingulate cortices, dorsolateral prefrontal cortices, insulae and amygdalae. t tests were run to compare connectivity maps of apathetic and non-apathetic patients. Age, education, Mini Mental State Examination score, gray matter volumes and gray matter fractions served as covariates. Results: At a pFWE < 0.05 threshold, apathetic patients had reduced connectivity between the left insula and right superior parietal cortex. Apathetic patients had also increased connectivity between the right dorsolateral prefrontal seed and the right superior parietal cortex. Patients with apathy were significantly more likely to experience other psychiatric symptoms. Conclusion: Our findings support a role of frontal and insular connections in coordinating value-based decisions in AD. Both down-regulation and maladaptive up-regulation mechanisms appear to be at play in these regions

Psychol Med

Background:Late-life depression (LLD) is characterized by differences in resting state functional connectivity within and between intrinsic functional networks. This study examined whether clinical improvement to antidepressant medications is associated with pre-randomization functional connectivity in intrinsic brain networks.Methods:Participants were 95 elders aged 60 years or older with major depressive disorder. After clinical assessments and baseline MRI, participants were randomized to escitalopram or placebo with a two-to-one allocation for 8 weeks. Non-remitting participants subsequently entered an 8-week trial of open-label bupropion. The main clinical outcome was depression severity measured by MADRS. Resting state functional connectivity was measured between a priori key seeds in the default mode (DMN), cognitive control, and limbic networks.Results:In primary analyses of blinded data, lower post-treatment MADRS score was associated with higher resting connectivity between: a) posterior cingulate cortex (PCC) and left medial prefrontal cortex; b) PCC and subgenual anterior cingulate cortex (ACC); c) right medial PFC and subgenual ACC; d) right orbitofrontal cortex and left hippocampus. Lower post-treatment MADRS was further associated with lower connectivity between: e) the right orbitofrontal cortex and left amygdala; and f) left dorsolateral PFC and left dorsal ACC. Secondary analyses associated mood improvement on escitalopram with anterior DMN hub connectivity. Exploratory analyses of the bupropion open-label trial associated improvement with subgenual ACC, frontal, and amygdala connectivity.Conclusions:Response to antidepressants in LLD is related to connectivity in the DMN, cognitive control and limbic networks. Future work should focus on clinical markers of network connectivity informing prognosis.R01 MH121620/MH/NIMH NIH HHSUnited States/R01 MH102246/MH/NIMH NIH HHSUnited States/UL1TR002243/TR/NCATS NIH HHSUnited States/K24 MH110598/MH/NIMH NIH HHSUnited States/UL1 TR002243/TR/NCATS NIH HHSUnited States/S10 OD021771/OD/NIH HHSUnited States/S10 OD021771/CD/ODCDC CDC HHSUnited States/R01 MH121620/MH/NIMH NIH HHSUnited States/UL1TR002243/TR/NCATS NIH HHSUnited States/S10 OD021771/CD/ODCDC CDC HHSUnited States