Journal
NEUROPSYCHOPHARMACOLOGY
Volume 42, Issue 6, Pages 1210-1219Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/npp.2016.186
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Funding
- National Institute of Mental Health of the National Institutes of Health [K23MH094707]
- Iris & Junming Le Foundation
- Brain and Behavior Research Foundation (NARSAD awards)
- NIH National Center for Advancing Translational Sciences [UL1TR000067]
- Patterson Trust Award
- NIHM [K23MH101498]
- US Department of Veterans Affairs via VA National Center for PTSD-Clinical Neurosciences Division
- US Department of Veterans Affairs via Office of Academic Affairs Advanced Fellowship in Mental Illness Research and Treatment
- Janssen Pharmaceutical
- Avanir Pharmaceutical
- National Institutes of Health
- Brain and Behavioral Research Foundation
- American Foundation for Suicide Prevention
- Department of Defense
- American Psychiatric Foundation
- Robert E. Leet and Clara Guthrie Patterson Trust
- Mount Sinai School of Medicine from Alkermes
- Astra Zeneca
- Brainsway
- Euthymics Bioscience Inc
- Neosync
- Roche
- Shire
- US Department of Defense
- NIH
- NIH/NIMH
- NARSAD
- USAMRAA
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Capitalizing on recent advances in resting-state functional connectivity magnetic resonance imaging (rs-fcMRI) and the distinctive paradigm of rapid mood normalization following ketamine treatment, the current study investigated intrinsic brain networks in major depressive disorder (MDD) during a depressive episode and following treatment with ketamine. Medication-free patients with MDD and healthy control subjects (HC) completed baseline rs-fcMRI. MDD patients received a single infusion of ketamine and underwent repeated rs-fcMRI at 24 h posttreatment. Global brain connectivity with global signal regression (GBCr) values were computed as the average of correlations of each voxel with all other gray matter voxels in the brain. MDD group showed reduced GBCr in the prefrontal cortex (PFC) but increased GBCr in the posterior cingulate, precuneus, lingual gyrus, and cerebellum. Ketamine significantly increased GBCr in the PFC and reduced GBCr in the cerebellum. At baseline, 2174 voxels of altered GBCr were identified, but only 310 voxels significantly differed relative to controls following treatment (corrected alpha<0.05). Responders to ketamine showed increased GBCr in the lateral PFC, caudate, and insula. Follow-up seed-based analyses illustrated a pattern of dysconnectivity between the PFC/subcortex and the rest of the brain in MDD, which appeared to normalize postketamine. The extent of the functional dysconnectivity identified in MDD and the swift and robust normalization following treatment suggest that GBCr may serve as a treatment response biomarker for the development of rapid acting antidepressants. The data also identified unique prefrontal and striatal circuitry as a putative marker of successful treatment and a target for antidepressants' development.
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