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Katharine Dunlop

Researcher at Cornell University

Publications -  49
Citations -  3243

Katharine Dunlop is an academic researcher from Cornell University. The author has contributed to research in topics: Transcranial magnetic stimulation & Resting state fMRI. The author has an hindex of 16, co-authored 39 publications receiving 2340 citations. Previous affiliations of Katharine Dunlop include Toronto Western Hospital & University Health Network.

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Cortico-Striatal-Thalamic Loop Circuits of the Salience Network: A Central Pathway in Psychiatric Disease and Treatment.

TL;DR: Clinical and experimental evidence for abnormalities in SN cortico-striatal-thalamic loop circuits in major depression, substance use disorders (SUD), anxiety disorders, schizophrenia and eating disorders (ED), and novel invasive and non-invasive brain stimulation treatments may exert therapeutic effects by normalizing abnormalities in the SN loop are reviewed.
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Anhedonia and Reward-Circuit Connectivity Distinguish Nonresponders from Responders to Dorsomedial Prefrontal Repetitive Transcranial Magnetic Stimulation in Major Depression

TL;DR: Two distinct depression subtypes are suggested, one with preserved hedonic function and responsive to dorsomedial rTMS and another with disrupted hedono-reward circuit integrity, abnormally lateralized connectivity through ventromedial prefrontal cortex, and unresponsive to dorsifiedial RTMS.
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Resting-State Cortico-Thalamic-Striatal Connectivity Predicts Response to Dorsomedial Prefrontal rTMS in Major Depressive Disorder

TL;DR: It is found that successful treatment was associated with increased dmPFC-thalamic connectivity and decreased subgenual cingulate cortex-caudate connectivity, which provides insight into which individuals might respond to rTMS treatment and the mechanisms through which these treatments work.
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Noninvasive brain stimulation treatments for addiction and major depression.

TL;DR: Noninvasive brain stimulation techniques, including rTMS and tDCS, have been used to enhance cortico–striatal–thalamic activity through the core SN nodes in the dorsal anterior cingulate cortex, dorsolateral prefrontal cortex, and anterior insula, and inhibition of the VMN appears promising in preclinical studies for quenching the pathological incentive salience underlying SUDs and MDD.