Publications by authors named "Sarah E Cote"

The nature of data obtainable from the commercial smartphone - bolstered by a translational model emphasizing the impact of social and physical zeitgebers on circadian rhythms and mood - offers the possibility of scalable and objective vital signs for major depression. Our objective was to explore associations between passively sensed behavioral smartphone data and repeatedly measured depressive symptoms to suggest which features could eventually lead towards vital signs for depression. We collected continuous behavioral data and bi-weekly depressive symptoms (PHQ-8) from 131 psychiatric outpatients with a lifetime DSM-5 diagnosis of depression and/or anxiety over a 16-week period.

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Objective: Lower white matter integrity of frontal-subcortical circuitry has been associated with late-life depression in normally aging older adults and with the presence of multiple sclerosis (MS). Frontal-striatal white matter tracts involved in executive, cognitive, emotion, and motor function may underlie depression in older adults with MS. The present study examined the association between depression score and frontal-striatal white matter integrity in older adults with MS and controls.

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Background: Apathy is common in multiple sclerosis (MS) and neurological disease, but its presence and underlying brain mechanisms in older adults with MS (OAMS) have not been evaluated.

Objective: Examine apathy and its association with caudate nuclei volume in OAMS and controls. We hypothesized that compared to controls, OAMS would demonstrate: a) greater apathy; b) stronger associations between apathy and caudate nuclei volumes.

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We generated cortical interneurons (cINs) from induced pluripotent stem cells derived from 14 healthy controls and 14 subjects with schizophrenia. Both healthy control cINs and schizophrenia cINs were authentic, fired spontaneously, received functional excitatory inputs from host neurons, and induced GABA-mediated inhibition in host neurons in vivo. However, schizophrenia cINs had dysregulated expression of protocadherin genes, which lie within documented schizophrenia loci.

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