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Neural substrates for late-life depression: A selective review of structural neuroimaging studies

Authors
Kim, Yong-KuHan, Kyu-Man
Issue Date
10-1월-2021
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
Late-life depression; Geriatric depression; Magnetic resonance imaging; Structural neuroimaging; White matter hyperintensity; Antidepressant
Citation
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, v.104
Indexed
SCIE
SCOPUS
Journal Title
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
Volume
104
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/50128
DOI
10.1016/j.pnpbp.2020.110010
ISSN
0278-5846
Abstract
Recent neuroimaging studies have characterized the pathophysiology of late-life depression (LLD) as a dysfunction of the brain networks involved in the regulation of emotion, motivational behavior, cognitive control, executive function, and self-referential thinking. In this article, we reviewed LLD-associated structural neuroimaging markers such as white matter hyperintensity (WMH), white matter integrity measured by diffusion tensor imaging, cortical and subcortical volumes, and cortical thickness, which may provide a structural basis for brain network dysfunction in LLD. LLD was associated with greater severity or volumes of deep, periventricular, or overall WMH and with decreased white matter integrity in the brain regions belonging to the fronto-striatallimbic circuits and reduced white matter tract integrity which connects these circuits, such as the cingulum, corpus callosum, or uncinate fasciculus. Decreased volumes or cortical thickness in the prefrontal cortex, orbitofrontal cortex, anterior and posterior cingulate cortex, several temporal and parietal regions, hippocampus, amygdala, striatum, thalamus, and the insula were associated with LLD. These structural neuroimaging findings were also associated with cognitive dysfunction, which is a prominent clinical feature in LLD. Several structural neuroimaging markers including the WMH burden, white matter integrity, and cortical and subcortical volumes predicted antidepressant response in LLD. These structural neuroimaging findings support the hypothesis that disruption of the brain networks involved in emotion regulation and cognitive processing by impaired structural connectivity is strongly associated with the pathophysiology of LLD.
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