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White Matter Track Based Analysis at Limbic Abnormalities in Cognitive Impairment

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R Juh

R Juh1*, T Suh2 , J Han1 , C Kim1 , C Oh1 , (1) Seoul National University Bundang Hospital, Seongnamsi, GyeonggiDo ,(2) The catholic university of Korea, Seoul, N/A


SU-F-I-17 (Sunday, July 31, 2016) 3:00 PM - 6:00 PM Room: Exhibit Hall

Purpose: Mild cognitive impairment with depression (MCID) is common and associated with disability and cognitive impairment, with high probability of relapse. Hypothesize that a sign of WM disintegration would be observed in MCID than MCI nondepression (MCIND), especially in frontal and limbic regions and patients with depression would show reduced GM density in the hippocampus, amygdala, anterior gyrus cingulate, and dorsolateral prefrontal cortex (DLPFC) and dorsomedial prefrontal cortex (DMPFC) the abnormalities of long association fiber tracts integrity are correlated with geriatric depression.

Methods: Forty-two subjects (20 nondepressed, 22 depressed) underwent DTI and cognitive assessment. Depression was initially assessed by means of the Korean version of the 30-item Geriatric Depression Scale (K-GDS). All patients scoring 19 or higher on the K-GDS were screened as depressed. An automated tract-based statistical analysis method was used to derive estimates of fractional anisotropy (FA) for each subject. Group effects and correlations with clinical features on DTI parameters were examined.

Results: We found cross-sectional differences in WM tract disintegration on posterior cingulum, splenium of corpus callosum, uncinate fasciculus, genu, thalamus, internal and external capsule of limbic in MCID. These results support changes in the structural integrity of neuronal cells in these specific important brain regions constituting a fronto-limbic-cerebellar network during depressive and in particular during the course of depression. The different parts of the frontal lobes have afferent and efferent connections with other neocortical, limbic, and subcortical regions and participate in the limbic–cortico–striatal–pallidal–thalamic circuits.

Conclusion: Findings are suggestive of loss of integrity in WM fiber within frontal, temporal and limbic regions, increasing the evidence that implicates disruptions to the limbic–orbitofrontal networks in the pathogenesis of MCID. These neuroanatomical circuits play an important role in the regulation and modulation of affect and emotion, and contribute to the pathogenesis of late-life depression.

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