OBJECTIVE: Functional deactivation of the posteromedial cortex (PMC) seems to be a physiologic process underlying normal memory. The authors examined whether older subjects with subsyndromal depressive symptoms show impaired PMC deactivation. DESIGN: Subjects underwent 4T functional magnetic resonance imaging scan while performing a novel and familiar face-name associative encoding task. The Beck-II Depression Inventory (BDI) was used to self-rate depression symptoms. A novel-minus-familiar encoding contrast was built into a simple regression model showing brain activation magnitudes that covaried with BDI score. A region-of-interest mask was applied to isolate the PMC and other midline structures of the default-mode network. SETTING: The study was conducted at a university-based medical center. PARTICIPANTS: Participants included 62 nondemented subjects aged 55-85, with and without mild memory deficits. BDI scores ranged from 0 to 17. RESULTS: Analysis revealed a distinct PMC cluster confined to the dorsal posterior cingulate cortex (BA 31) whose activity correlated significantly with BDI score. A multiple regression model further showed that BDI score, as well as a history of depression and current use of antidepressants, had a significant effect on cluster variance, while age, education, gender, and mini-mental state exam scores did not. CONCLUSIONS: Our findings raise the hypothesis that subsyndromal depressive symptoms in late life may impair physiological PMC deactivation in the dorsal posterior cingulate cortex. A prospective study of a full spectrum of depressed patients may be warranted.
OBJECTIVE: Functional deactivation of the posteromedial cortex (PMC) seems to be a physiologic process underlying normal memory. The authors examined whether older subjects with subsyndromal depressive symptoms show impaired PMC deactivation. DESIGN: Subjects underwent 4T functional magnetic resonance imaging scan while performing a novel and familiar face-name associative encoding task. The Beck-II Depression Inventory (BDI) was used to self-rate depression symptoms. A novel-minus-familiar encoding contrast was built into a simple regression model showing brain activation magnitudes that covaried with BDI score. A region-of-interest mask was applied to isolate the PMC and other midline structures of the default-mode network. SETTING: The study was conducted at a university-based medical center. PARTICIPANTS: Participants included 62 nondemented subjects aged 55-85, with and without mild memory deficits. BDI scores ranged from 0 to 17. RESULTS: Analysis revealed a distinct PMC cluster confined to the dorsal posterior cingulate cortex (BA 31) whose activity correlated significantly with BDI score. A multiple regression model further showed that BDI score, as well as a history of depression and current use of antidepressants, had a significant effect on cluster variance, while age, education, gender, and mini-mental state exam scores did not. CONCLUSIONS: Our findings raise the hypothesis that subsyndromal depressive symptoms in late life may impair physiological PMC deactivation in the dorsal posterior cingulate cortex. A prospective study of a full spectrum of depressedpatients may be warranted.
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