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Longitudinal studies of cerebral glucose metabolism in late‐life depression and normal aging
Author(s) -
Marano Christopher M.,
Workman Clifford I.,
Kramer Elisse,
Hermann Carol R.,
Ma Yilong,
Dhawan Vijay,
Chaly Thomas,
Eidelberg David,
Smith Gwenn S.
Publication year - 2013
Publication title -
international journal of geriatric psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.28
H-Index - 129
eISSN - 1099-1166
pISSN - 0885-6230
DOI - 10.1002/gps.3840
Subject(s) - late life depression , dementia , medicine , cognitive decline , posterior cingulate , depression (economics) , carbohydrate metabolism , positron emission tomography , psychology , endocrinology , cognition , psychiatry , hippocampal formation , nuclear medicine , disease , economics , macroeconomics
Objective Late‐life depression (LLD) has a substantial public health impact and is both a risk factor for and a prodrome of dementia. Positron emission tomography (PET) studies of cerebral glucose metabolism have demonstrated sensitivity in evaluating neural circuitry involved in depression, aging, incipient cognitive decline, and dementia. The present study evaluated the long term effects of a course of antidepressant treatment on glucose metabolism in LLD patients. Methods Nine LLD patients and seven non‐depressed control subjects underwent clinical and cognitive evaluations as well as brain magnetic resonance imaging and PET studies of cerebral glucose metabolism at baseline, after 8 weeks of treatment with citalopram for a major depressive episode (patients only), and at an approximately 2‐year follow‐up. Results The majority of LLD patients were remitted at follow‐up (7/9). Neither patients nor controls showed significant cognitive decline. The patients showed greater increases in glucose metabolism than the controls in regions associated with mood symptoms (anterior cingulate and insula). Both groups showed decreases in metabolism in posterior association cortices implicated in dementia. Conclusions Longitudinal changes in cerebral glucose metabolism are observed in controls and in LLD patients without significant cognitive decline that are more extensive than the decreases in brain volume. Longer duration follow‐up studies and the integration of other molecular imaging methods will have implications for understanding the clinical and neurobiological significance of these metabolic changes. Copyright © 2012 John Wiley & Sons, Ltd.