Citation

Kumar A, Kepe V, Barrio JR, Siddarth P, Manoukian V, Elderkin-Thompson V, Small GW. Arch. Gen. Psychiatry 2011; 68(11): 1143-1150.

Affiliation

Department of Psychiatry, University of Illinois at Chicago, 1601 W Taylor, Ste 573, MC 912, Chicago, IL 60612. akumar@psych.uic.edu.

Copyright

(Copyright © 2011, American Medical Association)

DOI

10.1001/archgenpsychiatry.2011.122

PMID

22065530

Abstract

CONTEXT: Depression has been identified as a risk factor and a prodrome of dementia. Common neurobiological mechanisms may underlie this clinical and phenomenologic overlap. OBJECTIVE: To examine and compare protein (amyloid and tau) binding in critical brain regions in patients diagnosed as having late-life major depressive disorder (MDD) and healthy control individuals using 2-(1-{6-[(2-[(18)F]fluoroethyl)(methyl)-amino]-2-naphthyl}ethylidene) malononitrile ([(18)F]FDDNP) positron emission tomography. DESIGN: A cross-section neuroimaging study using positron emission tomography. SETTING: University of California, Los Angeles. Patients  Our samples comprised 20 patients diagnosed as having MDD and 19 healthy control individuals of comparable age, sex, and educational level. Main Outcome Measure  Relative distribution volume in regions of interest was used as the measure of [(18)F]FDDNP binding in all study participants. RESULTS: When compared with controls, [(18)F]FDDNP binding was significantly higher overall and in the posterior cingulate and lateral temporal regions in the MDD group. CONCLUSIONS: These findings suggest that neuronal injury associated with higher protein load in critical brain regions might provide a mechanism in the pathophysiologic manifestation of MDD in late life and have implications for the therapeutics of depression in elderly individuals.

Language: en