Depression, Antidepressants, and Plasma Amyloid β (Beta) Peptides in Those Elderly Who Do Not Have Cardiovascular Disease

Background Low plasma amyloid-β peptide 42 (Aβ42) is associated with depressive symptoms independently of cardiovascular disease (CVD) in the elderly. It is critical to investigate whether antidepressants modify this relationship. Methods We evaluated 324 elders without CVD in a cross-sectional stud...

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Veröffentlicht in:Biological psychiatry (1969) 2007-12, Vol.62 (12), p.1413-1417
Hauptverfasser: Sun, Xiaoyan, Mwamburi, D. Mkaya, Bungay, Kathleen, Prasad, Jasmin, Yee, Jacqueline, Lin, Yu-min, Liu, Timothy C, Summergrad, Paul, Folstein, Marshal, Qiu, Wei Qiao
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Sprache:eng
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Zusammenfassung:Background Low plasma amyloid-β peptide 42 (Aβ42) is associated with depressive symptoms independently of cardiovascular disease (CVD) in the elderly. It is critical to investigate whether antidepressants modify this relationship. Methods We evaluated 324 elders without CVD in a cross-sectional study. Depression was evaluated with the Center for Epidemiological Studies Depression (CES-D) scale. Antidepressants were documented. Plasma Aβ40 and Aβ42 were measured. Results In the absence of CVD, those with depression had lower plasma Aβ42 (median: 13.7 vs. 18.8 pg/mL, p = .003) than those without. Depressed subjects on antidepressant treatment had a lower concentration of plasma Aβ40 (median: 97.8 vs. 133.5 pg/mL, p = .008), but not Aβ42, than those without the treatment. Multivariate logistic regression showed that antidepressant use did not influence the relationship between depression and low plasma Aβ42 (odds ratio = .55; 95% CI = .33, .90; p = .02) after adjusting for confounders, but its use interacted with plasma Aβ40 in the model. Conclusions Lower concentration of plasma Aβ42 is associated with depression in the absence of CVD that is not related to the antidepressant use by those subjects. Prospective studies are needed to determine whether depression associated with low plasma Aβ42 predicts the onset of Alzheimer’s disease.
ISSN:0006-3223
1873-2402
DOI:10.1016/j.biopsych.2007.01.003