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A Prodromal Depression of Alzheimer Disease?

Xiaoyan Sun, MD, PhD; David C. Steffens, MD; Rhoda Au, PhD; Marshal Folstein, MD; Paul Summergrad, MD; Jacqueline Yee, BA; Irwin Rosenberg, MD; D. Mkaya Mwamburi, MD, PhD; Wei Qiao Qiu, MD, PhD

Arch Gen Psychiatry. 2008;65(5):542-550.

Context  A high ratio of plasma amyloid-β peptide 40 (Aβ₄₀) to Aβ₄₂, determined by both high Aβ₄₀ and low Aβ₄₂ levels, increases the risk of Alzheimer disease. In a previous study, we reported that depression is also associated with low plasma Aβ₄₂ levels in the elderly population.

Objective  To characterize plasma Aβ₄₀:Aβ₄₂ ratio and cognitive function in elderly individuals with and without depression.

Design  Cross-sectional study.

Setting  Homecare agencies.

Participants  A total of 995 homebound elderly individuals of whom 348 were defined as depressed by a Center for Epidemiological Studies Depression score of 16 or greater.

Main Outcome Measures  Cognitive domains of memory, language, executive, and visuospatial functions according to levels of plasma Aβ₄₀ and Aβ₄₂ peptides.

Results  Subjects with depression had lower plasma Aβ₄₂ levels (median, 14.1 vs 19.2 pg/mL; P = .006) and a higher plasma Aβ₄₀:Aβ₄₂ ratio (median, 8.9 vs 6.4; P < .001) than did those without depression in the absence of cardiovascular disease and antidepressant use. The interaction between depression and plasma Aβ₄₀:Aβ₄₂ ratio was associated with lower memory score (β = –1.9, SE = 0.7, P = .006) after adjusting for potentially confounders. Relative to those without depression, "amyloid-associated depression," defined by presence of depression and a high plasma Aβ₄₀:Aβ₄₂ ratio, was associated with greater impairment in memory, visuospatial ability, and executive function; in contrast, nonamyloid depression was not associated with memory impairment but with other cognitive disabilities.

Conclusion  Amyloid-associated depression may define a subtype of depression representing a prodromal manifestation of Alzheimer disease.

Author Affiliations: Department of Psychiatry, Tufts–New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts (Drs Sun, Folstein, Summergrad, and Qiu); Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University (Drs Sun, Folstein, and Qiu and Ms Yee); Department of Psychiatry, Duke University Medical Center, Durham, North Carolina (Dr Steffens); Department of Neurology, Boston University School of Medicine and Framingham Heart Study (Dr Au); Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (Dr Rosenberg); and Department of Public Health and Family Medicine, Tufts University (Dr Mwamburi).

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