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The article presents a cross-sectional study that characterizes plasma amyloid-β peptide 40 (Aβ40): Aβ42 ratio and cognitive function in elderly individuals with and without depression. It aimed to measure the cognitive domains of memory, language, executive and visuospatial functions according to levels of plasma Aβ40 and A-β42 peptide. The study concludes that amyloid-associated depression may define a subtype of depression that represents a prodormal manifestation of Alzheimer disease.

High levels of homocysteine are associated with cerebrovascular disease, monoamine neurotransmitters, and depression of mood. A plausible hypothesis for these associations is that high homocysteine levels cause cerebral vascular disease and neurotransmitter deficiency, which cause depression of mood. The homocysteine depression hypothesis, if true, would mandate inclusions of imaging studies for cerebrovascular disease and measures of homocysteine, folate, and B12 and B6 vitamins in the clinical evaluation of older depressed patients. Longitudinal studies and clinical trials should be designed to challenge the hypothesis. [ABSTRACT FROM AUTHOR]

OBJECTIVES: To describe patterns of cognitive deficits and activities of daily living (ADLs) in older people with diabetes mellitus. DESIGN: Cross-sectional, population-based study. SETTING: Three homecare agency areas in Boston, Massachusetts. PARTICIPANTS: Two hundred ninety-one homebound people aged 60 and older; 40% with diabetes mellitus. MEASUREMENTS: Demographic data; evidence of diabetes mellitus and other diseases; Mini-Mental State Examination and tests of memory and executive function; ADLs. RESULTS: Executive and visuospatial functions were more impaired in individuals with diabetes mellitus than in those without, as assessed using Block Design (mean score±standard deviation 17.1±8.6 vs 20.5±9.6, P=.003) and Trails B (median seconds to accomplish the task: 255 vs 201, P=.03). For memory, word retention score was lower in those with diabetes mellitus than without (39.1±28.9 vs 48.0±29.7, P=.01), but the other memory tests did not show a difference between these two subgroups. More individuals with diabetes mellitus suffered from depressive symptoms than those without (55% vs 42%, P=.03). The ADL scores of those with diabetes mellitus were higher than those without. CONCLUSION: The pattern of cognitive deficits in people with diabetes mellitus suggests frontal-subcortical dysfunction, as seen in microvascular disease of the brain. The impairment in ADLs may be associated with this executive dysfunction, which cerebral microvascular disease in diabetes mellitus may cause. [ABSTRACT FROM AUTHOR]

Five patients with trisomy 21 (Down's syndrome (DS], referred to us for evaluation of dementia, were instead found to have major depression. All had shown cognitive and behavioural deterioration and this had led to a mistaken diagnosis of Alzheimer's disease in two. We outline and contrast the features of major depression and Alzheimer's disease in DS, and suggest that electroconvulsive therapy is an effective treatment for major depression in DS. [ABSTRACT FROM AUTHOR]

Determines the prevalence rates of major depressive disorder and of depressive symptoms and their relationship to mortality in nursing homes. Factors associated with depression; Characteristics that have made nursing homes a major focus of care for the elderly; Risks of acquiring depressive symptoms.

For each of 41 index patients with probable Alzheimer's disease and a first episode of major depression and 71 nondepressed Alzheimer's disease patients, two first-degree relatives were interviewed by a rater blind to presence or absence of depression in the proband. The depressed patients had significantly more first- and second-degree relatives with depression than did control subjects. The lifetime risk for major depression, adjusted for differences in age distribution, was significantly greater in first-degree relatives of index patients, suggesting that depression in Alzheimer's disease is genetically related to primary affective disorder. Alzheimer's disease may be useful for studying aspects of depressive pathophysiology. [ABSTRACT FROM AUTHOR]

Abstract: Background: Depression is associated with an increase in the incidence of type 2 diabetes, but the mechanism is unclear. We aimed to study the relationship between depression and glycemic intake in the elderly, and examine whether antidepressant use modified this relationship. Design, setting and participants: We evaluated 976 homebound elders in a cross-sectional study. Depression was defined by having a Center for Epidemiological Studies Depression (CES-D) score ≥16. Antidepressant use was documented. Glycemic index (GI), Glycemic load (GL), and fasting blood insulin levels were measured. Results: Depressed elders had slightly higher GI (Mean±SD: 55.8±3.8 vs. 55.1±3.7, P=0.003) and higher insulin levels (Median: 84.0 vs. 74.4pmol/ml, P=0.05) than non-depressed elders. Depressed elders receiving antidepressants, primarily selective serotonin reuptake inhibitors (SSRI), had lower GI (Mean±SD: 55.1±4.7 vs. 56.2±3.4, P=0.002) and GL (Median: 170.3 vs. 6826.3, P=0.03) than those not taking antidepressants. After adjusting for potential confounding variables, GI remained positively associated with depression (β=+0.65, SE=0.28, P=0.02); the logarithm of GL was positively associated with depression (β=+0.33, SE=0.17, P=0.05) and negatively associated with antidepressant use (β=−0.54, SE=0.18, P=0.003). Conclusions: Prospective studies are needed to examine whether high glycemic intake is a mediating factor between late life depression and the risk of type 2 diabetes. [Copyright &y& Elsevier]

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. [Copyright &y& Elsevier]