Depression and the Risk of Alzheimer Disease
ABSTRACT Background: Several epidemiologic studies have examined depression as a risk factor for Alzheimer disease with conflicting results. Most studies relied on self-reported depression, but the agreement between self-reported depression and clinical diagnosis has been reported to be weak, thereby diluting the association.
Methods: A population-based cohort in Odense, Denmark, of 3346 persons age 65-84 years was examined at baseline (1992-1994) and after 2 years (1994-1996) and 5 years (1997-1999). History of depression was collected at baseline as self-report. We used logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs).
Results: Persons with a history of depression had an increased risk of Alzheimer disease both at baseline (OR = 1.7; CI = 1.0-2.7) and at follow up (at 2 years, 1.9 [1.0-3.3] and at 5 years, 1.6 [0.9-2.7]).
Conclusions: Depression was associated with an increased risk of Alzheimer disease. The odds ratios were lower than generally reported from follow-up studies and are similar to cross-sectional studies.
SourceAvailable from: Saira Saeed Mirza[Show abstract] [Hide abstract]
ABSTRACT: Background Whether depression is a long-term risk factor for dementia or represents a dementia prodrome is unclear. Therefore, we examined the relationship between depressive symptoms and dementia during short and long follow-up in a population-based cohort. Methods In the Rotterdam Study, 4393 nondemented individuals were followed for incident dementia for 13.7 years by continuous monitoring. Cox proportional hazards models for different time intervals were used to estimate the risk of incident dementia. Results Five-hundred eighty-two participants developed dementia during 13.7 years. Persons with depressive symptoms had an 8% increased risk of dementia compared with those without depressive symptoms during the overall follow-up. The risk was highest in the short and intermediate follow-up, particularly in men. We did not find an association in the follow-up period beyond 10 years. Conclusion Our results suggest that late-life depressive symptoms are part of a dementia prodrome rather than an independent risk factor of dementia.Alzheimer's & dementia: the journal of the Alzheimer's Association 10/2014; DOI:10.1016/j.jalz.2013.10.006 · 14.48 Impact Factor
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ABSTRACT: Affective disorders are associated with cognitive disturbances but their role as risk factors for dementia is still not fully investigated. To evaluate the risk of developing dementia in individuals with a history of affective disorder. We conducted a systematic review of case-control and cohort studies addressing the risk of developing dementia in people with affective disorders. To the best of our knowledge, this is the first systematic review that has included studies evaluating this risk specifically in people with bipolar disorder. Fifty-one studies were included. Most of the studies found an increased risk for developing dementia in individuals with depression. Greater frequency and severity of depressive episodes seem to increase this risk. The evidence is contradictory regarding whether there is a difference in risk in people with early- or late-onset depression. The few available risk estimates for dementia in people with bipolar disorder suggest an even higher risk than for those with depression. Affective disorders appear to be associated with an increased risk of developing dementia, and one that is dependent on clinical and demographic variables. Depression may be both a prodrome and a risk factor for dementia. Future research should aim to elucidate the mechanisms that mediate these links.The British journal of psychiatry: the journal of mental science 03/2013; 202(3):177-86. DOI:10.1192/bjp.bp.111.101931 · 6.62 Impact Factor
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ABSTRACT: The current study investigated the hypothesis that the duration of the proinflammatory environment plays a critical role in the brain's response that results in negative consequences on cognition, biochemistry, and pathology. Lipopolysaccharide or artificial cerebrospinal fluid was slowly (250 ηg/h) infused into the fourth ventricle of young (3-month-old), adult (9-month-old), or aged (23-month-old) male F-344 rats for 21 or 56 days. The rats were then tested in the water pool task and endogenous hippocampal levels of pro- and anti-inflammatory proteins and genes and indicators of glutamatergic function were determined. The duration of the lipopolysaccharide infusion, compared with the age of the rat, had the greatest effect on (1) spatial working memory; (2) the density and distribution of activated microglia within the hippocampus; and (3) the cytokine protein and gene expression profiles within the hippocampus. The duration- and age-dependent consequences of neuroinflammation might explain why human adults respond positively to anti-inflammatory therapies and aged humans do not.Neurobiology of aging 04/2013; 34(10). DOI:10.1016/j.neurobiolaging.2013.03.034 · 5.94 Impact Factor