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Late-life depression increases risk of dementia

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Late-life depression increases risk of dementia

By: CHRISTINE LEHMANN

 

05/07/13

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Depression in late life can accelerate cognitive decline. A new study shows that depression in older adults significantly increased the risk of all-cause dementia, Alzheimer’s disease, and vascular dementia.

Depression after age 50 years increased the risk of all-cause dementia by 1.85 times, Alzheimer’s disease by 1.65 times, and vascular dementia by 2.52 times, according to the results of a study published in the May issue of the British Journal of Psychiatry.

The meta-analysis, conducted by Dr. Breno S. Diniz and his associates at Western Psychiatric Institute and Clinic at the University of Pittsburgh Medical Center, is the first of its kind to examine both the risk of Alzheimer’s disease and vascular dementia in older adults with depression. Alzheimer’s disease is the most common form of dementia, followed by vascular dementia, which is characterized by impaired judgment or an inability to plan and complete tasks.

Dr. Breno S. Diniz

Dr. Diniz and his colleagues said their study also distinguished itself in another way. “This is the first study to show that late-life depression increases the risk of vascular dementia, and that the risk of vascular dementia is greater than the risk of Alzheimer’s disease for older adults with depression,” they wrote.

A meta-analysis of 23 prospective community-based cohort studies was conducted to calculate the pooled risk of all-cause dementia, Alzheimer’s disease, and vascular dementia. Only studies with baseline cases of depression in adults aged 50 years or older were included. Data from 49,612 participants were used for the pooled analysis for all-cause dementia; 28,746 participants were included in the pooled analysis for Alzheimer’s disease; and 14,901 participants were included in the pooled analysis for vascular dementia. The median follow-up interval for all-cause dementia studies was 5 years. For Alzheimer’s disease studies, the median follow-up interval was 5 years and for vascular dementia studies, it was 6.1 years (Br. J. Psychiatry 2013;202:329-35).

After excluding studies that did not report risk measures adjusted for multiple confounders, a reduced, although statistically significant, association was found between late-life depression and the risk of all-cause dementia, Alzheimer’s disease, and vascular dementia. The adjusted pooled risk for all-cause dementia was 1.59 and 1.55 for Alzheimer’s. For vascular dementia, the adjusted pooled risk was 2.02, with a confidence interval of 95%.

They said their results were in line with a report showing an increased risk of all three conditions among participants with mid- and late-life depression. These findings came from a retrospective analysis of 13,535 older participants who were followed on the Kaiser Permanente Medical Care Program of Northern California (Arch. Gen. Psychiatry 2012;69:493-8).

In the current meta-analysis, the researchers recommended conducting new clinical trials to investigate the potential impact of depression prevention on the risk of cognitive impairment and dementia among older adults.

“Also, the prevention and treatment of cardiovascular risk factors and an improvement of general health in people with late-life depression may have a significant impact not only in a reduction of late-life depression cases but also [in the] reduction of dementia cases (vascular dementia and Alzheimer’s disease) associated with this disorder,” the authors commented.

The researchers cited several limitations. Among them is that their meta-analysis was limited to PubMed and Scopus databases. A search of international databases such as EMBASE and PsychINFO might have led to additional studies, but they believe that their literature search was comprehensive.

In the past 3 years, Dr. Diniz received payment for lectures from Novartis and has had travel/meeting expenses covered by Pfizer. His colleagues reported associations with several organizations, including Northstar Neuroscience, Medtronic, Bristol-Myers Squibb, and Forest Laboratories This work was supported in part by the John Hartford Foundation, the University of Pittsburgh Medical Center Endowment in Geriatric Psychiatry, and the National Institutes of Health.

 


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