Decreasing hazards of Alzheimer 's disease with the use of antidepressants: mitigating the risk of depression and apolipoprotein E
Year: 2017
Type: article
Study design: Observational Study
Abstract: OBJECTIVE: Alzheimer's disease (AD) is a neurodegenerative disease, manifesting in clinically observable deficits in memory, thinking, and behavior that disproportionately affects older adults. Susceptibility genes, such as apolipoprotein ε4, have long been associated with an increased risk of AD diagnosis. Studies have shown associations between depression and increased risk of AD development. Furthermore, findings from previous investigations suggest mixed effects in the use of psychotropic medication in older adults. The hypothesis for this study is that antidepressant use modifies the increased hazard of depression or such that a non-significant hazard will result with respect to eventual AD development. METHODS: Utilizing data from the National Alzheimer's Coordinating Center, we examined evaluations of 11,443 cognitively intact participants. Survival analysis was used to explore relationships between depression, apolipoprotein E, AD diagnosis, and antidepressant use. RESULTS: An analytical sample of 8732 participants with normal cognition was examined. Among users of antidepressant medication, the hazard, in most cases, was no longer statistically significant. One generic medication showed protective benefits for users (p < 0.001). In addition, there was a statistically significant relationship between recent depression (n = 2083; p < 0.001), lifetime depression (n = 2068; p < 0.05), and ε4 carrier status (n = 2470; p < 0.001) and AD development. CONCLUSIONS: The findings suggest that a mechanism related to antidepressant use may reduce the hazard of eventual AD. Furthermore, the findings reinforce the association between depression, apolipoprotein E (APOE) ε4, and AD diagnosis. This study contributes to the emerging literature exploring interventions aimed at decreasing the risk of AD by targeting potentially modifiable psychosocial risk factors such as depression. Copyright © 2017 John Wiley & Sons, Ltd.
DOI: 10.1002/gps.4709
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: G1017046091, G1053905225, G1228824270, UC Davis Alzheimer's Disease Core Center, Indiana Alzheimer Disease Center, G1417337112, G1602633198, G2515091901, Neurobiology of Alzheimer's Disease and Aging, G2984989008, National Alzheimer's Coordinating Center, Alzheimer's Disease Research Center, G3632542342, G36881302, G384347443, G3919444319, G40706755, G4076092645, G413369726, G423967958, Alzheimer's Disease Core Center, The Alzheimer's Disease Research Center at the University of California, Irvine, G4417220376, Oregon Alzheimer's Disease Center, G556672640, G5640525220, G5977822913, G603598372, G611802359, Wisconsin Alzheimer's Disease Research Center, University of Kansas Alzheimer's Disease Core Centers, Alzheimer's Disease Research Center, Alzheimer Disease Research Center, Yale Alzheimer Disease Research Center, Arizona Alzheimer's Disease Core Center, Johns Hopkins Alzheimer's Disease Research Center, Boston University Alzheimer's Disease Center, Alzheimer's Disease Core Center, Emory Alzheimer's Disease Center, University of Florida - Mt. Sinai Medical Center AD Research Center, G828200374, Mayo Alzheimer's Disease Research Center
OpenAlex ID: W2618335481
