Robert Stempel College of Public Health and Social Work, School of Social Work, Florida International University, Miami, FL, USA.
Simmons College School of Social Work, Boston, MA, USA.
Int J Geriatr Psychiatry. 2018 Jan;33(1):200-211. doi: 10.1002/gps.4709. Epub 2017 May 31.
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.
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.
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.
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.
阿尔茨海默病（AD）是一种神经退行性疾病，临床上表现为记忆、思维和行为的明显缺陷， disproportionately 影响老年人。载脂蛋白 E4 等易感基因 long 以来一直与 AD 诊断风险增加相关。研究表明 depression 与 AD 发展风险增加之间存在关联。此外，先前的调查结果表明，在老年人中使用精神药物的效果mixed。本研究的假设是，使用抗抑郁药会改变 depression 或增加的风险，从而导致最终 AD 发展的风险无显著增加。
利用国家阿尔茨海默病协调中心的数据，我们对 11443 名认知正常的参与者进行了评估。生存分析用于探索 depression、载脂蛋白 E、AD 诊断和抗抑郁药使用之间的关系。
我们对 8732 名认知正常的参与者进行了分析样本检查。在使用抗抑郁药的患者中，大多数情况下，风险不再具有统计学意义。一种通用药物对使用者具有保护作用（p < 0.001）。此外，最近的 depression（n = 2083；p < 0.001）、lifetime depression（n = 2068；p < 0.05）和 ε4 携带者状态（n = 2470；p < 0.001）与 AD 发展之间存在统计学显著关系。
这些发现表明，与抗抑郁药使用相关的机制可能会降低最终 AD 的风险。此外，这些发现强化了 depression、载脂蛋白 E（APOE）ε4 与 AD 诊断之间的关联。这项研究有助于探索通过针对 depression 等潜在可改变的社会心理风险因素来降低 AD 风险的干预措施的新兴文献。版权所有 © 2017 约翰威立父子公司
