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Broadening the etiological discourse on Alzheimer's disease to include trauma and posttraumatic stress disorder as psychosocial risk factors

机译:扩大关于阿尔茨海默氏病的病因学论述,将创伤和创伤后应激障碍纳入为社会心理危险因素

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Biomedical perspectives have long dominated research on the etiology and progression of Alzheimer's disease (AD); yet these approaches do not solely explain observed variations in individual AD trajectories. More robust biopsychosocial models regard the course of AD as a dialectical interplay of neuropathological and psychosocial influences. Drawing on this broader conceptualization, we conducted an extensive review of empirical and theoretical literature on the associations of trauma, posttraumatic stress disorder (PTSD) and AD to develop a working model that conceptualizes the role of psychosocial stressors and physiological mechanisms in the onset and course of AD. The proposed model suggests two pathways. In the first, previous life trauma acts as a risk factor for later-life onset of AD, either directly or mediated by PTSD or PTSD correlates. In the second, de novo AD experiential trauma is associated with accelerated cognitive decline, either directly or mediated through PTSD or PTSD correlates. Evidence synthesized in this paper indicates that previous life trauma and PTSD are strong candidates as psychosocial risk factors for AD and warrant further empirical scrutiny. Psychosocial and neurological-based intervention implications are discussed. A biopsychosocial approach has the capacity to enhance understanding of individual AD trajectories, moving the field toward 'person-centered' models of care.
机译:生物医学观点长期以来一直是阿尔茨海默氏病(AD)病因和进展研究的主导。然而,这些方法并不能仅解释单个AD轨迹中观察到的变化。更强大的生物心理社会模型将AD的过程视为神经病理学和社会心理影响的辩证相互作用。在此更广泛的概念化基础上,我们对创伤,创伤后应激障碍(PTSD)和AD的关系进行了经验和理论文献的广泛回顾,以开发一种工作模型,将心理社会压力源和生理机制在发病过程和过程中的作用概念化的。提出的模型提出了两种途径。首先,以前的生活创伤是直接或通过PTSD或PTSD相关因素介导AD发作的危险因素。第二,从头AD经历性创伤与直接或通过PTSD或PTSD相关的加速的认知下降相关。本文综合的证据表明,先前的生活创伤和PTSD是AD的社会心理危险因素,因此有待进一步的实证研究。讨论了基于社会心理和神经学的干预含义。生物心理社会学方法具有增强对个体AD轨迹的理解的能力,使该领域向“以人为本”的护理模式发展。

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