The majority of research works to date suggest that Major Depressive Disorder (MDD) is a risk factor for dementia and may predispose to cognitive decline in both early and late onset variants. The presence of depression may not, however, reflect the cause, rather, an effect: it may be a response to cognitive impairment or alters the threshold at which cognitive impairment might manifest or be detected. An alternative hypothesis is that depression may be part of a prodrome to Alzheimer's Disease (AD), suggesting a neurobiological association rather than one of psychological response alone. Genetic polymorphisms may explain some of the variances in shared phenomenology between the diagnoses, the instance, when the conditions arise comorbidly, the order in which they are detected that may depend on individual cognitive and physical reserves, as well as the medical history and individual vulnerability. This hypothesis is biologically sound but has not been systematically investigated to date. The current review highlights how genetic variations are involved in the development of both AD and MDD, and the risk conferred by these variations on the expression of these two disorders comorbidly is an important consideration for future studies of pathoaetiological mechanisms and in the stratification of study samples for randomised controlled trials.

中文翻译：

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痴呆症中的抑郁症还是抑郁症中的痴呆症？对研究和假设的系统评价。

迄今为止，大多数研究工作表明，重度抑郁症（MDD）是痴呆症的危险因素，可能会导致早期和晚期发作变异的认知能力下降。但是，抑郁症的出现可能并不能反映出原因，而是一种影响：它可能是对认知障碍的反应，或者改变了可能出现或检测到认知障碍的阈值。另一种假设是，抑郁症可能是阿尔茨海默氏病（AD）的一部分，表明存在神经生物学联系，而不仅仅是心理反应之一。遗传多态性可以解释诊断之间共享现象学的某些差异，例如，当条件并发出现时，检测它们的顺序可能取决于个人的认知和身体储备，以及病史和个人脆弱性。该假设在生物学上是合理的，但迄今为止尚未进行系统的研究。本综述着重介绍了遗传变异如何参与AD和MDD的发展，以及这些变异对这两种疾病的表达所造成的风险并存，这是未来病原学机制研究和研究样本分层的重要考虑因素用于随机对照试验。