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痴呆中抑郁还是抑郁中痴呆?研究和假说的系统综述。

Depression in Dementia or Dementia in Depression? Systematic Review of Studies and Hypotheses.

机构信息

Department of Old Age Psychiatry and Psychotic Disorders, Medical University of Lodz, Lodz, Poland.

Centre for Psychiatry, Wolfson Institute for Preventive Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University London, London E14NS, United Kingdom.

出版信息

Curr Alzheimer Res. 2020;17(1):16-28. doi: 10.2174/1567205017666200217104114.

DOI:10.2174/1567205017666200217104114
PMID:32065103
Abstract

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.

摘要

迄今为止,大多数研究表明,重度抑郁症(MDD)是痴呆的一个风险因素,可能导致早发性和晚发性变异的认知能力下降。然而,抑郁的存在可能并不反映原因,而是反映结果:它可能是对认知障碍的反应,或者改变了认知障碍表现或被检测出来的阈值。另一种假设是,抑郁可能是阿尔茨海默病(AD)前驱期的一部分,这表明存在神经生物学关联,而不仅仅是心理反应。遗传多态性可能可以解释这两种诊断之间共享现象学的一些差异,例如,当这些病症同时出现时,它们被检测到的顺序可能取决于个体的认知和身体储备,以及病史和个体脆弱性。这一假设在生物学上是合理的,但迄今为止尚未得到系统研究。目前的综述强调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同时出现的风险,这是未来研究病理发病机制和随机对照试验研究样本分层的重要考虑因素。

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