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淀粉样蛋白负担与临床前阿尔茨海默病患者抑郁症状的发生。

Amyloid burden and incident depressive symptoms in preclinical Alzheimer's disease.

机构信息

Department of Psychology, School of Health and Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia; Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, Parkville, Victoria, Australia.

Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia.

出版信息

J Affect Disord. 2018 Mar 15;229:269-274. doi: 10.1016/j.jad.2017.12.101. Epub 2018 Jan 3.

Abstract

BACKGROUND

Relationships between depression and Alzheimer's disease (AD) may become clearer if studied in preclinical AD where dementia is not present.

METHOD

The aim of this study was to evaluate prospectively, relationships between brain amyloid-β (Aβ), depressive symptoms and screen positive depression in cognitively normal (CN) older adults. Depressive symptoms were measured with the Geriatric Depression Inventory (GDS-15) in CN adults from the Australian Imaging Biomarkers and Lifestyle (AIBL) study without depression at baseline and classified as having abnormally high (Aβ+; n = 136) or low (Aβ-; n = 449) Aβ according to positron emission tomography at 18-month intervals over 72 months.

RESULTS

Incident cases of screen positive depression were not increased in Aβ+ CN adults although small increases in overall depressive symptoms severity (d = - 0.25; 95% CI, - 0.45, - 0.05) and apathy-anxiety symptoms (d = - 0.28; 95% CI - 0.48, - 0.08) were.

LIMITATIONS

As the AIBL sample is an experimental sample, no individuals had severe medical illnesses or significant psychiatric disorders. Additionally, individuals who had evidence of screen-positive depression at screening were excluded from enrolment in the AIBL study. Thus, the current data can be considered only as providing a foundation for understanding relationships between Aβ and depression in preclinical AD.

CONCLUSIONS

These results suggest that the presence of a depressive disorder or even increased depressive symptoms are themselves unlikely to be a direct consequence of increasing Aβ. New depressive disorders presenting in CN older adults could therefore be investigated for aetiologies beyond AD.

摘要

背景

如果在没有痴呆的临床前阿尔茨海默病(AD)中进行研究,抑郁与 AD 之间的关系可能会更加清晰。

方法

本研究的目的是前瞻性评估认知正常(CN)老年人中脑淀粉样蛋白-β(Aβ)、抑郁症状与筛查阳性抑郁之间的关系。CN 成年人使用老年抑郁量表(GDS-15)测量抑郁症状,这些成年人来自澳大利亚成像生物标志物和生活方式(AIBL)研究,基线时无抑郁,并根据正电子发射断层扫描在 72 个月的 18 个月间隔内分为 Aβ 阳性(Aβ+;n=136)或 Aβ 阴性(Aβ-;n=449)。

结果

Aβ+CN 成年人中未增加筛查阳性抑郁的病例,尽管总体抑郁症状严重程度(d=-0.25;95%CI,-0.45,-0.05)和淡漠-焦虑症状(d=-0.28;95%CI-0.48,-0.08)略有增加。

局限性

由于 AIBL 样本是一个实验样本,没有个体患有严重的医疗疾病或严重的精神疾病。此外,在筛查时出现筛查阳性抑郁的个体被排除在 AIBL 研究的入组之外。因此,目前的数据只能被认为是为理解临床前 AD 中 Aβ 与抑郁之间的关系提供了基础。

结论

这些结果表明,抑郁障碍的存在,甚至抑郁症状的增加,本身不太可能是 Aβ 增加的直接后果。因此,可以对 CN 老年人群中新出现的抑郁障碍进行 AD 以外病因的研究。

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