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抑郁与痴呆症发病风险。

Depression and risk of developing dementia.

机构信息

Department of Psychiatry, University of California, San Francisco and San Francisco Veterans Affairs Medical Center, 4150 Clement Street (116H), San Francisco, CA 94121, USA.

出版信息

Nat Rev Neurol. 2011 May 3;7(6):323-31. doi: 10.1038/nrneurol.2011.60.

DOI:10.1038/nrneurol.2011.60
PMID:21537355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3327554/
Abstract

Depression is highly common throughout the life course and dementia is common in late life. Depression has been linked with dementia, and growing evidence implies that the timing of depression may be important in defining the nature of this association. In particular, earlier-life depression (or depressive symptoms) has consistently been associated with a more than twofold increase in dementia risk. By contrast, studies of late-life depression and dementia risk have been conflicting; most support an association, yet the nature of this association (for example, if depression is a prodrome or consequence of, or risk factor for dementia) remains unclear. The likely biological mechanisms linking depression to dementia include vascular disease, alterations in glucocorticoid steroid levels and hippocampal atrophy, increased deposition of amyloid-β plaques, inflammatory changes, and deficits of nerve growth factors. Treatment strategies for depression could interfere with these pathways and alter the risk of dementia. Given the projected increase in dementia incidence in the coming decades, understanding whether treatment for depression alone, or combined with other regimens, improves cognition is of critical importance. In this Review, we summarize and analyze current evidence linking late-life and earlier-life depression and dementia, and discuss the primary underlying mechanisms and implications for treatment.

摘要

抑郁症在整个生命过程中非常普遍,而痴呆症在晚年很常见。抑郁症与痴呆症有关,越来越多的证据表明,抑郁症的发病时间在定义这种关联的性质方面可能很重要。特别是,早发性抑郁症(或抑郁症状)与痴呆风险增加两倍以上一直相关。相比之下,关于老年期抑郁症和痴呆风险的研究一直存在争议;大多数研究支持这种关联,但这种关联的性质(例如,抑郁症是否是痴呆的前驱期、后果或危险因素)仍不清楚。将抑郁症与痴呆联系起来的可能生物学机制包括血管疾病、糖皮质激素水平的改变和海马体萎缩、β淀粉样斑块沉积增加、炎症变化以及神经生长因子缺乏。治疗抑郁症的策略可能会干扰这些途径,并改变痴呆的风险。鉴于未来几十年痴呆症发病率预计会增加,了解仅治疗抑郁症、还是联合其他治疗方案是否可以改善认知,这一点至关重要。在这篇综述中,我们总结和分析了目前将老年期和早发性抑郁症与痴呆联系起来的证据,并讨论了主要的潜在机制及其对治疗的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/335c/3327554/7171d4d9d90d/nihms-352655-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/335c/3327554/7171d4d9d90d/nihms-352655-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/335c/3327554/7171d4d9d90d/nihms-352655-f0001.jpg

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