The vascular depression hypothesis: mechanisms linking vascular disease with depression.
The vascular depression hypothesis: mechanisms linking vascular disease with depression.
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DOI：
10.1038/mp.2013.20
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发表时间：
2013-09
影响因子：
11
通讯作者：
Alexopoulos, G. S.
中科院分区：
文献类型：
--
作者：
Taylor, W. D.;Aizenstein, H. J.;Alexopoulos, G. S.
“血管性抑郁”假说认为，脑血管疾病可能诱发、沉淀或延续某些老年抑郁综合征。这一假设刺激了许多研究，提高了我们对晚年抑郁症（LLD）、血管危险因素和认知之间复杂关系的理解。简而言之，在晚年抑郁、血管危险因素和大脑高信号（血管抑郁的放射学标志）之间有明确的关系。认知功能障碍在老年抑郁症中很常见，尤其是执行功能障碍，这一发现预示着抗抑郁药物的不良反应。随着时间的推移，高强度和认知缺陷的进展预示着抑郁症的不良病程，并可能反映血管疾病的潜在恶化。这项工作为研究血管疾病影响脑回路和影响抑郁症的发展和过程的机制奠定了基础。我们回顾了测试血管抑郁假说的数据，重点是确定潜在的潜在血管机制。我们提出一个断连假说，其中局灶性血管损伤和白质病变位置是影响神经连通性的关键因素，有助于临床症状。我们还提出了炎症和灌注不足假说，这些概念将潜在的血管过程与影响抑郁症发展的脑功能的不利影响联系起来。测试这些假设不仅将告知血管疾病和抑郁症之间的关系，而且还将为可能改善晚年抑郁症结果的药理学药物的潜在重新用途提供指导。
The ‘Vascular Depression’ hypothesis posits that cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive syndromes. This hypothesis stimulated much research that has improved our understanding of the complex relationships between late-life depression (LLD), vascular risk factors, and cognition. Succinctly, there are well-established relationships between late-life depression, vascular risk factors, and cerebral hyperintensities, the radiological hallmark of vascular depression. Cognitive dysfunction is common in late-life depression, particularly executive dysfunction, a finding predictive of poor antidepressant response. Over time, progression of hyperintensities and cognitive deficits predicts a poor course of depression and may reflect underlying worsening of vascular disease. This work laid the foundation for examining the mechanisms by which vascular disease influences brain circuits and influences the development and course of depression. We review data testing the vascular depression hypothesis with a focus on identifying potential underlying vascular mechanisms. We propose a disconnection hypothesis, wherein focal vascular damage and white matter lesion location is a crucial factor influencing neural connectivity that contributes to clinical symptomatology. We also propose inflammatory and hypoperfusion hypotheses, concepts that link underlying vascular processes with adverse effects on brain function that influence the development of depression. Testing such hypotheses will not only inform the relationship between vascular disease and depression but also provide guidance on the potential repurposing of pharmacological agents that may improve late-life depression outcomes.
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DOI：
10.1176/appi.ajp.2011.10060853
发表时间：
2011-10
期刊：
The American journal of psychiatry
影响因子：
--
作者：
Aizenstein HJ;Andreescu C;Edelman KL;Cochran JL;Price J;Butters MA;Karp J;Patel M;Reynolds CF 3rd
通讯作者：
Reynolds CF 3rd
影响因子：
7.2
作者：
Alexopoulos, GS
通讯作者：
Alexopoulos, GS
影响因子：
17.7
作者：
Alexopoulos, George S.;Murphy, Christopher F.;Hoptman, Matthew J.
通讯作者：
Hoptman, Matthew J.
影响因子：
11
作者：
Baghai, T. C.;Binder, E. B.;Bondy, B.
通讯作者：
Bondy, B.
影响因子：
6.6
作者：
Alexopoulos, George S.;Murphy, Christopher F.;Gunning-Dixon, Faith M.;Glatt, Charles E.;Latoussakis, Vassilios;Kelly, Robert E., Jr.;Kanellopoulos, Dora;Klimstra, Sibel;Lim, Kelvin O.;Young, Robert C.;Hoptman, Matthew J.
通讯作者：
Hoptman, Matthew J.