Schweitzer Isaac, Tuckwell Virginia, O'Brien John, Ames David
Department of Psychiatry, University of Melbourne, Australia.
Int J Geriatr Psychiatry. 2002 Nov;17(11):997-1005. doi: 10.1002/gps.525.
Recent research suggests there are clinical and biological differences between late onset depression (LOD) and early-onset depression (EOD).
In this paper we review clinical, epidemiological, structural neuroimaging and genetic investigations of late life depression that have been performed over the past two decades and offer evidence that LOD is often a prodromal disorder for dementia.
LOD patients are more likely to have cognitive impairment and to have more deep white matter lesions (DWMLs). Evidence concerning cortical and temporal lobe atrophy is conflicting, while the ApoE 4 allele is not associated with LOD.
It is likely that LOD is not a prodrome for a particular type of dementia, but the majority of patients who do develop dementia will acquire Alzheimer's disease (AD) or a vascular dementia, as these are by far the most common causes of dementia. This issue requires further clarification with follow-up of patients over the long term.
近期研究表明，晚发性抑郁症（LOD）与早发性抑郁症（EOD）在临床和生物学方面存在差异。
在本文中，我们回顾了过去二十年中对老年抑郁症进行的临床、流行病学、结构神经影像学和遗传学研究，并提供证据表明LOD通常是痴呆症的前驱疾病。
LOD患者更有可能出现认知障碍，并且有更多的深部白质病变（DWMLs）。关于皮质和颞叶萎缩的证据存在矛盾，而载脂蛋白E4等位基因与LOD无关。
LOD可能不是特定类型痴呆症的前驱症状，但大多数确实发展为痴呆症的患者将患上阿尔茨海默病（AD）或血管性痴呆，因为这些是迄今为止最常见的痴呆症病因。这个问题需要通过对患者的长期随访进一步阐明。
