Montine Thomas J, Quinn Joseph F, Montine Kathleen S, Kaye Jeffrey A, Breitner John C S
Department of Pathology, University of Washington, Seattle, WA 98104, USA.
J Alzheimers Dis. 2005 Mar;8(4):359-67. doi: 10.3233/jad-2005-8405.
Dementia from Alzheimer's disease (AD) represents a significant and growing public health burden and presents a clear therapeutic imperative. Key to success in this undertaking will be biomarkers for the objective assessment of disease progression and response to therapeutics. Oxidative damage is one facet of AD pathogenesis for which there are experimentally validated quantitative in vivo biomarkers, the F2-isoprostanes (IsoPs). While plasma- or urine-based assays are desirable, consistent and reproducible cross-sectional data for increased F2-IsoPs in AD and mild cognitive impairment have been obtained only for CSF. In addition, measurement of CSF F2-IsoPs can increase the accuracy of laboratory-based classification of geriatric dementias, and have been used to assess objectively the response to anti-oxidant interventions in AD.
阿尔茨海默病（AD）所致的痴呆构成了日益严重的重大公共卫生负担，明确显示出治疗的紧迫性。这项工作取得成功的关键将是用于客观评估疾病进展和治疗反应的生物标志物。氧化损伤是AD发病机制的一个方面，对此已有经实验验证的体内定量生物标志物——F2-异前列腺素（IsoPs）。虽然基于血浆或尿液的检测方法较为理想，但仅在脑脊液中获得了AD和轻度认知障碍患者F2-IsoPs升高的一致且可重复的横断面数据。此外，脑脊液F2-IsoPs的测量可以提高基于实验室的老年痴呆分类的准确性，并已用于客观评估AD中抗氧化干预的反应。
