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阿尔茨海默病病理学的分子成像

Molecular imaging of Alzheimer disease pathology.

作者信息

Kantarci K

机构信息

From the Department of Radiology, Mayo Clinic, Rochester, Minnesota.

出版信息

AJNR Am J Neuroradiol. 2014 Jun;35(6 Suppl):S12-7. doi: 10.3174/ajnr.A3847. Epub 2014 Feb 6.

Abstract

Development of molecular imaging agents for fibrillar β-amyloid positron-emission tomography during the past decade has brought molecular imaging of Alzheimer disease pathology into the spotlight. Large cohort studies with longitudinal follow-up in cognitively normal individuals and patients with mild cognitive impairment and Alzheimer disease indicate that β-amyloid deposition can be detected many years before the onset of symptoms with molecular imaging, and its progression can be followed longitudinally. The utility of β-amyloid PET in the differential diagnosis of Alzheimer disease is greatest when there is no pathologic overlap between 2 dementia syndromes, such as in frontotemporal lobar degeneration and Alzheimer disease. However β-amyloid PET alone may be insufficient in distinguishing dementia syndromes that commonly have overlapping β-amyloid pathology, such as dementia with Lewy bodies and vascular dementia, which represent the 2 most common dementia pathologies after Alzheimer disease. The role of molecular imaging in Alzheimer disease clinical trials is growing rapidly, especially in an era when preventive interventions are designed to eradicate the pathology targeted by molecular imaging agents.

摘要

在过去十年中,用于纤维状β淀粉样蛋白正电子发射断层扫描的分子成像剂的开发,使阿尔茨海默病病理学的分子成像成为焦点。对认知正常个体、轻度认知障碍患者和阿尔茨海默病患者进行纵向随访的大型队列研究表明,使用分子成像技术可以在症状出现前许多年检测到β淀粉样蛋白沉积,并且可以纵向跟踪其进展。当两种痴呆综合征之间没有病理重叠时,例如额颞叶变性和阿尔茨海默病,β淀粉样蛋白PET在阿尔茨海默病的鉴别诊断中的效用最大。然而,仅靠β淀粉样蛋白PET可能不足以区分通常具有重叠β淀粉样蛋白病理学的痴呆综合征,如路易体痴呆和血管性痴呆,它们是继阿尔茨海默病之后最常见的两种痴呆病理学类型。分子成像在阿尔茨海默病临床试验中的作用正在迅速增长,尤其是在一个预防性干预旨在根除分子成像剂所针对的病理学的时代。

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