Bacskai Brian J, Frosch Matthew P, Freeman Stefanie H, Raymond Scott B, Augustinack Jean C, Johnson Keith A, Irizarry Michael C, Klunk William E, Mathis Chester A, Dekosky Steven T, Greenberg Steven M, Hyman Bradley T, Growdon John H
MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Charlestown, MA 02129, USA.
Arch Neurol. 2007 Mar;64(3):431-4. doi: 10.1001/archneur.64.3.431.
To determine the correspondence between uptake of Pittsburgh Compound B (PiB) in life and measures of beta-amyloid (Abeta) in postmortem tissue analysis. Patient A 76-year-old man with a clinical diagnosis of dementia with Lewy bodies underwent fluorodeoxyglucose (18)F and PiB positron emission tomographic brain scans. Imaging revealed marked region specific binding of PiB and abnormal fluorodeoxyglucose uptake. Intervention Autopsy was performed 3 months after the PiB scan.
Autopsy confirmed the clinical diagnosis; in addition, there was severe cerebral amyloid angiopathy and only moderate numbers of parenchymal Abeta plaques. Biochemical measures revealed a positive correlation between Abeta levels and regional PiB binding.
This report confirms that PiB detects Abeta in the living patient and demonstrates that amyloid deposited as cerebral amyloid angiopathy can be the dominant source of signal.
确定活体中匹兹堡化合物B（PiB）摄取与死后组织分析中β-淀粉样蛋白（Aβ）测量值之间的对应关系。患者 一名76岁临床诊断为路易体痴呆的男性接受了氟脱氧葡萄糖（18）F和PiB正电子发射断层脑扫描。成像显示PiB有明显的区域特异性结合以及氟脱氧葡萄糖摄取异常。干预 在PiB扫描3个月后进行尸检。
尸检证实了临床诊断；此外，存在严重的脑淀粉样血管病，实质Aβ斑块数量仅为中等。生化测量显示Aβ水平与区域PiB结合之间存在正相关。
本报告证实PiB可在活体患者中检测到Aβ，并表明作为脑淀粉样血管病沉积的淀粉样蛋白可能是信号的主要来源。
