Ng Steven Y, Villemagne Victor L, Masters Colin L, Rowe Christopher C
Department of Nuclear Medicine and Centre for Positron Emission Tomography, Austin Health, Melbourne, Australia.
Arch Neurol. 2007 Aug;64(8):1140-4. doi: 10.1001/archneur.64.8.1140.
A progressive decline in episodic memory affecting activities of daily living is the usual clinical presentation of Alzheimer disease. However, patients presenting with atypical or focal clinical symptoms such as language or visuospatial dysfunction often pose a diagnostic challenge.
To explore the presence and topography of beta amyloid (Abeta) as measured by carbon 11-labeled Pittsburgh Compound B ((11)C-PiB) in patients with atypical presentations of dementia.
DESIGN, SETTING, AND PARTICIPANTS: At a tertiary referral center for memory disorders, 15 healthy controls, 10 patients with Alzheimer disease, a patient with primary progressive aphasia (PPA), and a patient with posterior cortical atrophy (PCA) underwent (11)C-PiB positron emission tomographic studies. Retention of (11)C-PiB was compared between different groups using statistical parametric mapping.
The topography of cortical (11)C-PiB binding in atypical vs typical Alzheimer disease.
Cortical (11)C-PiB binding was higher in the group with Alzheimer disease and in the patients with PPA and PCA than the controls (P < .001). Both patients with atypical dementia had a similar (11)C-PiB binding pattern to Alzheimer disease although (11)C-PiB retention was higher on the left cerebral hemisphere in the patient with PPA (P < .01) and higher in the occipital cortex in the patient with PCA (P < .01).
The presence of distinctive focal (11)C-PiB retention patterns was demonstrated in 2 patients with atypical onset of dementia. Pittsburgh Compound B has the potential to facilitate differential diagnosis of dementia and identify patients who could benefit from specific therapeutic strategies aimed at beta amyloid reduction.
情景记忆进行性减退并影响日常生活活动是阿尔茨海默病常见的临床表现。然而，出现非典型或局灶性临床症状（如语言或视觉空间功能障碍）的患者常常带来诊断挑战。
探讨以碳11标记的匹兹堡化合物B（（11）C-PiB）测量的β淀粉样蛋白（Aβ）在非典型痴呆表现患者中的存在情况及分布。
设计、地点和参与者：在一家记忆障碍三级转诊中心，15名健康对照者、10名阿尔茨海默病患者、1名原发性进行性失语（PPA）患者和1名后皮质萎缩（PCA）患者接受了（11）C-PiB正电子发射断层扫描研究。使用统计参数映射比较不同组之间（11）C-PiB的滞留情况。
非典型与典型阿尔茨海默病中皮质（11）C-PiB结合的分布。
阿尔茨海默病组、PPA患者和PCA患者的皮质（11）C-PiB结合高于对照组（P <.001）。两名非典型痴呆患者的（11）C-PiB结合模式与阿尔茨海默病相似，尽管PPA患者左脑半球的（11）C-PiB滞留更高（P <.01），PCA患者枕叶皮质的（11）C-PiB滞留更高（P <.01）。
在2例非典型起病的痴呆患者中证实存在独特的局灶性（11）C-PiB滞留模式。匹兹堡化合物B有潜力促进痴呆的鉴别诊断，并识别可能从旨在降低β淀粉样蛋白的特定治疗策略中获益的患者。
