In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging
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DOI：
10.1073/pnas.1409952112
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发表时间：
2015-04-21
影响因子：
11.1
通讯作者：
Kepe, Vladimir
中科院分区：
文献类型：
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作者：
Barrio, Jorge R.;Small, Gary W.;Kepe, Vladimir
慢性创伤性脑病（CTE）是一种获得性原发性tau蛋白病，具有与单次、间歇性或重复性创伤性脑损伤（TBI）持续的累积脑损伤相关的各种认知、行为和运动症状。目前尚无明确的临床诊断。在这项工作中，我们使用[F-18]FDDNP PET检测疑似CTE的退役职业美式足球运动员（n = 14）的神经病理分布的大脑模式，并将结果与认知完整的对照组（n = 28）和阿尔茨海默氏痴呆症（AD）患者（n = 24）进行比较，AD是一种与CTE相关的认知疾病。[F-18]退役运动员的FDDNP PET成像结果表明，存在与脑震荡模型一致的神经病理学模式，其中脑干白色物质束经历早期轴突损伤和沿着皮层下、边缘系统和皮层脑回路的累积轴突损伤，这些轴突损伤支持情绪、情感和行为。这种沉积模式与AD中神经病理学的进行性模式[成对螺旋丝（PHF）-tau和淀粉样蛋白-β]明显不同，后者通常始于内侧颞叶，沿着皮质默认模式网络进展，不涉及或极少涉及皮质下结构。在疑似CTE病例中的这种特定[F-18]FDDNP PET成像模式也主要与在具有轻度TBI病史和尸检确认的CTE诊断的受试者中尸检时观察到的PHF-tau分布一致。
Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.