McKee Ann C, Cairns Nigel J, Dickson Dennis W, Folkerth Rebecca D, Keene C Dirk, Litvan Irene, Perl Daniel P, Stein Thor D, Vonsattel Jean-Paul, Stewart William, Tripodis Yorghos, Crary John F, Bieniek Kevin F, Dams-O'Connor Kristen, Alvarez Victor E, Gordon Wayne A
Department of Neurology, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA.
Department of Pathology, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA.
Acta Neuropathol. 2016 Jan;131(1):75-86. doi: 10.1007/s00401-015-1515-z. Epub 2015 Dec 14.
Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. Like many other neurodegenerative conditions, at present, CTE can only be definitively diagnosed by post-mortem examination of brain tissue. As the first part of a series of consensus panels funded by the NINDS/NIBIB to define the neuropathological criteria for CTE, preliminary neuropathological criteria were used by 7 neuropathologists to blindly evaluate 25 cases of various tauopathies, including CTE, Alzheimer's disease, progressive supranuclear palsy, argyrophilic grain disease, corticobasal degeneration, primary age-related tauopathy, and parkinsonism dementia complex of Guam. The results demonstrated that there was good agreement among the neuropathologists who reviewed the cases (Cohen's kappa, 0.67) and even better agreement between reviewers and the diagnosis of CTE (Cohen's kappa, 0.78). Based on these results, the panel defined the pathognomonic lesion of CTE as an accumulation of abnormal hyperphosphorylated tau (p-tau) in neurons and astroglia distributed around small blood vessels at the depths of cortical sulci and in an irregular pattern. The group also defined supportive but non-specific p-tau-immunoreactive features of CTE as: pretangles and NFTs affecting superficial layers (layers II-III) of cerebral cortex; pretangles, NFTs or extracellular tangles in CA2 and pretangles and proximal dendritic swellings in CA4 of the hippocampus; neuronal and astrocytic aggregates in subcortical nuclei; thorn-shaped astrocytes at the glial limitans of the subpial and periventricular regions; and large grain-like and dot-like structures. Supportive non-p-tau pathologies include TDP-43 immunoreactive neuronal cytoplasmic inclusions and dot-like structures in the hippocampus, anteromedial temporal cortex and amygdala. The panel also recommended a minimum blocking and staining scheme for pathological evaluation and made recommendations for future study. This study provides the first step towards the development of validated neuropathological criteria for CTE and will pave the way towards future clinical and mechanistic studies.
慢性创伤性脑病(CTE)是一种神经退行性疾病,其特征是大脑内异常磷酸化的tau蛋白异常蓄积。与许多其他神经退行性疾病一样,目前,CTE只能通过对脑组织进行尸检来明确诊断。作为由美国国立神经疾病和中风研究所(NINDS)/美国国立生物医学成像和生物工程研究所(NIBIB)资助的一系列共识小组的第一部分,旨在确定CTE的神经病理学标准,7名神经病理学家使用初步神经病理学标准对25例各种tau蛋白病进行了盲法评估,包括CTE、阿尔茨海默病、进行性核上性麻痹、嗜银颗粒病、皮质基底节变性、原发性年龄相关性tau蛋白病以及关岛帕金森病痴呆综合征。结果表明,审查病例的神经病理学家之间具有良好的一致性(科恩kappa系数,0.67),审查者与CTE诊断之间的一致性甚至更好(科恩kappa系数,0.78)。基于这些结果,该小组将CTE的特征性病变定义为异常磷酸化tau(p-tau)在皮质沟深处围绕小血管分布的神经元和星形胶质细胞中蓄积,且呈不规则模式。该小组还将CTE的支持性但非特异性p-tau免疫反应性特征定义为:影响大脑皮质浅层(II-III层)的前缠结和神经原纤维缠结;海马体CA2区的前缠结、神经原纤维缠结或细胞外缠结以及CA4区的前缠结和近端树突肿胀;皮质下核中的神经元和星形胶质细胞聚集;软脑膜和脑室周围区域胶质界膜处的棘状星形胶质细胞;以及大颗粒状和点状结构。支持性非p-tau病理学包括海马体、颞叶内侧前皮质和杏仁核中的TDP-43免疫反应性神经元胞质内含物和点状结构。该小组还推荐了用于病理评估的最低限度封闭和染色方案,并对未来研究提出了建议。这项研究为制定经过验证的CTE神经病理学标准迈出了第一步,并将为未来的临床和机制研究铺平道路。