Correlations between cortical and subcortical tau pathology
Correlations between cortical and subcortical tau pathology
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DOI：
10.1111/j.1365-2990.2011.01244.x
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发表时间：
2012-10-01
影响因子：
5
通讯作者：
Jellinger, K.
中科院分区：
文献类型：
--
作者：
Attems, J.;Thomas, A.;Jellinger, K.
J. atts， A. Thomas和K. Jellinger（2012）神经病理学和应用神经生物学38,582590皮层和皮层下tau病理的相关性目的：最近的研究表明，阿尔茨海默病（AD）的tau病理最初并不表现在大脑皮层，而是表现在特定的皮层下核，特别是蓝斑核（LC）。在这项研究中，我们将嗅觉和脑干tau病理与神经性Braak分期联系起来。方法：239例未选择的尸检病例（女性57.3%，男性42.7%；年龄55102岁，平均82.8±9.7 SD年；AD 44.8%；非痴呆对照组31.8%；帕金森病5.0%；伴路易体痴呆2.5%；AD +路易体病15.9%）。标准化神经病理学检查包括LC、黑质（SN）、迷走神经背运动核（dmX）和嗅球（OB）的tau病变免疫组织化学和半定量评估。结果：在Braak 0期，OB中有52.9%出现tau病理（通常是非常稀疏的缠结前物质），SN/LC中有44%。随着Braak分期的增加，OB和皮层下tau病理的患病率也随之增加，在Braak分期中，OB、SN和LC分别达到100%，dmX达到95.2%。OB和皮质下核中tau病理的严重程度与Braak分期显著相关（P < 0.001），在控制相应区域伴随的a-突触核蛋白病理时，这些相关性仍然具有统计学意义。结论：我们发现OB、LC、SN和dmX tau病理在AD中的患病率和严重程度随着Braak分期的增加而增加，这表明这些区域在AD进展过程中越来越多地参与，而不是代表最初受AD相关tau病理影响的部位。
J. Attems, A. Thomas and K. Jellinger (2012) Neuropathology and Applied Neurobiology38, 582590 Correlations between cortical and subcortical tau pathology Aim: Recent studies indicate that tau pathology in Alzheimer's disease (AD) does not initially manifest in the cerebral cortex but in selected subcortical nuclei, in particular the locus ceruleus (LC). In this study we correlate both olfactory and brainstem tau pathology with neuritic Braak stages. Methods: We examined 239 unselected autopsy cases (57.3% female, 42.7% male; aged 55102, mean 82.8 +/- 9.7 SD years; AD, 44.8%; non-demented controls, 31.8%; Parkinson's disease, 5.0%; dementia with Lewy bodies, 2.5%; AD + Lewy body disease, 15.9%). Neuropathological examination according to standardized methods included immunohistochemistry and semiquantitative assessment of tau lesions in LC, substantia nigra (SN), dorsal motor nucleus of nervus vagus (dmX), and olfactory bulb (OB). Results: In Braak stage 0, tau pathology (usually very sparse pretangle material) was seen in the OB in 52.9% and in the SN/LC in 44%. The prevalence of OB and subcortical tau pathology increased with increasing Braak stages and reached 100% in OB, SN and LC and 95.2% in dmX in Braak stage VI, respectively. The severity of tau pathology in OB and subcortical nuclei significantly (P < 0.001) correlated with Braak stages and these correlations remained statistically significant when controlling for concomitant a-synuclein pathology in the respective regions. Conclusions: Our finding of an increase in both prevalence and severity of OB, LC, SN and dmX tau pathology in AD with increasing Braak stages suggests that these regions become increasingly involved during AD progression rather than representing sites initially affected by AD-associated tau pathology.