Nelson Peter T, Abner Erin L, Scheff Stephen W, Schmitt Frederick A, Kryscio Richard J, Jicha Gregory A, Smith Charles D, Patel Ela, Markesbery William R
Department of Pathology and Division of Neuropathology, University of Kentucky Medical Center, Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky, Lexington, KY 40536, USA.
Neurosci Lett. 2009 Feb 6;450(3):336-9. doi: 10.1016/j.neulet.2008.11.006. Epub 2008 Nov 8.
We studied Alzheimer's disease (AD) pathology in the precuneus and surrounding brain areas. Anatomically, the precuneus corresponds to the medial portion of human cerebral cortical Brodmann Area 7. This study utilized patients from the University of Kentucky Alzheimer's Disease Center autopsy cohort. Data from 47 brains were used comprising patients of differing antemortem cognitive impairment severities, each with longitudinal clinical data and extensive neuropathological data. We assessed whether the precuneus and surrounding areas are differentially vulnerable to AD-type pathological lesions (diffuse amyloid plaques, neuritic amyloid plaques, and neurofibrillary tangles). Eleven areas of brain were evaluated for each case: amygdala, hippocampal CA1, subiculum, entorhinal cortex, frontal cortex, superior and middle temporal gyri, inferior parietal lobule, occipital cortex, posterior cingulate gyrus, Brodmann Area 31, and the precuneus proper. Like other areas of neocortex, the precuneus demonstrated increased diffuse and neuritic amyloid plaques early in the evolution in AD, and increased neurofibrillary tangles late in AD. Correcting for the antemortem cognitive status of the patients, there was no evidence of an increase in the density of AD-type pathology in the precuneus or neighboring areas relative to other areas of cerebral neocortex. Our results are not consistent with the idea that the precuneus is involved in a special way with plaques or tangles relative to other areas of neocortex.
我们研究了楔前叶及周围脑区的阿尔茨海默病（AD）病理学。从解剖学角度来看，楔前叶相当于人类大脑皮质布罗德曼第7区的内侧部分。本研究使用了来自肯塔基大学阿尔茨海默病中心尸检队列的患者。研究采用了47例大脑的数据，这些患者生前认知障碍严重程度各异，均有纵向临床数据和广泛的神经病理学数据。我们评估了楔前叶及周围区域是否对AD型病理病变（弥漫性淀粉样斑块、神经炎淀粉样斑块和神经原纤维缠结）具有不同的易损性。对每个病例的11个脑区进行了评估：杏仁核、海马CA1区、海马下脚、内嗅皮质、额叶皮质、颞上回和颞中回、顶下小叶、枕叶皮质、后扣带回、布罗德曼第31区以及楔前叶本身。与新皮质的其他区域一样，楔前叶在AD病程早期显示出弥漫性和神经炎淀粉样斑块增加，在AD病程晚期显示出神经原纤维缠结增加。校正患者生前的认知状态后，没有证据表明楔前叶或邻近区域的AD型病理密度相对于大脑新皮质的其他区域有所增加。我们的结果与楔前叶相对于新皮质其他区域以特殊方式参与斑块或缠结形成的观点不一致。
