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非痴呆的阿尔茨海默病病理学中间阶段个体的神经元基因表达。

Neuronal gene expression in non-demented individuals with intermediate Alzheimer's Disease neuropathology.

机构信息

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ 85004, USA.

出版信息

Neurobiol Aging. 2010 Apr;31(4):549-66. doi: 10.1016/j.neurobiolaging.2008.05.013. Epub 2008 Jun 24.

Abstract

While the clinical and neuropathological characterization of Alzheimer's Disease (AD) is well defined, our understanding of the progression of pathologic mechanisms in AD remains unclear. Post-mortem brains from individuals who did not fulfill clinical criteria for AD may still demonstrate measurable levels of AD pathologies to suggest that they may have presented with clinical symptoms had they lived longer or are able to stave off disease progression. Comparison between such individuals and those clinically diagnosed and pathologically confirmed to have AD will be key in delineating AD pathogenesis and neuroprotection. In this study, we expression profiled laser capture microdissected non-tangle bearing neurons in 6 post-mortem brain regions that are differentially affected in the AD brain from 10 non-demented individuals demonstrating intermediate AD neuropathologies (NDAD; Braak stage of II through IV and CERAD rating of moderate to frequent) and evaluated this data against that from individuals who have been diagnosed with late onset AD as well as healthy elderly controls. We identified common statistically significant expression changes in both NDAD and AD brains that may establish a degenerative link between the two cohorts, in addition to NDAD specific transcriptomic changes. These findings pinpoint novel targets for developing earlier diagnostics and preventative therapies for AD prior to diagnosis of probable AD. We also provide this high-quality, low post-mortem interval (PMI), cell-specific, and region-specific NDAD/AD reference data set to the community as a public resource.

摘要

虽然阿尔茨海默病(AD)的临床和神经病理学特征已经得到很好的定义,但我们对 AD 病理机制进展的理解仍不清楚。没有达到 AD 临床标准的个体死后大脑中仍可能存在可测量水平的 AD 病理学,这表明如果他们活得更长或能够延缓疾病进展,他们可能已经出现了临床症状。比较这些个体与那些临床诊断和病理证实患有 AD 的个体,对于阐明 AD 的发病机制和神经保护至关重要。在这项研究中,我们对 6 个死后大脑区域的非缠结神经元进行了激光捕获显微解剖,并对 10 名具有中间 AD 神经病理学(AD 大脑中受影响不同的 Braak 阶段 II 至 IV 和 CERAD 评分为中度至频繁)的非痴呆个体进行了表达谱分析,并将这些数据与被诊断为晚期 AD 的个体以及健康的老年对照组进行了比较。我们在 NDAD 和 AD 大脑中都发现了常见的统计学上显著的表达变化,这些变化可能在这两个队列之间建立了一种退行性联系,除了 NDAD 特定的转录组变化。这些发现为 AD 的早期诊断和预防治疗提供了新的靶点,从而可以在可能的 AD 诊断之前进行诊断。我们还为社区提供了这个高质量、低死后间隔(PMI)、细胞特异性和区域特异性的 NDAD/AD 参考数据集,作为公共资源。

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