首页> 外文期刊>Neuropathology and applied neurobiology >Inflammatory pathology markers (activated microglia and reactive astrocytes) in early and late onset Alzheimer disease: a post mortem post mortem study
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Inflammatory pathology markers (activated microglia and reactive astrocytes) in early and late onset Alzheimer disease: a post mortem post mortem study

机译:炎症病理学标志物(活性微胶质细胞和活性星形胶质细胞)早期和晚期发作的阿尔茨海默病:后验尸验尸研究

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摘要

Aims The association between the pathological features of AD and dementia is stronger in younger old persons than in older old persons suggesting that additional factors are involved in the clinical expression of dementia in the oldest old. Cumulative data suggests that neuroinflammation plays a prominent role in Alzheimer′s disease (AD) and different studies reported an age‐associated dysregulation of the neuroimmune system. Consequently, we sought to characterize the pattern of microglial cell activation and astrogliosis in brain post mortem tissue of pathologically confirmed cases of early and late onset AD (EOAD and LOAD) and determine their relation to age. Methods Immunohistochemistry (CD68 and glial fibrillary acidic protein) with morphometric analysis of astroglial profiles in 36 cases of AD and 28 similarly aged controls. Results Both EOAD and LOAD groups had higher microglial scores in CA1, entorhinal and temporal cortices, and higher astroglial response in CA1, dentate gyrus, entorhinal and temporal cortices, compared to aged matched controls. Additionally, EOAD had higher microglial scores in subiculum, entorhinal and temporal subcortical white matter, and LOAD higher astrogliosis in CA2 region. Conclusions Overall, we found that the neuroinflammatory pathological markers in late stage AD human tissue to have a similar pattern in both EOAD and LOAD, though the severity of the pathological markers in the younger group was higher. Understanding the age effect in AD will be important when testing modifying agents that act on the neuroinflammation.
机译:旨在比老年人的广告和痴呆症的病理特征与痴呆症之间的关联比老年人更强大,这表明其他因素参与了最古老的痴呆症的痴呆症的临床表达。累积数据表明,神经引发在阿尔茨海默病(AD)中起着突出的作用,不同的研究报告了神经免疫系统的年龄相关的失调。因此,我们试图表征在病理证实早期和后期发病广告(eaod和Load)的病理证实病例的脑后验尸组织中的小细胞细胞活化和星分泌的模式,并确定其与年龄的关系。方法采用免疫组织化学(CD68和胶质纤维酸性酸性蛋白),36例AD和28例同样老化对照中的26例时差分析。结果EAD和负载基团在CA1,跑车和时间皮质中具有较高的显微痛解,以及CA1中的较高的星形响应,与老化的对照相比,CA1,牙齿齿轮,颞叶和颞蜂窝。此外,eaoid在诸例中具有较高的小胶质痛评分,并且在CA2区域中负载较高的星形症。结论总体而言,我们发现晚期AD人体组织的神经炎病理标志物在eaad和载荷中具有类似的模式,尽管较年轻群体的病理标志物的严重程度较高。了解AD中的年龄效应在测试对神经引起的炎症作用的改性剂时非常重要。

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    Neuropathology UnitCentro Hospitalar do PortoPorto Portugal;

    Life and Health Sciences Research InstituteUniversity of MinhoBraga Portugal;

    Neuropathology UnitCentro Hospitalar do PortoPorto Portugal;

    Division of Neuroscience and Experimental PsychologyUniversity of ManchesterSalford UK;

    Neuropathology UnitCentro Hospitalar do PortoPorto Portugal;

    Life and Health Sciences Research InstituteUniversity of MinhoBraga Portugal;

    Division of Neuroscience and Experimental PsychologyUniversity of ManchesterSalford UK;

    Neuropathology UnitCentro Hospitalar do PortoPorto Portugal;

    Life and Health Sciences Research InstituteUniversity of MinhoBraga Portugal;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 病理学;
  • 关键词

    ageing; Alzheimer′s disease; astrocytes; microglia; pathology;

    机译:老化;阿尔茨海默病;星形胶质细胞;小胶质细胞;病理学;

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