Department of Old Age Psychiatry and Psychotic Disorders, Medical University of Lodz, 8/10 Czechosłowacka st., 92-216 Lodz, Poland.
Folia Neuropathol. 2012;50(1):74-84.
Microglia are the resident immune cells of the CNS. They are involved in the pathogenesis of diverse neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease, prion diseases as well as multiple sclerosis, amyotrophic lateral sclerosis and AIDS dementia complex. Activated microglia up-regulate many surface receptors such as the major histocompatibility complex (MHC) or complement receptors and secrete a variety of soluble biologically active factors, which are either neurotrophic (e.g. Glia-Derived Neurotrophic Factor [GDNF]) or proinflammatory and neurotoxic (e.g. tumour necrosis factor alpha [TNF-α], interleukin 1β [IL-1β], nitric oxide [NO], superoxide, eicosanoids, quinolinic acid).
The aim of this work was to assess differences in the expression of microglial markers (ferritin, CD68, and HLA-DR) between AD and Creutzfeldt-Jakob disease (CJD) brains.
Analyses were performed on 65 slices derived from 26 brains [46 CJD (20 brains), 12 AD (4 brains) and 7 controls (2 brains)]. Slices were labelled immunohistochemically using anti-ferritin, anti-HLA-DR and anti-CD68 antibodies. The nonparametric Mann-Whitney U test was used to assess quantitative differences between groups.
The expression of microglia markers (HLA-DR and CD68) is more noticeable in CJD than in AD or control brains. There is no difference between AD and controls. The latter statement is only true in the case of using HLA-DR or CD-68 labelling. Furthermore, ferritin is not a recommended marker in this context.
CNS inflammation is more prominent in CJD than in AD or controls. The lack of differences between AD and controls may result from a relatively advanced neurodegeneration in AD brains. In late phases of AD, inflammation is no longer present, in contrast to the early stages of the disease.
小胶质细胞是中枢神经系统的固有免疫细胞。它们参与多种神经退行性疾病的发病机制，如阿尔茨海默病（AD）、帕金森病、朊病毒病以及多发性硬化症、肌萎缩侧索硬化症和艾滋病痴呆综合征。激活的小胶质细胞上调许多表面受体，如主要组织相容性复合体（MHC）或补体受体，并分泌多种具有生物活性的可溶性因子，这些因子既有神经营养作用（如胶质细胞源性神经营养因子[GDNF]），也有促炎和神经毒性作用（如肿瘤坏死因子-α[TNF-α]、白细胞介素 1β[IL-1β]、一氧化氮[NO]、超氧化物、类花生酸、喹啉酸）。
本研究旨在评估 AD 和克雅氏病（CJD）大脑中小胶质细胞标志物（铁蛋白、CD68 和 HLA-DR）表达的差异。
对 26 例脑标本（46 例 CJD[20 例]、12 例 AD[4 例]和 7 例对照[2 例]）的 65 个切片进行了分析。使用抗铁蛋白、抗 HLA-DR 和抗 CD68 抗体对切片进行免疫组织化学标记。采用非参数 Mann-Whitney U 检验评估组间的定量差异。
CJD 大脑中小胶质细胞标志物（HLA-DR 和 CD68）的表达比 AD 或对照大脑更明显。AD 与对照之间无差异。后一种说法仅在使用 HLA-DR 或 CD-68 标记时成立。此外，铁蛋白在此情况下不是推荐的标志物。
CNS 炎症在 CJD 中比在 AD 或对照中更为明显。AD 与对照之间无差异可能是由于 AD 大脑中神经退行性变相对较晚。在 AD 的晚期，炎症不再存在，而在疾病的早期则存在炎症。
