Slevin Mark, Liu Donghui, Ferris Glenn, Al-Hsinawi Malik, Al-Baradie Raid, Krupinski Jerzy
Manchester Metropolitan University, School of Healthcare Science, Manchester, United Kingdom.
Turk Patoloji Derg. 2017;33(1):25-29. doi: 10.5146/tjpath.2016.01374.
We have previously shown that monomeric-C-reactive protein is deposited in significant quantities within the brain parenchyma after stroke. Since we have recently identified a possible role of this protein in supporting neurodegeneration and aberrant vascular development we identified a small group of post-mortem brain samples from individuals who had Alzheimer's disease and evidence of tissue infarction/ micro-infarction on histological examination.
We used immunohistochemistry staining to identify the monomeric-C-reactive protein expressed in the infarcted brain tissues.
We showed that monomeric-C-reactive protein deposition was highest in those regions affected by stroke or vascular disruption, and that within those same areas, there was more interaction and co-localization between major classical proteins of neurodegeneration (β-amyloid and tau).
We hypothesise that vascular disruption and concomitant release of monomeric-C-reactive protein within the brain tissue could exacerbate ongoing neurological damage via stimulation of neuro-inflammation and from direct consequences of its action on both neuronal and vascular cells.
我们之前已经表明，单体C反应蛋白在中风后大量沉积于脑实质内。由于我们最近发现该蛋白在支持神经退行性变和异常血管发育方面可能发挥作用，因此我们从患有阿尔茨海默病且在组织学检查中有组织梗死/微梗死证据的个体中挑选了一小批尸检脑样本。
我们使用免疫组织化学染色来鉴定梗死脑组织中表达的单体C反应蛋白。
我们发现，单体C反应蛋白沉积在受中风或血管破坏影响的区域最高，并且在这些相同区域内，神经退行性变的主要经典蛋白（β淀粉样蛋白和tau蛋白）之间存在更多的相互作用和共定位。
我们推测，脑组织内的血管破坏和单体C反应蛋白的伴随释放可能通过刺激神经炎症以及其对神经元和血管细胞作用的直接后果，加剧正在进行的神经损伤。
