Lue L F, Brachova L, Civin W H, Rogers J
L.J. Roberts Center, Sun Health Research Institute, Sun City, AZ 85372, USA.
J Neuropathol Exp Neurol. 1996 Oct;55(10):1083-8.
We evaluated entorhinal cortex and superior frontal gyrus for hallmarks of Alzheimer's disease (AD) pathology, including inflammation, in three patient sets: AD patients, nondemented elderly patients with few or no neurofibrillary tangles (NFTs) and amyloid beta peptide (A beta) deposits, i.e. normal controls (NC), and nondemented elderly patients with profuse entorhinal cortex NFTs and neocortical A beta deposits, i.e. high pathology controls (HPC). Membrane attack complex (C5b-9) immunoreactivity and immune activation of microglia (MHCII expression) were used as general markers for inflammation. Compared to NC patients, AD patients exhibited significant cortical synapse loss, A beta deposition, NFT formation, and inflammation. HPC patients also had significantly elevated A beta deposition and NFT formation, but there was no evidence of synapse loss and little or no evidence of inflammation. Across patients and brain regions the measures of inflammation each accounted for significant percentages of the variance in synaptophysin immunoreactivity and each was more highly correlated with synapse estimates than NFT formation or A beta deposition.
我们在三组患者中评估了内嗅皮质和额上回是否存在阿尔茨海默病（AD）病理特征，包括炎症，这三组患者分别是：AD患者、神经原纤维缠结（NFTs）和淀粉样β肽（Aβ）沉积很少或没有的非痴呆老年患者，即正常对照（NC），以及内嗅皮质NFTs丰富且新皮质有Aβ沉积的非痴呆老年患者，即高病理对照（HPC）。膜攻击复合物（C5b - 9）免疫反应性和小胶质细胞的免疫激活（MHCII表达）被用作炎症的一般标志物。与NC患者相比，AD患者表现出显著的皮质突触丢失、Aβ沉积、NFT形成和炎症。HPC患者的Aβ沉积和NFT形成也显著升高，但没有突触丢失的证据，几乎没有或没有炎症的证据。在所有患者和脑区中，炎症指标在突触素免疫反应性的方差中各自占显著比例，并且与突触估计值的相关性均高于NFT形成或Aβ沉积。
