摘要  

       我们报告气球状神经元 (BN) 的存在是嗜银颗粒病 (AgD) 患者杏仁核的一个恒定特征。 在 10 例 AgD 病例中，BN 随机分散在整个杏仁核中，并与不同数量的嗜银颗粒 (ArG) 和 tau 免疫反应性非球囊神经元相关。 BN 被针对 αB-晶状体蛋白、磷酸化 tau（AT8、PHF-1）和磷酸化神经丝（SMI-31）的抗体强烈标记。 相比之下，AT8 免疫反应性非球囊神经元和 ArGs 始终没有被 αB-晶状体蛋白抗体染色。 我们的研究结果表明，在 AgD 中，两种不同的病理机制可能在边缘神经元中起作用：（1）tau 蛋白的异常磷酸化可能与 ArGs 的形成有关，而没有细胞膨胀或 αB-晶状体蛋白表达； (2) 过度磷酸化的 tau 蛋白和 αB-晶状体蛋白表达的积累导致与 ArGs 形成无关的细胞膨胀。 

       We report the presence of ballooned neurons (BNs) as a constant feature of amygdaloid nuclei in patients with argyrophilic grain disease (AgD). In 10 cases with AgD BNs were randomly dispersed throughout the amygdala and were associated with various numbers of argyrophilic grains (ArGs) and tau immunoreactive non-ballooned neurons. BNs were strongly labelled with antibodies against αB-crystallin, phosphorylated tau (AT8, PHF-1) and phosphorylated neurofilament (SMI-31). In contrast AT8-immunoreactive non-ballooned neurons and ArGs remained consistently unstained with the αB-crystallin antibody. Our findings suggest that in AgD two different pathological mechanisms may operate in limbic neurons: (1) abnormal phosphorylation of tau protein probably linked to the formation of ArGs without cell ballooning or αB-crystallin expression; (2) accumulation of hyperphosphorylated tau protein and αB-crystallin expression leading to cell ballooning not related to ArGs formation.
https://www.sciencedirect.com/science/article/abs/pii/S030439409800250X