Marschalek Nils, Albert Frank, Afshordel Sarah, Meske Volker, Eckert Gunter P, Ohm Thomas G
Institut für Integrative Neuroanatomie, Charité, Universitätsmedizin Berlin, Berlin, Germany.
J Neurochem. 2015 Apr;133(1):153-61. doi: 10.1111/jnc.12959. Epub 2015 Feb 5.
Niemann Pick type C (NPC1) is a rare fatal hereditary cholesterol storage disease associated with a massive Purkinje cells loss. The mechanisms leading to neurodegeneration are still poorly understood. Different laboratories pointed to hypersensitivity to cytotoxic effects of statins (HMG-CoA reductase inhibitors) in NPC1 and suggested an underlying lack of geranylgeranyl pyrophosphate (GGPP). GGPP is a non-sterol isoprenoid essential for cell survival and differentiation. We measured GGPP levels in cerebella of a NPC1 mouse model and of wild-type littermates and found a physiological increase of GGPP levels between post-natal days 21 and 49 in wild-type mice but not in NPC mice. This further supports the hypothesis that Purkinje cell loss may be due to an extremely low level of GGPP. The progressive Purkinje cell loss in NPC starts between p21 and p49. To test the hypothesis, we used long-term organotypic slice cultures of NPC1 mice that display the natural history of NPC1 disease in vitro and tested if chronic administration of GGPP might prevent Purkinje cell loss. We did not see a beneficial effect. This suggests, in contrast to the expectations, that the relative lack of GGPP may not significantly contribute to mechanisms of Purkinje cell loss in NPC1.
尼曼-皮克C型病(NPC1)是一种罕见的致命性遗传性胆固醇贮积病,与大量浦肯野细胞丧失有关。导致神经退行性变的机制仍不清楚。不同实验室指出NPC1对他汀类药物(HMG-CoA还原酶抑制剂)的细胞毒性作用高度敏感,并提示潜在的香叶基香叶基焦磷酸(GGPP)缺乏。GGPP是细胞存活和分化所必需的一种非甾醇类异戊二烯。我们测量了NPC1小鼠模型和野生型同窝小鼠小脑内的GGPP水平,发现野生型小鼠在出生后第21天至49天之间GGPP水平有生理性升高,而NPC小鼠则没有。这进一步支持了浦肯野细胞丧失可能是由于GGPP水平极低这一假说。NPC中浦肯野细胞的进行性丧失始于出生后第21天至49天之间。为了验证这一假说,我们使用了能在体外展现NPC1疾病自然病程的NPC1小鼠长期器官型脑片培养物,并测试了长期给予GGPP是否能预防浦肯野细胞丧失。我们没有看到有益效果。这表明,与预期相反,GGPP的相对缺乏可能对NPC1中浦肯野细胞丧失的机制没有显著影响。