Yang Wendy W, Dodge James C, Passini Marco A, Taksir Tatyana V, Griffiths Denise, Schuchman Edward H, Cheng Seng H, Shihabuddin Lamya S
Genzyme Corporation, One Mountain Road, Framingham, MA 01701-9322, USA.
Exp Neurol. 2007 Oct;207(2):258-66. doi: 10.1016/j.expneurol.2007.06.017. Epub 2007 Jul 10.
Niemann-Pick A disease (NPD-A) is caused by a deficiency of acid sphingomyelinase (ASM) leading to the intracellular accumulation of sphingomyelin and cholesterol in lysosomes. We evaluated the effects of direct intraparenchymal brain injections of purified recombinant human ASM (hASM) at correcting the storage pathology in a mouse model of NPD-A (ASMKO). Different doses (0.1 ng to 10 mug of hASM) were injected into the right hemisphere of the hippocampus and thalamus of 12- to 14-week-old ASMKO mice. Immunohistochemical analysis after 1 week indicated that animals treated with greater than 1 mug hASM/site showed detectable levels of enzyme around the injected regions. However, localized clearance of sphingomyelin and cholesterol storage were observed in animals administered lower doses of enzyme, starting at 100 ng hASM/site. Areas of correction were also noted at distal sites such as in the contralateral hemispheres. Indications of storage re-accumulation were seen after 2 weeks post-injection. Injections of hASM did not cause any significant cell infiltration, astrogliosis, or microglial activation. These results indicate that intraparenchymal injection of hASM is associated with minimal toxicity and can lead to regional reductions in storage pathology in the ASMKO mouse.
尼曼-匹克病A型(NPD-A)是由酸性鞘磷脂酶(ASM)缺乏引起的,导致溶酶体中鞘磷脂和胆固醇在细胞内蓄积。我们评估了在NPD-A小鼠模型(ASMKO)中经脑实质内直接注射纯化的重组人ASM(hASM)对纠正储存病理的效果。将不同剂量(0.1纳克至10微克的hASM)注射到12至14周龄ASMKO小鼠的海马体和丘脑右半球。1周后的免疫组织化学分析表明,每部位注射大于1微克hASM治疗的动物在注射区域周围显示出可检测到的酶水平。然而,在每部位注射低至100纳克hASM的动物中观察到鞘磷脂和胆固醇储存的局部清除。在诸如对侧半球等远端部位也注意到了纠正区域。注射后2周出现储存再蓄积迹象。注射hASM未引起任何明显的细胞浸润、星形胶质细胞增生或小胶质细胞活化。这些结果表明,脑实质内注射hASM毒性极小,可导致ASMKO小鼠储存病理的区域减少。