Sunaga K, Takahashi H, Chuang D M, Ishitani R
Group on Cellular Neurobiology, Josai University, Saitama, Japan.
Neurosci Lett. 1995 Nov 17;200(2):133-6. doi: 10.1016/0304-3940(95)12098-o.
The age-induced apoptotic death of cerebellar neurons in culture is associated with over-expression of a 38-kDa particulate protein identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Both the age-induced apoptosis and the 38-kDa protein overexpression were effectively suppressed by the presence of tetrahydroaminoacridine, an antidementia drug, or aurintricarboxylic acid. This over-expressed 38-kDa protein and purified GAPDH were found to react with a monoclonal antibody (mAb), Am-3, which was raised against amyloid plaques from Alzheimer's brain, but not with mAb, AmT-1, which was produced using synthetic amyloid beta peptide. These results raise the possibility that GAPDH is also involved in the neurodegeneration during the development of Alzheimer's disease.
培养的小脑神经元因年龄增长而发生的凋亡性死亡与一种被鉴定为甘油醛-3-磷酸脱氢酶(GAPDH)的38 kDa颗粒蛋白的过度表达有关。抗痴呆药物四氢氨基吖啶或金精三羧酸的存在有效地抑制了年龄诱导的凋亡和38 kDa蛋白的过度表达。发现这种过度表达的38 kDa蛋白和纯化的GAPDH与一种针对阿尔茨海默病大脑淀粉样斑块产生的单克隆抗体(mAb)Am-3发生反应,但不与使用合成淀粉样β肽产生的mAb AmT-1发生反应。这些结果增加了GAPDH也参与阿尔茨海默病发展过程中神经退行性变的可能性。