FAMILIAL ALZHEIMER'S DISEASE PRESENLIN I (PSI)MUTATIONS AND

我们构建了表达人APP和PSI的细胞系 蛋白质使用小鼠neuroplastorna细胞（N2 a细胞），并研究了 通过分析AP肽分析PSI突变对AP产生的影响 转染的细胞调节的细胞培养基中的组合物 与人类APP和PSI的cDNA。 我们还研究了PSI的作用 通过分析蛋白水解降解， 培养细胞中合成AP肽的产物（API-40和API-42 用野生型和突变型人PSI cDNA转染。 最后，我们 分析人脑脊液中的AP肽。 脑脊液（CSF）和脑 具有PSI突变的AD患者的组织样本，以确定是否 我们可以确定患者的异常模式和水平， 疾病

We have constructed a cell line for expressing human APP and PSI proteins using mouse neuroplastorna cells (N2a cell) and studied the effect of PSI mutations on AP production by analyzing AP peptide composition in cell culture media conditioned by cells transfected with human APP and PSI cDNAs. We have also studied the effect of PSI mutations on AP degradation by analyzing proteolytic degradation products of synthetic AP peptide (API-40 and API-42) in cultured cells transfectes with wildtype and mutant human PSI cDNAs. Finally, we are analyzing AP peptides in human cerebrospinal. fluid (CSF) and brain tissue specimens of AD patient with PSI mutations to determine whether we can determine abnon-nal pattern and levels in patients with disease.