Yoshizawa T, Komatsuzaki Y, Iwamoto H, Mizusawa H, Kanazawa I
Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Japan.
J Neurol Sci. 1993 Jul;117(1-2):12-5. doi: 10.1016/0022-510x(93)90147-q.
We investigated a C to T transition at base pair 2149 in the amyloid precursor protein gene in 41 Japanese cases of early-onset familial Alzheimer's disease (FAD), late-onset FAD and sporadic Alzheimer's disease (AD) by polymerase chain reaction and restriction enzyme polymorphism with BclI. Among 9 early-onset FAD patients derived from independent families, only one patient had the mis-sense mutation. Neither 5 patients with late-onset FAD nor 27 patients with sporadic AD had the mutation. Our result and the previous reports from Japan indicate that this type of mis-sense mutation is present in several cases of Japanese early-onset FAD. On the other hand, our data suggest that this mutation is not a common cause of Japanese early-onset FAD. Moreover, this mutation could be absent in late-onset FAD and sporadic AD in Japan. Because the mutation has been reported to be rare in Caucasian early-onset FAD and to be absent in Caucasian late-onset FAD and sporadic AD, the situation of this mutation in Alzheimer's disease may be common beyond the ethnic background.
我们通过聚合酶链反应和BclI限制性酶切多态性,对41例日本早发型家族性阿尔茨海默病(FAD)、晚发型FAD和散发性阿尔茨海默病(AD)患者的淀粉样前体蛋白基因第2149位碱基对处的C到T转换进行了研究。在来自独立家族的9例早发型FAD患者中,只有1例患者存在错义突变。5例晚发型FAD患者和27例散发性AD患者均未发生该突变。我们的研究结果以及日本之前的报道表明,这种错义突变在部分日本早发型FAD病例中存在。另一方面,我们的数据表明该突变并非日本早发型FAD的常见病因。此外,在日本的晚发型FAD和散发性AD中可能不存在这种突变。由于据报道该突变在白种人早发型FAD中罕见,在白种人晚发型FAD和散发性AD中不存在,因此在阿尔茨海默病中这种突变的情况可能不受种族背景影响而普遍存在。