Bird T D, Levy-Lahad E, Poorkaj P, Sharma V, Nemens E, Lahad A, Lampe T H, Schellenberg G D
Department of Neurology, VA Medical Center, University of Washington Medical School, Seattle, USA.
Ann Neurol. 1996 Dec;40(6):932-6. doi: 10.1002/ana.410400619.
Mutations in three different genes on chromosomes 1, 14, and 21 cause autosomal dominant forms of familial Alzheimer's disease (FAD). Most result in an early-onset phenotype. However, several kindreds of Volga German ancestry have the same chromosome 1 gene mutation and demonstrate a relatively older mean age of onset and include individuals with late age of onset. In these families, the mean age of onset is 54.9 +/- 8.4 years (range, 40-75 years), mean age at death is 65.9 +/- 10.2 years (range, 43-88 years), and mean disease duration is 11.3 +/- 4.6 years (range, 5-23 years). This contrasts with a group of 7 families with chromosome 14 mutations in which the mean age of onset is 44.8 +/- 4.8 years (range, 30-55 years), mean age at death is 52.6 +/- 5.7 years (range, 39-65 years), and mean disease duration is 7.6 +/- 3.2 years (range, 2-17 years). (All means are significantly different in the 2 groups of families, p < 0.005.) In the chromosome 1 families, 7 persons (16%) had an age of onset at or older than 65 years and 22 (54%) survived to age 65 or older versus none in the chromosome 14 families. An example of probable nonpenetrance of disease at age 89 was also found in a chromosome 1 kindred. It is concluded that, unlike the chromosome 14 gene, mutations in the chromosome 1 FAD gene may result in individuals with a late age of onset overlapping with the more common sporadic form of the disease occurring in the general population. In light of the great variability in age of onset in persons with identical mutations, study of the genetic and environmental factors contributing to delayed onset of disease in chromosomal 1 FAD kindreds will be an important area for further investigation. Apolipoprotein E genotype may be one such factor that plays a partial role in this variability.
位于1号、14号和21号染色体上的三种不同基因发生突变会导致常染色体显性遗传形式的家族性阿尔茨海默病(FAD)。大多数突变会导致早发型表型。然而,一些具有伏尔加德意志人血统的家族具有相同的1号染色体基因突变,其发病平均年龄相对较大,其中还包括发病较晚的个体。在这些家族中,发病平均年龄为54.9±8.4岁(范围为40 - 75岁),死亡平均年龄为65.9±10.2岁(范围为43 - 88岁),平均病程为11.3±4.6年(范围为5 - 23年)。这与一组有14号染色体突变的7个家族形成对比,其发病平均年龄为44.8±4.8岁(范围为30 - 55岁),死亡平均年龄为52.6±5.7岁(范围为39 - 65岁),平均病程为7.6±3.2年(范围为2 - 17年)。(两组家族的所有平均值均存在显著差异,p < 0.005。)在1号染色体家族中,7人(16%)发病年龄在65岁及以上,22人(54%)存活至65岁及以上,而14号染色体家族中则无人如此。在一个1号染色体家族中还发现了一个89岁时可能未发病的例子。得出的结论是,与14号染色体基因不同,1号染色体FAD基因突变可能导致个体发病较晚,与普通人群中更常见的散发性疾病形式重叠。鉴于具有相同突变的个体发病年龄差异很大,研究导致1号染色体FAD家族疾病发病延迟的遗传和环境因素将是进一步研究的一个重要领域。载脂蛋白E基因型可能是在这种变异性中起部分作用的一个因素。