Heckmann Jeannine M, Low Wee-Chuang, de Villiers Cora, Rutherfoord Stuart, Vorster Alvera, Rao Harpal, Morris Christopher M, Ramesar Raj S, Kalaria Raj N
Division of Neurology, Groote Schur Hospital and University of Cape Town, South Africa.
Brain. 2004 Jan;127(Pt 1):133-42. doi: 10.1093/brain/awh009. Epub 2003 Oct 21.
Genetically determined Alzheimer's disease (AD) is virtually unknown in Africa. We report clinicopathological findings and a presenilin 1 (PS1) mutation associated with early-onset AD in a large Xhosa family from Southern Africa. Twelve individuals spanning four generations were affected, four of whom underwent clinical and psychometric evaluation. Their phenotype was characterized by memory impairment beginning in the early part of the fifth decade, with progressive dementing illness lasting 6-7 years that did not appear to be modified by the presence of an apolipoprotein E (APOE)-epsilon 4 allele. Initial linkage-based analysis using known DNA markers suggested allele cosegregation with a locus on chromosome 14. Direct sequencing of the PS1 gene disclosed a novel I143M (ATT to ATG at nucleotide 677) mutation that lies in a cluster in the second transmembrane domain of the protein. Examination of the proband's brain at autopsy revealed severe AD pathology characterized by neuronal loss, abundant beta amyloid (A beta) neuritic plaques (A beta 42) and neurofibrillary degeneration extending into the brainstem. The phenotype of the I143M mutation was clearly associated with a high degree of neurofibrillary change compared with early-onset sporadic AD cases. Although sporadic cases of AD do exist in African populations, our study confirms the existence of early-onset familial AD among indigenous Southern Africans.
在非洲,由基因决定的阿尔茨海默病(AD)几乎无人知晓。我们报告了来自南部非洲一个大型科萨族家庭中与早发性AD相关的临床病理发现及早老素1(PS1)突变。四代人中的12人患病,其中4人接受了临床和心理测量评估。他们的表型特征为在50岁出头开始出现记忆障碍,患有进行性痴呆疾病,病程持续6至7年,载脂蛋白E(APOE)-ε4等位基因的存在似乎并未改变病情。最初使用已知DNA标记进行的基于连锁的分析表明,等位基因与14号染色体上的一个位点共分离。PS1基因的直接测序揭示了一个新的I143M(第677位核苷酸处的ATT突变为ATG)突变,该突变位于该蛋白第二个跨膜结构域的一个簇中。尸检时对先证者大脑的检查显示出严重的AD病理特征,包括神经元丢失、大量β淀粉样蛋白(Aβ)神经炎性斑块(Aβ42)以及延伸至脑干的神经原纤维变性。与早发性散发性AD病例相比,I143M突变的表型显然与高度的神经原纤维变化有关。尽管非洲人群中确实存在散发性AD病例,但我们的研究证实了南部非洲原住民中存在早发性家族性AD。