Mayeux R, Ottman R, Maestre G, Ngai C, Tang M X, Ginsberg H, Chun M, Tycko B, Shelanski M
Gertrude H. Sergievsky Center, Columbia University, New York, NY 10032.
Neurology. 1995 Mar;45(3 Pt 1):555-7. doi: 10.1212/wnl.45.3.555.
The apolipoprotein-epsilon 4 allele increases the risk of Alzheimer's disease (AD), but cerebral deposition of beta-amyloid with age, a genetic mutation, or head injury may contribute to the pathogenesis of this disease. We examined the risks of AD associated with traumatic head injury and apolipoprotein-epsilon 4 in 236 community-dwelling elderly persons. A 10-fold increase in the risk of AD was associated with both apolipoprotein-epsilon 4 and a history of traumatic head injury, compared with a two-fold increase in risk with apolipoprotein-epsilon 4 alone. Head injury in the absence of an apolipoprotein-epsilon 4 allele did not increase risk. These data imply that the biological effects of head injury may increase the risk of AD, but only through a synergistic relationship with apolipoprotein-epsilon 4.
载脂蛋白ε4等位基因会增加患阿尔茨海默病（AD）的风险，但随着年龄增长、基因突变或头部受伤导致的β-淀粉样蛋白在大脑中的沉积可能会促使该病的发病。我们对236名居住在社区的老年人进行了研究，以检测与创伤性脑损伤及载脂蛋白ε4相关的AD风险。与仅携带载脂蛋白ε4时风险增加两倍相比，载脂蛋白ε4和有创伤性脑损伤病史都会使AD风险增加10倍。不存在载脂蛋白ε4等位基因时的头部损伤不会增加风险。这些数据表明，头部损伤的生物学效应可能会增加AD风险，但仅通过与载脂蛋白ε4的协同关系来实现。
