美国一项新研究显示，一个被称为CLU的阿尔茨海默氏症（早老性痴呆症）风险基因早在患者发病前50年就开始损害大脑。研究人员说，这种损害不会表现出症状，但能通过核磁共振扫描观察到。
CLU基因是在2009年与另外两个阿尔茨海默氏症风险基因一起被发现的。当时有研究认为，携带CLU基因的人罹患这种痴呆症的风险要高16%，但其作用机制并没有弄清。
美国加州大学洛杉矶分校的研究人员在新一期《神经科学期刊》网络上报告说，CLU基因损害覆盖在大脑神经元外侧起保护作用的髓鞘质，使其功能减弱，最终导致阿尔茨海默氏症在晚年发作。
研究人员表示，携带CLU基因的人，在青少年时期并不会出现认知能力减退，因为大脑能自动修补。但随着年龄增长，自动修补能力减弱，认知能力就会逐渐减退。
研究人员还发现，CLU基因并非少数人才有，白人携带这种基因的比例高达88%。
报告主要撰稿人、神经学教授保罗·汤普森说，认识这一基因可帮助阿尔茨海默氏症潜在病人提前50年采取预防措施，包括坚持锻炼身体及保持健康的饮食习惯等。（生物谷Bioon.com）
生物谷推荐原文出处：
The Journal of Neuroscience DOI:10.1523/?JNEUROSCI.5794-10.2011
Common Alzheimer's Disease Risk Variant Within the CLU Gene Affects White Matter Microstructure in Young Adults
Meredith N. Braskie1, Neda Jahanshad, Jason L. Stein1, Marina Barysheva, Katie L. McMahon, Greig I. de Zubicaray, Nicholas G. Martin, Margaret J. Wright, John M. Ringman, Arthur W. Toga1, and Paul M. Thompson1
There is a strong genetic risk for late-onset Alzheimer's disease (AD), but so far few gene variants have been identified that reliably contribute to that risk. A newly confirmed genetic risk allele C of the clusterin (CLU) gene variant rs11136000 is carried by ～88% of Caucasians. The C allele confers a 1.16 greater odds of developing late-onset AD than the T allele. AD patients have reductions in regional white matter integrity. We evaluated whether the CLU risk variant was similarly associated with lower white matter integrity in healthy young humans. Evidence of early brain differences would offer a target for intervention decades before symptom onset. We scanned 398 healthy young adults (mean age, 23.6 ± 2.2 years) with diffusion tensor imaging, a variation of magnetic resonance imaging sensitive to white matter integrity in the living brain. We assessed genetic associations using mixed-model regression at each point in the brain to map the profile of these associations with white matter integrity. Each C allele copy of the CLU variant was associated with lower fractional anisotropy—a widely accepted measure of white matter integrity—in multiple brain regions, including several known to degenerate in AD. These regions included the splenium of the corpus callosum, the fornix, cingulum, and superior and inferior longitudinal fasciculi in both brain hemispheres. Young healthy carriers of the CLU gene risk variant showed a distinct profile of lower white matter integrity that may increase vulnerability to developing AD later in life.
