Cruts Marc, Van Broeckhoven Christine
Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB, Antwerp, Belgium.
Trends Genet. 2008 Apr;24(4):186-94. doi: 10.1016/j.tig.2008.01.004. Epub 2008 Mar 6.
Frontotemporal lobar degeneration (FTLD) represents a collection of neurodegenerative diseases of frontal and temporal brain regions. It has long been associated with mutations in microtubule-associated protein tau (MAPT), and more recently with loss-of-function mutations in progranulin (PGRN). Phenotypes of PGRN and MAPT mutation carriers overlap, although disease onset in PGRN carriers is a decade later. Mutations in PGRN might influence susceptibility to a wider range of neurodegenerative diseases including Alzheimer and Parkinson diseases. The recent demonstration that mutations in PGRN result in FTLD provided a novel entrance point to the molecular mechanisms leading to this disorder. The high variability in onset age and age-dependent penetrance suggests that the PGRN pathway is highly susceptible to modulating factors that might be exploited to delay the disease processes.
额颞叶变性(FTLD)是一组累及额叶和颞叶脑区的神经退行性疾病。长期以来,它一直与微管相关蛋白tau(MAPT)的突变有关,最近又与原颗粒蛋白(PGRN)的功能丧失突变有关。PGRN和MAPT突变携带者的表型有重叠,尽管PGRN携带者的疾病发病时间要晚十年。PGRN的突变可能会影响对包括阿尔茨海默病和帕金森病在内的更广泛神经退行性疾病的易感性。最近有研究表明,PGRN的突变会导致FTLD,这为导致这种疾病的分子机制提供了一个新的切入点。发病年龄的高度变异性和年龄依赖性外显率表明,PGRN通路对可能被用于延缓疾病进程的调节因子高度敏感。