Center for Mind and Brain, University of California, Davis, California 95618, USA.
Mov Disord. 2011 Jun;26(7):1329-36. doi: 10.1002/mds.23646. Epub 2011 Apr 11.
Older male premutation carriers of the FMR1 gene are associated with the risk of developing a late-onset neurodegenerative disorder, fragile X-associated tremor/ataxia syndrome. Although previous postmortem and in vivo magnetic resonance imaging studies have indicated white matter pathology, the regional selectivity of abnormalities, as well as their relationship with molecular variables of the FMR1 gene, has not been investigated. In this study, we used diffusion tensor imaging to study male premutation carriers with and without fragile X-associated tremor/ataxia syndrome and healthy sex-matched controls. We performed a tract of interest analysis for fractional anisotropy and axial and radial diffusivities of major white matter tracts in the cerebellar-brain stem and limbic systems. Compared with healthy controls, patients with fragile X-associated tremor/ataxia syndrome showed significant reductions of fractional anisotropy in multiple white matter tracts, including the middle cerebellar peduncle, superior cerebellar peduncle, cerebral peduncle, and the fornix and stria terminalis. Significant reduction of fractional anisotropy in these tracts was confirmed by voxel-wise analysis using tract-based spatial statistics. Analysis of axial and radial diffusivities showed significant elevation of these measures in middle cerebellar peduncle, even among premutation carriers without fragile X-associated tremor/ataxia syndrome. Furthermore, regression analyses demonstrated a clear inverted U-shaped relationship between CGG-repeat size and axial and radial diffusivities in middle cerebellar peduncle. These results provide new evidence from diffusion tensor imaging for white matter abnormalities in the cerebellar-brain stem and limbic systems among individuals with the fragile X premutation and suggest the involvement of molecular mechanisms related to the FMR1 gene in their white matter pathology.
携带 FMR1 基因前突变的老年男性与发生迟发性神经退行性疾病,脆性 X 相关震颤/共济失调综合征的风险相关。尽管之前的尸检和体内磁共振成像研究表明存在白质病理学,但异常的区域选择性以及它们与 FMR1 基因的分子变量之间的关系尚未得到研究。在这项研究中,我们使用弥散张量成像研究了携带脆性 X 相关震颤/共济失调综合征和无脆性 X 相关震颤/共济失调综合征的男性前突变携带者以及健康的性别匹配对照者。我们对小脑-脑干和边缘系统的主要白质束的分数各向异性以及轴向和径向弥散系数进行了感兴趣区分析。与健康对照组相比,脆性 X 相关震颤/共济失调综合征患者的多个白质束的分数各向异性明显降低,包括小脑中脑脚、上小脑脚、大脑脚和穹窿和终纹。使用基于束的空间统计学的体素分析证实了这些束中的分数各向异性的明显降低。对轴向和径向弥散系数的分析表明,即使在没有脆性 X 相关震颤/共济失调综合征的前突变携带者中,这些束中的这些指标也明显升高。此外,回归分析表明,在小脑中脑脚中,CGG 重复大小与轴向和径向弥散系数之间存在明显的倒 U 形关系。这些结果从弥散张量成像为脆性 X 前突变个体小脑-脑干和边缘系统中的白质异常提供了新的证据,并表明与 FMR1 基因相关的分子机制参与了其白质病理学。