Department of Neurology, Johns Hopkins Medicine, Baltimore, Maryland, United States of America.
PLoS One. 2012;7(2):e29522. doi: 10.1371/journal.pone.0029522. Epub 2012 Feb 16.
Careful characterization of the phenotype and genotype of Huntington disease (HD) can foster better understanding of the condition.
We conducted a cohort study in the United States, Canada, and Australia of members of families affected by HD. We collected demographic and clinical data, conducted the Unified Huntington's Disease Rating Scale and Mini-Mental State Examination, and determined Huntingtin trinucleotide CAG repeat length. We report primarily on cross-sectional baseline data from this recently completed prospective, longitudinal, observational study.
As of December 31, 2009, 2,318 individuals enrolled; of these, 1,985 (85.6%) were classified into six analysis groups. Three groups had expanded CAG alleles (36 repeats or more): individuals with clinically diagnosed HD [n = 930], and clinically unaffected first-degree relatives who had previously pursued [n = 248] or not pursued [n = 112] predictive DNA testing. Three groups lacked expanded alleles: first-degree relatives who had previously pursued [n = 41] or not pursued [n = 224] genetic testing, and spouses and caregivers [n = 430]. Baseline mean performance differed across groups in all motor, behavioral, cognitive, and functional measures (p<0.001). Clinically unaffected individuals with expanded alleles weighed less (76.0 vs. 79.6 kg; p = 0.01) and had lower cognitive scores (28.5 vs. 29.1 on the Mini Mental State Examination; p = 0.008) than individuals without expanded alleles. The frequency of "high normal" repeat lengths (27 to 35) was 2.5% and repeat lengths associated with reduced penetrance (36 to 39) was 2.7%.
Baseline analysis of COHORT study participants revealed differences that emerge prior to clinical diagnosis. Longitudinal investigation of this cohort will further characterize the natural history of HD and genetic and biological modifiers.
Clinicaltrials.gov NCT00313495.
对亨廷顿病(HD)的表型和基因型进行仔细描述可以帮助我们更好地了解这种疾病。
我们在美国、加拿大和澳大利亚开展了一项针对受 HD 影响的家族成员的队列研究。我们收集了人口统计学和临床数据,进行了统一亨廷顿病评定量表和简易精神状态检查,并确定了亨廷顿三核苷酸 CAG 重复长度。我们主要报告了这项最近完成的前瞻性、纵向、观察性研究的横断面基线数据。
截至 2009 年 12 月 31 日,共有 2318 人入组;其中,1985 人(85.6%)分为六个分析组。三组具有扩展的 CAG 等位基因(36 次重复或以上):有临床诊断 HD 的个体[n=930],以及之前进行过[ n=248]或未进行过[n=112]预测性 DNA 检测的无临床症状的一级亲属。三组没有扩展的等位基因:之前进行过[n=41]或未进行过[n=224]基因检测的一级亲属,以及配偶和护理人员[n=430]。所有运动、行为、认知和功能测量指标的组间基线平均表现均存在差异(p<0.001)。具有扩展等位基因的无临床症状个体体重较轻(76.0 与 79.6kg;p=0.01),认知评分较低(简易精神状态检查中 28.5 与 29.1;p=0.008)。“高正常值”重复长度(27 至 35)的频率为 2.5%,而与低外显率相关的重复长度(36 至 39)的频率为 2.7%。
COHORT 研究参与者的基线分析显示出在临床诊断之前出现的差异。对该队列的纵向研究将进一步描述 HD 的自然病史以及遗传和生物学修饰剂。
Clinicaltrials.gov NCT00313495。