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[脆性X智力低下1号基因前突变携带者——他们真的没有症状吗?]

[FMR1 PREMUTATION CARRIERS - ARE THEY REALLY ASYMPTOMATIC?].

作者信息

Elizur Shai, Berkenstadt Michal, Ries-Levavi Liat, Gruber Noah, Pinhas-Hamiel Orit, Hassin-Baer Sharon, Raas-Rothschild Annick, Raanani Hila, Cukierman-Yaffe Tali, Orvieto Raoul, Cohen Yoram, Gabis Lidia

机构信息

IVF Unit, Sheba Medical Center, Tel Hashomer.

The Sackler Faculty of Medicine, Tel-Aviv University, Israel.

出版信息

Harefuah. 2018 Apr;157(4):241-244.

Abstract

Fragile X Syndrome (FXS), the most common form of inherited mental retardation, is caused by a trinucleotide repeat expansion (CGG) in the 5'-untranslated region of the Fragile X Mental Retardation 1 (FMR1) gene located at Xq27.3. Patients with fragile X -related mental retardation, carry the full mutation CGG-repeat expansions (>200 CGG repeats), which are generally accompanied by hypermethylation of the promoter region, with the consequent transcriptional silencing of the FMR1 gene and absence of the encoded FMR1 protein (FMRP). Expansion of the CGG triplet number above the normal range (n=5-54) towards the so-called premutation status (n=55-199) is associated with increased risk for Fragile X-Associated Premature Ovarian Insufficiency (FXPOI) in females and Fragile X-Associated Tremor/ Ataxia Syndrome (FXTAS) predominantly in males. In addition, premutation women carriers are at increased risk for learning disabilities, as well as psychologic, endocrine, autoimmune and metabolic disorders. The observation that premutation carriers, both males and females, have increased FMR1 transcript levels, led researchers to suggest a similar molecular pathogenesis in both FXPOI and FXTAS. Two models have been proposed as the culprits of FXTAS and FXPOI: The toxic RNA gain-of-function model and the Repeat Associated Non-AUG initiated (RAN) translation protein toxicity model. The Fragile X Multidisciplinary Center in Sheba Medical Center, at Tel Hashomer includes a team of geneticists, fertility specialists, endocrinologists, psychologists and neurologists who work together in order to provide early detection of FMR1 premutation carriers and offer FMR1 premutation carriers and their families adequate multidisciplinary medical consultation, follow-up and care.

摘要

脆性X综合征(FXS)是遗传性智力障碍最常见的形式,由位于Xq27.3的脆性X智力障碍1(FMR1)基因5'非翻译区的三核苷酸重复扩增(CGG)引起。患有脆性X相关智力障碍的患者携带完全突变的CGG重复扩增(>200个CGG重复),通常伴有启动子区域的高甲基化,从而导致FMR1基因转录沉默以及编码的FMR1蛋白(FMRP)缺失。CGG三联体数量从正常范围(n = 5 - 54)扩展到所谓的前突变状态(n = 55 - 199)与女性脆性X相关早发性卵巢功能不全(FXPOI)风险增加以及主要在男性中出现的脆性X相关震颤/共济失调综合征(FXTAS)相关。此外,前突变女性携带者患学习障碍以及心理、内分泌、自身免疫和代谢紊乱的风险增加。前突变携带者(包括男性和女性)FMR1转录水平升高这一观察结果,促使研究人员提出FXPOI和FXTAS具有相似的分子发病机制。已经提出了两种模型作为FXTAS和FXPOI的病因:有毒RNA功能获得模型和重复相关非AUG起始(RAN)翻译蛋白毒性模型。位于特拉哈希默的谢巴医疗中心的脆性X多学科中心有一组遗传学家、生育专家、内分泌学家、心理学家和神经学家,他们共同努力以便早期检测FMR1前突变携带者,并为FMR1前突变携带者及其家庭提供充分的多学科医学咨询、随访和护理。

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