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NRCAM 基因的双等位基因功能丧失变异与以运动为主的轴索性多发性神经病相关;第二份报告。

Bi-allelic loss of function variant in the NRCAM gene is associated with motor-predominant axonal polyneuropathy; the second report.

机构信息

Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran.

Kariminejad-Najmabadi Pathology & Genetics Center, Tehran, Iran.

出版信息

Mol Genet Genomic Med. 2023 Apr;11(4):e2131. doi: 10.1002/mgg3.2131. Epub 2023 Jan 6.

DOI:10.1002/mgg3.2131
PMID:36606341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10094081/
Abstract

BACKGROUND

The role of biallelic variants in the NRCAM gene underlying a neurodevelopmental disorder has been defined recently. The phenotype is mainly recognized by varying severity of global developmental delay/intellectual disability, hypotonia, spasticity, and peripheral neuropathy.

METHODS

Here, we describe a patient with an initial diagnosis of motor-predominant axonal polyneuropathy or a form of distal SMA. Whole-exome sequencing (WES), in parallel with WES-based CNV detection and assessment of homozygosity runs, was performed to identify this patient's possible genetic cause.

RESULTS

Whole exome sequencing revealed a homozygous variant, c.73C > T (p.Gln25*), in the NRCAM gene, while the patient manifests a mild range of phenotypes compared to NRCAM-related disorder. He presented only motor-predominant axonal polyneuropathy with no other signs of central nervous system involvement.

CONCLUSIONS

This study is the second report of an association between biallelic NRCAM gene variants and a Mendelian disorder. The obtained clinical data, together with the molecular findings in this patient, expands the clinical and molecular spectrum of NRCAM-related disorder and highlights its phenotypic complexity. Although patients with loss of function variants in this gene have previously presented severe clinical features, we show that type of the pathogenic variant does not necessarily determine the severity of this phenotype.

摘要

背景

最近已经确定了神经发育障碍中 NRCAM 基因的双等位基因变异的作用。表型主要表现为不同严重程度的全面发育迟缓/智力残疾、低张力、痉挛和周围神经病。

方法

在这里,我们描述了一名最初被诊断为运动为主的轴索性多发性神经病或远端 SMA 的患者。进行了全外显子组测序 (WES),同时进行了 WES 基于的 CNV 检测和纯合子分析,以确定该患者的可能遗传原因。

结果

全外显子组测序显示 NRCAM 基因中的纯合变异 c.73C>T(p.Gln25*),而患者的表型与 NRCAM 相关疾病相比处于轻度范围。他仅表现为运动为主的轴索性多发性神经病,没有中枢神经系统受累的其他迹象。

结论

这项研究是关于双等位基因 NRCAM 基因变异与孟德尔疾病之间关联的第二份报告。获得的临床数据,以及该患者的分子发现,扩展了 NRCAM 相关疾病的临床和分子谱,并强调了其表型的复杂性。尽管该基因的功能丧失变异患者以前表现出严重的临床特征,但我们表明,致病性变异的类型不一定决定该表型的严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c3b/10094081/8e74525dd6b2/MGG3-11-e2131-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c3b/10094081/344d169722f6/MGG3-11-e2131-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c3b/10094081/8e74525dd6b2/MGG3-11-e2131-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c3b/10094081/344d169722f6/MGG3-11-e2131-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c3b/10094081/8e74525dd6b2/MGG3-11-e2131-g001.jpg

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2
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3
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Nature. 2020 May;581(7809):434-443. doi: 10.1038/s41586-020-2308-7. Epub 2020 May 27.
4
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J Pain. 2020 Jul-Aug;21(7-8):892-904. doi: 10.1016/j.jpain.2019.12.004. Epub 2020 Jan 7.
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Iranome: A catalog of genomic variations in the Iranian population.伊朗人基因组变异目录:伊朗人群中的基因组变异目录。
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6
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