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早发性痴呆症与 MBD5 基因中的杂合性、无义突变和新生变异相关。

Early-Onset Dementia Associated with a Heterozygous, Nonsense, and de novo Variant in the MBD5 Gene.

机构信息

Department of Neurology, Hospital Universitario 12 de Octubre, Madrid, Spain.

Group of Neurodegenerative Diseases, Instituto de Investigación Hospital 12 de Octubre (I+12), Madrid, Spain.

出版信息

J Alzheimers Dis. 2021;84(1):73-78. doi: 10.3233/JAD-210648.

Abstract

The haploinsufficiency of the methyl-binding domain protein 5 (MBD5) gene has been identified as the determinant cause of the neuropsychiatric disorders grouped under the name MBD5-neurodevelopment disorders (MAND). MAND includes patients with intellectual disability, behavioral problems, and seizures with a static clinical course. However, a few reports have suggested regression. We describe a non-intellectually disabled female, with previous epilepsy and personality disorder, who developed early-onset dementia. The extensive etiologic study revealed a heterozygous nonsense de novo pathogenic variant in the MBD5 gene. This finding could support including the MBD5 gene in the study of patients with atypical early-onset dementia.

摘要

甲基结合域蛋白 5(MBD5)基因的单倍体不足已被确定为神经精神障碍的决定因素,这些障碍被归为 MBD5-神经发育障碍(MAND)。MAND 包括伴有智力残疾、行为问题和癫痫发作且临床病程呈静态的患者。然而,有少数报道提示病情有进展。我们描述了一位非智力残疾的女性,她之前患有癫痫和人格障碍,后发展为早发性痴呆。广泛的病因学研究发现 MBD5 基因存在杂合无义新生致病性变异。这一发现可能支持将 MBD5 基因纳入非典型早发性痴呆患者的研究。

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