Department of Neuromuscular Diseases, University College London, Queen Square, Institute of Neurology, London WC1N 3BG, UK.
Department of Biology, Faculty of Science, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Brain. 2023 Dec 1;146(12):5031-5043. doi: 10.1093/brain/awad257.
MED27 is a subunit of the Mediator multiprotein complex, which is involved in transcriptional regulation. Biallelic MED27 variants have recently been suggested to be responsible for an autosomal recessive neurodevelopmental disorder with spasticity, cataracts and cerebellar hypoplasia. We further delineate the clinical phenotype of MED27-related disease by characterizing the clinical and radiological features of 57 affected individuals from 30 unrelated families with biallelic MED27 variants. Using exome sequencing and extensive international genetic data sharing, 39 unpublished affected individuals from 18 independent families with biallelic missense variants in MED27 have been identified (29 females, mean age at last follow-up 17 ± 12.4 years, range 0.1-45). Follow-up and hitherto unreported clinical features were obtained from the published 12 families. Brain MRI scans from 34 cases were reviewed. MED27-related disease manifests as a broad phenotypic continuum ranging from developmental and epileptic-dyskinetic encephalopathy to variable neurodevelopmental disorder with movement abnormalities. It is characterized by mild to profound global developmental delay/intellectual disability (100%), bilateral cataracts (89%), infantile hypotonia (74%), microcephaly (62%), gait ataxia (63%), dystonia (61%), variably combined with epilepsy (50%), limb spasticity (51%), facial dysmorphism (38%) and death before reaching adulthood (16%). Brain MRI revealed cerebellar atrophy (100%), white matter volume loss (76.4%), pontine hypoplasia (47.2%) and basal ganglia atrophy with signal alterations (44.4%). Previously unreported 39 affected individuals had seven homozygous pathogenic missense MED27 variants, five of which were recurrent. An emerging genotype-phenotype correlation was observed. This study provides a comprehensive clinical-radiological description of MED27-related disease, establishes genotype-phenotype and clinical-radiological correlations and suggests a differential diagnosis with syndromes of cerebello-lental neurodegeneration and other subtypes of 'neuro-MEDopathies'.
MED27 是 Mediator 多蛋白复合物的一个亚基,参与转录调控。最近有研究表明,双等位基因 MED27 变异与一种常染色体隐性神经发育障碍有关,该障碍表现为痉挛、白内障和小脑发育不良。我们通过对 30 个无关家庭的 57 名双等位基因 MED27 变异患者的临床和放射学特征进行描述,进一步阐明了 MED27 相关疾病的临床表型。通过外显子组测序和广泛的国际遗传数据共享,确定了 18 个独立家庭的 39 名双等位基因错义变异未发表的受影响个体(29 名女性,最后一次随访时的平均年龄为 17 ± 12.4 岁,范围为 0.1-45 岁)。从已发表的 12 个家庭中获得了随访和以前未报道的临床特征。对 34 例的脑 MRI 扫描进行了回顾。MED27 相关疾病表现为从发育性和癫痫性运动障碍性脑病到各种伴有运动异常的神经发育障碍的广泛表型连续谱。其特征是轻度至重度全面发育迟缓/智力障碍(100%)、双侧白内障(89%)、婴儿期低张力(74%)、小头畸形(62%)、步态共济失调(63%)、肌张力障碍(61%)、伴有癫痫(50%)、肢体痉挛(51%)、面部畸形(38%)和未成年前死亡(16%)。脑 MRI 显示小脑萎缩(100%)、白质体积减少(76.4%)、桥脑发育不良(47.2%)和基底节萎缩伴信号改变(44.4%)。以前未报道的 39 名受影响个体有 7 个纯合致病性错义 MED27 变异,其中 5 个为复发性变异。观察到一种新兴的基因型-表型相关性。本研究提供了 MED27 相关疾病的全面临床-放射学描述,建立了基因型-表型和临床-放射学相关性,并提出了与小脑-脑桥神经退行性变综合征和其他“神经-MED 病”亚型的鉴别诊断。