| Literature DB >> 26947546 |
Alberto Fernández-Jaén1, Sara Álvarez2, Eui Young So3, Toru Ouchi3, Mar Jiménez de la Peña4, Anna Duat5, Daniel Martín Fernández-Mayoralas6, Ana Laura Fernández-Perrone6, Jacobo Albert7, Beatriz Calleja-Pérez8.
Abstract
We describe a 4-year-old male child born to non-consanguineous Spanish parents with progressive encephalopathy (PE), microcephaly, and hypertonia. Whole exome sequencing revealed compound heterozygous BRAT1 mutations [c.1564G > A (p.Glu522Lys) and c.638dup (p.Val214Glyfs*189)]. Homozygous and compound heterozygous BRAT1 mutations have been described in patients with lethal neonatal rigidity and multifocal seizure syndrome (MIM# 614498). The seven previously described patients suffered from uncontrolled seizures, and all of those patients died in their first months of life. BRAT1 acts as a regulator of cellular proliferation and migration and is required for mitochondrial function. The loss of these functions may explain the cerebral atrophy observed in this case of PE. This case highlights the extraordinary potential of next generation technologies for the diagnosis of rare genetic diseases, including PE. Making a prompt diagnosis of PE is important for genetic counseling and disease management.Entities:
Keywords: BRAT1; Lethal neonatal rigidity; Progressive encephalopathy; Whole exome sequencing
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Year: 2016 PMID: 26947546 PMCID: PMC4979314 DOI: 10.1016/j.ejpn.2016.02.009
Source DB: PubMed Journal: Eur J Paediatr Neurol ISSN: 1090-3798 Impact factor: 3.140