| Literature DB >> 26354034 |
Chihiro Ohba1,2, Kazuhiro Haginoya3, Hitoshi Osaka4,5, Kazuo Kubota6, Akihiko Ishiyama6, Takuya Hiraide6, Hirofumi Komaki6, Masayuki Sasaki6, Satoko Miyatake1, Mitsuko Nakashima1, Yoshinori Tsurusaki1, Noriko Miyake1, Fumiaki Tanaka2, Hirotomo Saitsu1, Naomichi Matsumoto1.
Abstract
Recently, de novo KIF1A mutations were identified in patients with intellectual disability, spasticity and cerebellar atrophy and/or optic nerve atrophy. In this study, we analyzed a total of 62 families, including 68 patients with genetically unsolved childhood cerebellar atrophy, by whole-exome sequencing (WES). We identified five de novo missense KIF1A mutations, including only one previously reported mutation (p.Arg316Trp). All the mutations are located in the motor domain of KIF1A. In all patients, initial symptom onset was during the infantile period, and included developmental delay in three patients and gait disturbance in two. Thereafter, they showed gait disturbances, exaggerated deep tendon reflexes, cerebellar symptoms and cerebellar atrophy on brain magnetic resonance imaging. Four patients showed lower limb spasticity, upper limb clumsiness and visual disturbances. Nerve conduction study revealed peripheral neuropathy in three patients. This study further delineates clinical features of de novo KIF1A mutations. Genetic testing of KIF1A should be considered in children with developmental delay, cerebellar atrophy and pyramidal features.Entities:
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Year: 2015 PMID: 26354034 DOI: 10.1038/jhg.2015.108
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172