De novo KIF1A mutations cause intellectual deficit, cerebellar atrophy, lower limb spasticity and visual disturbance.
Chihiro OhbaKazuhiro HaginoyaHitoshi OsakaKazuo KubotaAkihiko IshiyamaTakuya HiraideHirofumi KomakiMasayuki SasakiSatoko MiyatakeMitsuko NakashimaYoshinori TsurusakiNoriko MiyakeFumiaki TanakaHirotomo SaitsuNaomichi MatsumotoPublished in: Journal of human genetics (2015)
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.
Keyphrases
- end stage renal disease
- ejection fraction
- magnetic resonance imaging
- upper limb
- newly diagnosed
- lower limb
- chronic kidney disease
- intellectual disability
- prognostic factors
- peritoneal dialysis
- spinal cord injury
- autism spectrum disorder
- young adults
- computed tomography
- multiple sclerosis
- patient reported
- cerebral palsy
- single cell
- white matter
- blood brain barrier
- cerebral ischemia