De novo variants in CAMTA1 cause a syndrome variably associated with spasticity, ataxia, and intellectual disability.
Iris G M WijnenHermine E Veenstra-KnolFleur VansenneErica H GerkesTom de KoningYvonne J VosMarina A J TijssenDeborah SivalNiklas DarinEls K VanhoutteMayke OosterlooMaartje PenningsBart P van de WarrenburgErik-Jan KamsteegPublished in: European journal of human genetics : EJHG (2020)
Previously, intragenic CAMTA1 copy number variants (CNVs) have been shown to cause non-progressive, congenital ataxia with or without intellectual disability (OMIM#614756). However, ataxia, intellectual disability, and dysmorphic features were all incompletely penetrant, even within families. Here, we describe four patients with de novo nonsense, frameshift or missense CAMTA1 variants. All four patients predominantly manifested features of ataxia and/or spasticity. Borderline intellectual disability and dysmorphic features were both present in one patient only, and other neurological and behavioural symptoms were variably present. Neurodevelopmental delay was found to be mild. Our findings indicate that also nonsense, frameshift and missense variants in CAMTA1 can cause a spastic ataxia syndrome as the main phenotype.
Keyphrases
- intellectual disability
- copy number
- mitochondrial dna
- autism spectrum disorder
- early onset
- genome wide
- case report
- botulinum toxin
- dna methylation
- end stage renal disease
- upper limb
- spinal cord injury
- cerebral palsy
- ejection fraction
- chronic kidney disease
- multiple sclerosis
- newly diagnosed
- prognostic factors
- congenital heart disease
- patient reported outcomes
- sleep quality