CACNA1G Causes Dominantly Inherited Myoclonus-Ataxia with Intellectual Disability: A Case Report

Cerebellum. 2024 Dec;23(6):2679-2683. doi: 10.1007/s12311-024-01734-6. Epub 2024 Sep 17.

Abstract

Spinocerebellar ataxias (SCAs) are characterized by substantial phenotypic variability. Among them, SCA42 is a rare non-expansion entity presenting with slowly progressive cerebellar syndrome but whose clinical spectrum may be also wider. A 53-year-old male presented with progressive myoclonus-ataxia and intellectual disability. Genetic screening revealed a novel c.3835G > A (p. Asp1279Asn) variant in the CACNA1G gene. SCA42 is a rare non-expansion SCA caused by mutations in CACNA1G on chromosome 17q21, encoding the Ca(V)3.1, a low-threshold voltage-gated T-type calcium channel. The novel variant we identified is potentially involved in channel activity. This case expands the knowledge regarding CACNA1G-associated phenotype and highlights the importance of genetic screening in myoclonus-ataxia disorders.

Keywords: CACNA1G; Ataxia; Genetic; Intellectual disability; Myoclonus.

Publication types

  • Case Reports

MeSH terms

  • Calcium Channels, T-Type* / genetics
  • Humans
  • Intellectual Disability* / genetics
  • Male
  • Middle Aged
  • Spinocerebellar Ataxias / complications
  • Spinocerebellar Ataxias / congenital
  • Spinocerebellar Ataxias / genetics

Substances

  • Calcium Channels, T-Type
  • CACNA1G protein, human