A novel TBK1 loss-of-function variant associated with ALS and parkinsonism phenotypes

Amyotroph Lateral Scler Frontotemporal Degener. 2024 Nov;25(7-8):791-794. doi: 10.1080/21678421.2024.2374374. Epub 2024 Jul 4.

Abstract

Loss-of-function (LoF) variants in the TANK binding kinase 1 (TBK1) gene are implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. In this study, we present the first familial cases of ALS and parkinsonism associated with a novel TBK1 variant. We describe two siblings: one diagnosed with classical ALS and the other with a unique syndrome overlapping ALS and parkinsonism. Comprehensive clinical and imaging evaluations supported these diagnoses. Genetic analysis through whole-genome sequencing revealed a previously unknown heterozygous splice site variant in TBK1. Functional assessments demonstrated that this splice site variant leads to abnormal splicing and subsequent degradation of the mutated TBK1 allele by nonsense-mediated decay, confirming its pathogenic impact. Our findings suggest a broader involvement of TBK1 in neurodegenerative diseases and underscore the need for further research into TBK1's role, advocating for screening for TBK1 variants in similar familial cases.

Keywords: Amyotrophic lateral sclerosis; Parkinsonism; TBK1; loss-of-function variant.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Aged
  • Amyotrophic Lateral Sclerosis* / diagnosis
  • Amyotrophic Lateral Sclerosis* / genetics
  • Female
  • Humans
  • Loss of Function Mutation / genetics
  • Male
  • Middle Aged
  • Parkinsonian Disorders* / genetics
  • Pedigree
  • Phenotype*
  • Protein Serine-Threonine Kinases* / genetics

Substances

  • Protein Serine-Threonine Kinases
  • TBK1 protein, human