| Literature DB >> 31244341 |
Veronica Hirsch-Reinshagen1, Omar A Alfaify2, Ging-Yuek R Hsiung2, Cyril Pottier3, Matt Baker3, Ralph B Perkerson3, Rosa Rademakers3, Hanna Briemberg2, Dean J Foti2, Ian R Mackenzie1.
Abstract
Mutations in the TANK binding kinase 1 gene (TBK1) are associated with amyotrophic lateral sclerosis and/or frontotemporal dementia; however, the range of clinical phenotypes and neuropathological changes associated with these mutations have not yet been completely elucidated. We present the detailed clinical, neuroimaging, and neuropathological features of two brothers carrying the TBK1 p.Gly272_Thr331del mutation. Both presented with very similar and unusual clinical features including primary progressive aphasia and asymmetric-onset primary lateral sclerosis (PLS). Repeated electrophysiological studies failed to reveal any lower motor neuron involvement. Neuropathological evaluation of both cases revealed frontotemporal lobar degeneration with TDP-43 proteinopathy type B and selective involvement of upper motor neurons with TDP-43 inclusions. The stereotypical clinical presentation and neuropathological findings in these cases widen the phenotypic spectrum of TBK1 mutations and provide insights into the pathogenesis of PLS.Entities:
Keywords: TBK1; TDP-43; neuropathology; primary lateral sclerosis; primary progressive aphasia
Year: 2019 PMID: 31244341 PMCID: PMC6768716 DOI: 10.1080/21678421.2019.1632347
Source DB: PubMed Journal: Amyotroph Lateral Scler Frontotemporal Degener ISSN: 2167-8421 Impact factor: 4.092