| Literature DB >> 31705535 |
Fabrizia Stregapede1,2, Lorena Travaglini1, Adriana P Rebelo3, Vivian Pedigone Cintra4, Emanuele Bellacchio5, Luca Bosco1, Paolo Alfieri6, Stefano Pro7, Stephan Zuchner3, Enrico Bertini1, Francesco Nicita1.
Abstract
Dominant mutations in ATP1A1, encoding the alpha-1 isoform of the Na+ /K+ -ATPase, have been recently reported to cause an axonal to intermediate type of Charcot-Marie-Tooth disease (ie, CMT2DD) and a syndrome with hypomagnesemia, intractable seizures and severe intellectual disability. Here, we describe the first case of hereditary spastic paraplegia (HSP) caused by a novel de novo (p.L337P) variant in ATP1A1. We provide evidence for the causative role of this variant with functional and homology modeling studies. This finding expands the phenotypic spectrum of the ATP1A1-related disorders, adds a piece to the larger genetic puzzle of HSP, and increases knowledge on the molecular mechanisms underlying inherited axonopathies (ie, CMT and HSP).Entities:
Keywords: CMT2; Charcot-Marie-Tooth; Na2+/K+-ATPase; axonopathies; hereditary spastic pararapesis; polyneuropathy
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Year: 2019 PMID: 31705535 DOI: 10.1111/cge.13668
Source DB: PubMed Journal: Clin Genet ISSN: 0009-9163 Impact factor: 4.438