Literature DB >> 27590285

Variants in SLC18A3, vesicular acetylcholine transporter, cause congenital myasthenic syndrome.

Gina L O'Grady1, Corien Verschuuren1, Michaela Yuen1, Richard Webster1, Manoj Menezes1, Johanna M Fock1, Natalie Pride1, Heather A Best1, Tatiana Benavides Damm1, Christian Turner1, Monkol Lek1, Andrew G Engel1, Kathryn N North1, Nigel F Clarke1, Daniel G MacArthur1, Erik-Jan Kamsteeg1, Sandra T Cooper2.   

Abstract

OBJECTIVE: To describe the clinical and genetic characteristics of presynaptic congenital myasthenic syndrome secondary to biallelic variants in SLC18A3.
METHODS: Individuals from 2 families were identified with biallelic variants in SLC18A3, the gene encoding the vesicular acetylcholine transporter (VAChT), through whole-exome sequencing.
RESULTS: The patients demonstrated features seen in presynaptic congenital myasthenic syndrome, including ptosis, ophthalmoplegia, fatigable weakness, apneic crises, and deterioration of symptoms in cold water for patient 1. Both patients demonstrated moderate clinical improvement on pyridostigmine. Patient 1 had a broader phenotype, including learning difficulties and left ventricular dysfunction. Electrophysiologic studies were typical for a presynaptic defect. Both patients showed profound electrodecrement on low-frequency repetitive stimulation followed by a prolonged period of postactivation exhaustion. In patient 1, this was unmasked only after isometric contraction, a recognized feature of presynaptic disease, emphasizing the importance of activation procedures.
CONCLUSIONS: VAChT is responsible for uptake of acetylcholine into presynaptic vesicles. The clinical and electrographic characteristics of the patients described are consistent with previously reported mouse models of VAChT deficiency. These findings make it very likely that defects in VAChT due to variants in SLC18A3 are a cause of congenital myasthenic syndrome in humans.
© 2016 American Academy of Neurology.

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Year:  2016        PMID: 27590285      PMCID: PMC5075972          DOI: 10.1212/WNL.0000000000003179

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


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