Brain monoamine vesicular transport disease caused by homozygous SLC18A2 variants: A study in 42 affected individuals

Ken Saida 1Reza Maroofian 2Toru Sengoku 3Tadahiro Mitani 4Alistair T Pagnamenta 5Dana Marafi 6Maha S Zaki 7Thomas J O'Brien 8Ehsan Ghayoor Karimiani 9Rauan Kaiyrzhanov 2Marina Takizawa 1Sachiko Ohori 1Huey Yin Leong 10Gulsen Akay 4Hamid Galehdari 11Mina Zamani 11Ratna Romy 12Christopher J Carroll 12Mehran Beiraghi Toosi 13Farah Ashrafzadeh 14Shima Imannezhad 15Hadis Malek 16Najmeh Ahangari 16Hoda Tomoum 17Vykuntaraju K Gowda 18Varunvenkat M Srinivasan 18David Murphy 19Natalia Dominik 2Hasnaa M Elbendary 7Karima Rafat 7Sanem Yilmaz 20Seda Kanmaz 20Mine Serin 20Deepa Krishnakumar 21Alice Gardham 21Anna Maw 22Tekki Sreenivasa Rao 23Sarah Alsubhi 24Myriam Srour 25Daniela Buhas 26Tamison Jewett 27Rachel E Goldberg 27Hanan Shamseldin 28Eirik Frengen 29Doriana Misceo 29Petter Strømme 30José Ricardo Magliocco Ceroni 31Chong Ae Kim 31Gozde Yesil 32Esma Sengenc 33Serhat Guler 34Mariam Hull 35Mered Parnes 35Dilek Aktas 36Banu Anlar 37Yavuz Bayram 38Davut Pehlivan 39Jennifer E Posey 4Shahryar Alavi 40Seyed Ali Madani Manshadi 41Hamad Alzaidan 42Mohammad Al-Owain 42Lama Alabdi 43Ferdous Abdulwahab 28Futoshi Sekiguchi 1Kohei Hamanaka 1Atsushi Fujita 1Yuri Uchiyama 44Takeshi Mizuguchi 1Satoko Miyatake 45Noriko Miyake 46Reem M Elshafie 47Kamran Salayev 48Ulviyya Guliyeva 49Fowzan S Alkuraya 50Joseph G Gleeson 51Kristin G Monaghan 52Katherine G Langley 52Hui Yang 52Mahsa Motavaf 53Saeid Safari 53Mozhgan Alipour 54Kazuhiro Ogata 3André E X Brown 8James R Lupski 55Henry Houlden 2Naomichi Matsumoto 56

Affiliations

01 January 2023

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doi: 10.1016/j.gim.2022.09.010


Abstract

Purpose: Brain monoamine vesicular transport disease is an infantile-onset movement disorder that mimics cerebral palsy. In 2013, the homozygous SLC18A2 variant, p.Pro387Leu, was first reported as a cause of this rare disorder, and dopamine agonists were efficient for treating affected individuals from a single large family. To date, only 6 variants have been reported. In this study, we evaluated genotype-phenotype correlations in individuals with biallelic SLC18A2 variants.

Methods: A total of 42 affected individuals with homozygous SLC18A2 variant alleles were identified. We evaluated genotype-phenotype correlations and the missense variants in the affected individuals based on the structural modeling of rat VMAT2 encoded by Slc18a2, with cytoplasm- and lumen-facing conformations. A Caenorhabditis elegans model was created for functional studies.

Results: A total of 19 homozygous SLC18A2 variants, including 3 recurrent variants, were identified using exome sequencing. The affected individuals typically showed global developmental delay, hypotonia, dystonia, oculogyric crisis, and autonomic nervous system involvement (temperature dysregulation/sweating, hypersalivation, and gastrointestinal dysmotility). Among the 58 affected individuals described to date, 16 (28%) died before the age of 13 years. Of the 17 patients with p.Pro237His, 9 died, whereas all 14 patients with p.Pro387Leu survived. Although a dopamine agonist mildly improved the disease symptoms in 18 of 21 patients (86%), some affected individuals with p.Ile43Phe and p.Pro387Leu showed milder phenotypes and presented prolonged survival even without treatment. The C. elegans model showed behavioral abnormalities.

Conclusion: These data expand the phenotypic and genotypic spectra of SLC18A2-related disorders.

Keywords: Brain monoamine vesicular transport disease; Dopamine agonist; Dystonia; SLC18A2; VMAT2.


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