Dystonia with brain manganese accumulation resulting from SLC30A10 mutations: A new treatable disorder-Reference-Cited by-同舟云学术

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Dystonia with brain manganese accumulation resulting from SLC30A10 mutations: A new treatable disorder

Published:2012-08-23 Issue:10 Volume:27 Page:1317-1322
ISSN:0885-3185
Container-title:Movement Disorders
language:en
Short-container-title:Mov. Disord.

Author:

Stamelou Maria¹,Tuschl Karin²,Chong W. K.³,Burroughs Andrew K.⁴,Mills Philippa B.²,Bhatia Kailash P.¹,Clayton Peter T.²

Affiliation:

1. Sobell Department of Motor Neuroscience and Movement Disorders, University College London Institute of Neurology, London, United Kingdom

2. Clinical and Molecular Genetics Unit, University College London Institute of Child Health, London, United Kingdom

3. Department of Radiology, Great Ormond Street Hospital for Children, London, United Kingdom

4. The Liver, Pancreatic, Biliary and Transplant Unit, The Wellington Hospital, London, United Kingdom

Publisher

Wiley

Subject

Clinical Neurology,Neurology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/mds.25138

Reference48 articles.

1. Syndrome of Hepatic Cirrhosis, Dystonia, Polycythemia, and Hypermanganesemia Caused by Mutations in SLC30A10 , a Manganese Transporter in Man

2. Hepatic cirrhosis, dystonia, polycythaemia and hypermanganesaemia—A new metabolic disorder

3. Mutations in SLC30A10 Cause Parkinsonism and Dystonia with Hypermanganesemia, Polycythemia, and Chronic Liver Disease

4. Regulation of the Erythropoietin Gene

5. Ferroportin is a manganese-responsive protein that decreases manganese cytotoxicity and accumulation

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