Associated Papers
Feasibility of Follow-Up Studies and Reclassification in Spinocerebellar Ataxia Gene Variants of Unknown Significance.
Ghorbani F et al.
Frontiers in Genetics, 2022
Spinocerebellar ataxia type 23 (SCA23): a review.
Wu F et al.
Journal of Neurology, 2021
Cerebellar developmental deficits underlie neurodegenerative disorder spinocerebellar ataxia type 23.
Smeets CJLM et al.
Brain Pathology (zurich, Switzerland), 2021
Altered secondary structure of Dynorphin A associates with loss of opioid signalling and NMDA-mediated excitotoxicity in SCA23.
Smeets CJ et al.
Human Molecular Genetics, 2016
Elevated mutant dynorphin A causes Purkinje cell loss and motor dysfunction in spinocerebellar ataxia type 23.
Smeets CJ et al.
Brain : a Journal of Neurology, 2015
The first Japanese familial case of spinocerebellar ataxia 23 with a novel mutation in the PDYN gene.
Saigoh K et al.
Parkinsonism & Related Disorders, 2015
The frequency of spinocerebellar ataxia type 23 in a UK population.
Fawcett K et al.
Journal of Neurology, 2013
Spinocerebellar ataxia type 23 is an uncommon SCA subtype in the Chinese Han population.
Liu YT et al.
Neuroscience Letters, 2012
Prodynorphin mutations cause the neurodegenerative disorder spinocerebellar ataxia type 23.
Bakalkin G et al.
American Journal of Human Genetics, 2010
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