Phenotypic evaluation of a childhood-onset parkinsonism-dystonia mouse model with inherent postural abnormalities.

Mouse models that replicate facets of human neurological diseases are often used at the pre-clinical stage to better understand the underlying mechanisms of a disease and test the target engagement of potential therapeutic interventions. We recently characterized a mouse model of childhood-onset parkinsonism-dystonia, a disease caused by a homozygous loss-of-function mutation in the SLC39A14 gene. The disease manifests itself phenotypically by impairments in locomotor behaviour and postural abnormalities. Our initial characterization of the model revealed that the Slc39a14

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Published by Elsevier Inc.