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The valosin-containing protein (VCP) is involved in a plethora of cellular processes including membrane dynamics, DNA damage response, and protein quality control.1 Its essential role in humans is highlighted by diverse clinical phenotypes linked to VCP mutations: (1) inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia (IBMPFD); (2) amyotrophic lateral sclerosis; (3) Charcot-Marie-Tooth disease type 2; and (4) hereditary spastic paraplegia (reviewed by Evangelista et al.2). Moreover, mutant VCP has been implicated in the pathogenesis of Parkinson disease (PD).3
Acknowledgments
Acknowledgment: The authors thank the patient and his family for consent to publish this study, Andreas Odparlik (University Clinic Halle/Saale) for SPECT images, and Frank Bittner for picture editing.
Footnotes
Author contributions: Martin Regensburger: clinical care, collection of data, initial draft of the manuscript. Matthias Türk: myopathologic analysis. Axel Pagenstecher: myopathologic analysis. Rolf Schröder: myopathologic analysis, draft of the manuscript. Jürgen Winkler: clinical care, critical revision of manuscript for intellectual content.
Study funding: M.R. was supported by the IZKF (Interdisciplinary Center for Clinical Research, University Hospital Erlangen; J52).
Disclosure: M. Regensburger, M. Türk, A. Pagenstecher, and R. Schröder report no disclosures relevant to the manuscript. J. Winkler reports personal fees outside of the submitted work from Astrum IT GmbH, Teva GmbH, Ever Pharma GmbH, Desitin Arzneimittel GmbH, AbbVie GmbH & Co. KG, Biogen GmbH, and GlaxoSmithKline GmbH & Co. KG. Go to Neurology.org for full disclosures.
- Received February 23, 2017.
- Accepted in final form May 4, 2017.
- © 2017 American Academy of Neurology
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