Nicolai Preisler
Nicolai Preisler
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Pascal Laforêt
Pascal Laforêt
Centre de Référence de Pathologie Neuromusculaire Paris-Est, Institut de Myologie, GH Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France
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Karen Lindhardt Madsen
Karen Lindhardt Madsen
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Edith Husu
Edith Husu
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Christoffer Rasmus Vissing
Christoffer Rasmus Vissing
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Gitte Hedermann
Gitte Hedermann
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Henrik Galbo
Henrik Galbo
Department of Inflammation Research, Rigshospitalet, Copenhagen, Denmark
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Christopher Lindberg
Christopher Lindberg
Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden
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John Vissing
John Vissing
Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Introduction Pompe disease (Glycogenosis type II; OMIM #232300) is caused by lysosomal acid alpha-glucosidase deficiency (EC# 3.2.1.20), which leads to a metabolic block in intra-lysosomal glycogen breakdown ( 1 ). In the late-onset forms of
