Neurodegenerative disease after hematopoietic stem cell transplantation in metachromatic leukodystrophy.


Journal

Annals of clinical and translational neurology
ISSN: 2328-9503
Titre abrégé: Ann Clin Transl Neurol
Pays: United States
ID NLM: 101623278

Informations de publication

Date de publication:
07 2023
Historique:
revised: 04 05 2023
received: 10 03 2023
accepted: 10 05 2023
medline: 19 7 2023
pubmed: 22 5 2023
entrez: 22 5 2023
Statut: ppublish

Résumé

Metachromatic leukodystrophy is a lysosomal storage disease caused by deficient arylsulfatase A. It is characterized by progressive demyelination and thus mainly affects the white matter. Hematopoietic stem cell transplantation may stabilize and improve white matter damage, yet some patients deteriorate despite successfully treated leukodystrophy. We hypothesized that post-treatment decline in metachromatic leukodystrophy might be caused by gray matter pathology. Three metachromatic leukodystrophy patients treated with hematopoietic stem cell transplantation with a progressive clinical course despite stable white matter pathology were clinically and radiologically analyzed. Longitudinal volumetric MRI was used to quantify atrophy. We also examined histopathology in three other patients deceased after treatment and compared them with six untreated patients. The three clinically progressive patients developed cognitive and motor deterioration after transplantation, despite stable mild white matter abnormalities on MRI. Volumetric MRI identified cerebral and thalamus atrophy in these patients, and cerebellar atrophy in two. Histopathology showed that in brain tissue of transplanted patients, arylsulfatase A expressing macrophages were clearly present in the white matter, but absent in the cortex. Arylsulfatase A expression within patient thalamic neurons was lower than in controls, the same was found in transplanted patients. Neurological deterioration may occur after hematopoietic stem cell transplantation in metachromatic leukodystrophy despite successfully treated leukodystrophy. MRI shows gray matter atrophy, and histological data demonstrate absence of donor cells in gray matter structures. These findings point to a clinically relevant gray matter component of metachromatic leukodystrophy, which does not seem sufficiently affected by transplantation.

Identifiants

pubmed: 37212343
doi: 10.1002/acn3.51796
pmc: PMC10351661
doi:

Substances chimiques

Cerebroside-Sulfatase EC 3.1.6.8

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1146-1159

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NINDS NIH HHS
ID : U54 NS115052
Pays : United States

Informations de copyright

© 2023 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

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Auteurs

Murtadha Al-Saady (M)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.

Shanice Beerepoot (S)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.
Center for Translational Immunology, University Medical Center Utrecht, Utrecht, the Netherlands.
Nierkens and Lindemans Group, Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands.

Bonnie C Plug (BC)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.
Department of Pathology, Amsterdam Leukodystrophy Center, Amsterdam University Medical Centers, VU University and Neuroscience Campus Amsterdam, Amsterdam, the Netherlands.

Marjolein Breur (M)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.
Department of Pathology, Amsterdam Leukodystrophy Center, Amsterdam University Medical Centers, VU University and Neuroscience Campus Amsterdam, Amsterdam, the Netherlands.

Hristina Galabova (H)

Department of Radiology and Nuclear Medicine, Neuroscience Campus Amsterdam, Amsterdam University Medical Centers, VU university, Amsterdam, the Netherlands.

Petra J W Pouwels (PJW)

Department of Radiology and Nuclear Medicine, Neuroscience Campus Amsterdam, Amsterdam University Medical Centers, VU university, Amsterdam, the Netherlands.

Jaap-Jan Boelens (JJ)

Stem Cell Transplantation and Cellular Therapies Program, Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Caroline Lindemans (C)

Stem Cell Transplantation and Cellular Therapies Program, Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Pediatric Blood and Bone Marrow Transplantation, Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands.

Peter M van Hasselt (PM)

Stem Cell Transplantation and Cellular Therapies Program, Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Ulrich Matzner (U)

Institute of Biochemistry and Molecular Biology, Medical Faculty, Rheinische Friedrich-Wilhelm University, Bonn, Germany.

Adeline Vanderver (A)

Division of Neurology, Department of Pediatrics, Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA, USA.

Marianna Bugiani (M)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.
Department of Pathology, Amsterdam Leukodystrophy Center, Amsterdam University Medical Centers, VU University and Neuroscience Campus Amsterdam, Amsterdam, the Netherlands.

Marjo S van der Knaap (MS)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.
Department of Integrative Neurophysiology, VU University, Amsterdam, the Netherlands.

Nicole I Wolf (NI)

Department of Child Neurology, Amsterdam Leukodystrophy Center, Emma Children's Hospital, Amsterdam University Medical Centers, and Amsterdam Neuroscience, Cellular & Molecular Mechanisms, Vrije Universiteit, Amsterdam, the Netherlands.

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