AAV9-Mediated Expression of SMN Restricted to Neurons Does Not Rescue the Spinal Muscular Atrophy Phenotype in Mice.


Journal

Molecular therapy : the journal of the American Society of Gene Therapy
ISSN: 1525-0024
Titre abrégé: Mol Ther
Pays: United States
ID NLM: 100890581

Informations de publication

Date de publication:
05 08 2020
Historique:
received: 12 03 2020
revised: 30 03 2020
accepted: 12 05 2020
pubmed: 30 5 2020
medline: 13 7 2021
entrez: 30 5 2020
Statut: ppublish

Résumé

Spinal muscular atrophy (SMA) is a neuromuscular disease mainly caused by mutations or deletions in the survival of motor neuron 1 (SMN1) gene and characterized by the degeneration of motor neurons and progressive muscle weakness. A viable therapeutic approach for SMA patients is a gene replacement strategy that restores functional SMN expression using adeno-associated virus serotype 9 (AAV9) vectors. Currently, systemic or intra-cerebrospinal fluid (CSF) delivery of AAV9-SMN is being explored in clinical trials. In this study, we show that the postnatal delivery of an AAV9 that expresses SMN under the control of the neuron-specific promoter synapsin selectively targets neurons without inducing re-expression in the peripheral organs of SMA mice. However, this approach is less efficient in restoring the survival and neuromuscular functions of SMA mice than the systemic or intra-CSF delivery of an AAV9 in which SMN is placed under the control of a ubiquitous promoter. This study suggests that further efforts are needed to understand the extent to which SMN is required in neurons and peripheral organs for a successful therapeutic effect.

Identifiants

pubmed: 32470325
pii: S1525-0016(20)30245-8
doi: 10.1016/j.ymthe.2020.05.011
pmc: PMC7403319
pii:
doi:

Substances chimiques

Survival of Motor Neuron 1 Protein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1887-1901

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.

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Auteurs

Aurore Besse (A)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

Stephanie Astord (S)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

Thibaut Marais (T)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

Marianne Roda (M)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

Benoit Giroux (B)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

François-Xavier Lejeune (FX)

Institut du Cerveau et de la Moelle épinière (ICM), Bioinformatics and Biostatistics Core Facility (iCONICS), Sorbonne Université, INSERM U1127, CNRS UMR 7225, GH Pitié-Salpêtrière, 75013 Paris, France.

Frederic Relaix (F)

Université Paris Est Créteil, INSERM, EnvA, AP-HP, 94000 Créteil, France.

Piera Smeriglio (P)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

Martine Barkats (M)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France.

Maria Grazia Biferi (MG)

Sorbonne Université, INSERM, Institute of Myology, Centre of Research in Myology, 75013 Paris, France. Electronic address: mg.biferi@institut-myologie.org.

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