Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes

Abstract WW domain‐containing oxidoreductase (WWOX) is an emerging neural gene‐regulating homeostasis of the central nervous system. Germline biallelic mutations in WWOX cause WWOX‐related epileptic encephalopathy (WOREE) syndrome and spinocerebellar ataxia and autosomal recessive 12 (SCAR12), two d...

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Main Authors: Srinivasarao Repudi, Irina Kustanovich, Sara Abu‐Swai, Shani Stern, Rami I Aqeilan
Format: Article
Language:English
Published: Springer Nature 2021-11-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.202114599
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author Srinivasarao Repudi
Irina Kustanovich
Sara Abu‐Swai
Shani Stern
Rami I Aqeilan
author_facet Srinivasarao Repudi
Irina Kustanovich
Sara Abu‐Swai
Shani Stern
Rami I Aqeilan
author_sort Srinivasarao Repudi
collection DOAJ
description Abstract WW domain‐containing oxidoreductase (WWOX) is an emerging neural gene‐regulating homeostasis of the central nervous system. Germline biallelic mutations in WWOX cause WWOX‐related epileptic encephalopathy (WOREE) syndrome and spinocerebellar ataxia and autosomal recessive 12 (SCAR12), two devastating neurodevelopmental disorders with highly heterogenous clinical outcomes, the most common being severe epileptic encephalopathy and profound global developmental delay. We recently demonstrated that neuronal ablation of murine Wwox recapitulates phenotypes of Wwox‐null mice leading to intractable epilepsy, hypomyelination, and postnatal lethality. Here, we designed and produced an adeno‐associated viral vector (AAV9) harboring murine Wwox or human WWOX cDNA and driven by the human neuronal Synapsin I promoter (AAV‐SynI‐WWOX). Testing the efficacy of AAV‐SynI‐WWOX delivery in Wwox‐null mice demonstrated that specific neuronal restoration of WWOX expression rescued brain hyperexcitability and seizures, hypoglycemia, myelination deficits, and the premature lethality and behavioral deficits of Wwox‐null mice. These findings provide a proof‐of‐concept for WWOX gene therapy as a promising approach to curing children with WOREE and SCAR12.
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spelling doaj-art-b0c97a48d8e64ff2bf3b116d611d7e9f2025-08-20T03:05:53ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842021-11-01131211510.15252/emmm.202114599Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypesSrinivasarao Repudi0Irina Kustanovich1Sara Abu‐Swai2Shani Stern3Rami I Aqeilan4The Concern Foundation Laboratories, The Lautenberg Center for Immunology and Cancer Research, Immunology and Cancer Research‐IMRIC, Hebrew University‐Hadassah Medical SchoolSagol Department of Neurobiology, University of HaifaThe Concern Foundation Laboratories, The Lautenberg Center for Immunology and Cancer Research, Immunology and Cancer Research‐IMRIC, Hebrew University‐Hadassah Medical SchoolSagol Department of Neurobiology, University of HaifaThe Concern Foundation Laboratories, The Lautenberg Center for Immunology and Cancer Research, Immunology and Cancer Research‐IMRIC, Hebrew University‐Hadassah Medical SchoolAbstract WW domain‐containing oxidoreductase (WWOX) is an emerging neural gene‐regulating homeostasis of the central nervous system. Germline biallelic mutations in WWOX cause WWOX‐related epileptic encephalopathy (WOREE) syndrome and spinocerebellar ataxia and autosomal recessive 12 (SCAR12), two devastating neurodevelopmental disorders with highly heterogenous clinical outcomes, the most common being severe epileptic encephalopathy and profound global developmental delay. We recently demonstrated that neuronal ablation of murine Wwox recapitulates phenotypes of Wwox‐null mice leading to intractable epilepsy, hypomyelination, and postnatal lethality. Here, we designed and produced an adeno‐associated viral vector (AAV9) harboring murine Wwox or human WWOX cDNA and driven by the human neuronal Synapsin I promoter (AAV‐SynI‐WWOX). Testing the efficacy of AAV‐SynI‐WWOX delivery in Wwox‐null mice demonstrated that specific neuronal restoration of WWOX expression rescued brain hyperexcitability and seizures, hypoglycemia, myelination deficits, and the premature lethality and behavioral deficits of Wwox‐null mice. These findings provide a proof‐of‐concept for WWOX gene therapy as a promising approach to curing children with WOREE and SCAR12.https://doi.org/10.15252/emmm.202114599AAV9DEE28hypomyelinationseizuresWOREE syndrome
spellingShingle Srinivasarao Repudi
Irina Kustanovich
Sara Abu‐Swai
Shani Stern
Rami I Aqeilan
Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes
EMBO Molecular Medicine
AAV9
DEE28
hypomyelination
seizures
WOREE syndrome
title Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes
title_full Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes
title_fullStr Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes
title_full_unstemmed Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes
title_short Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes
title_sort neonatal neuronal wwox gene therapy rescues wwox null phenotypes
topic AAV9
DEE28
hypomyelination
seizures
WOREE syndrome
url https://doi.org/10.15252/emmm.202114599
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AT irinakustanovich neonatalneuronalwwoxgenetherapyrescueswwoxnullphenotypes
AT saraabuswai neonatalneuronalwwoxgenetherapyrescueswwoxnullphenotypes
AT shanistern neonatalneuronalwwoxgenetherapyrescueswwoxnullphenotypes
AT ramiiaqeilan neonatalneuronalwwoxgenetherapyrescueswwoxnullphenotypes