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AAV5-miHTT Gene Therapy Demonstrates Broad Distribution and Strong Human Mutant Huntingtin Lowering in a Huntington's Disease Minipig Model

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    SYSNO ASEP0496209
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleAAV5-miHTT Gene Therapy Demonstrates Broad Distribution and Strong Human Mutant Huntingtin Lowering in a Huntington's Disease Minipig Model
    Author(s) Evers, M. (NL)
    Miniarikova, J. (NL)
    Juhás, Štefan (UZFG-Y) RID, ORCID
    Vallés, A. (NL)
    Bohuslavová, Božena (UZFG-Y) ORCID
    Juhásová, Jana (UZFG-Y) RID, ORCID
    Kupcová Skalníková, Helena (UZFG-Y) RID, ORCID
    Vodička, Petr (UZFG-Y) ORCID
    Valeková, Ivona (UZFG-Y) RID, ORCID
    Brouwers, C. (NL)
    Blits, B. (NL)
    Lubelski, J. (NL)
    Kovářová, Hana (UZFG-Y) RID, ORCID
    Ellederová, Zdeňka (UZFG-Y) RID, ORCID
    van Deventer, S. (NL)
    Petry, H. (NL)
    Motlík, Jan (UZFG-Y) RID, ORCID
    Konstantinová, P. (NL)
    Source TitleMolecular Therapy. - : Cell Press - ISSN 1525-0016
    Roč. 26, č. 9 (2018), s. 2163-2177
    Number of pages15 s.
    Publication formPrint - P
    Languageeng - English
    CountryUS - United States
    KeywordsHuntington´s disease ; minipig ; huntingtin
    Subject RIVFH - Neurology
    OECD categoryTechnologies involving identifying the functioning of DNA, proteins and enzymes and how they influence the onset of disease and maintenance of well-being (gene-based diagnostics and therapeutic interventions (pharmacogenomics, gene-based therapeutics)
    R&D ProjectsLO1609 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Institutional supportUZFG-Y - RVO:67985904
    UT WOS000447756800010
    EID SCOPUS85049723970
    DOI https://doi.org/10.1016/j.ymthe.2018.06.021
    AnnotationHuntington's disease (HD) is a fatal neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the huntingtin gene. Previously, we showed strong huntingtin reduction and prevention of neuronal dysfunction in HD rodents using an engineered microRNA targeting human huntingtin, delivered via adeno-associated virus (AAV) serotype 5 vector with a transgene encoding an engineered miRNA against HTT mRNA (AAV5-miHTT). One of the challenges of rodents as a model of neurodegenerative diseases is their relatively small brain, making successful translation to the HD patient difficult. This is particularly relevant for gene therapy approaches, where distribution achieved upon local administration into the parenchyma is likely dependent on brain size and structure. Here, we aimed to demonstrate the translation of huntingtin-lowering gene therapy to a large-animal brain. We investigated the feasibility, efficacy, and tolerability of one-time intracranial administration of AAV5-miHTT in the transgenic HD(tgHD) minipig model. We detected widespread dose-dependent distribution of AAV5-miHTT throughout the tgHD minipig brain that correlated with the engineered microRNA expression. Both human mutant huntingtin mRNA and protein were significantly reduced in all brain regions transduced by AAV5-miHTT. The combination of widespread vector distribution and extensive huntingtin lowering observed with AAV5-miHTT supports the translation of a huntingtin-lowering gene therapy for HD from preclinical studies into the clinic.
    WorkplaceInstitute of Animal Physiology and Genetics
    ContactJana Zásmětová, knihovna@iapg.cas.cz, Tel.: 315 639 554
    Year of Publishing2019
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