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<https://opendata.unex.es/recurso/ciencia-tecnologia/investigacion/publicaciones/Publicacion/2024-1010> bibo:eissn "2051-5960";
    dcterms:contributor "Markovinovic A. et al.";
    dcterms:title "Stimulating VAPB-PTPIP51 ER-mitochondria tethering corrects FTD/ALS mutant TDP43 linked Ca2+ and synaptic defects";
    bibo:volume "12";
    ou:urlScopus <https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85185963881&origin=inward>;
    dcterms:publisher "Acta Neuropathologica Communications";
    ou:bibtex "@article{f26a07a645114578a6be1e6066db7c75, title = 'Stimulating VAPB-PTPIP51 ER-mitochondria tethering corrects FTD/ALS mutant TDP43 linked Ca2+ and synaptic defects', abstract = 'Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are clinically linked major neurodegenerative diseases. Notably, TAR DNA-binding protein-43 (TDP43) accumulations are hallmark pathologies of FTD/ALS and mutations in the gene encoding TDP43 cause familial FTD/ALS. There are no cures for FTD/ALS. FTD/ALS display damage to a broad range of physiological functions, many of which are regulated by signaling between the endoplasmic reticulum (ER) and mitochondria. This signaling is mediated by the VAPB-PTPIP51 tethering proteins that serve to recruit regions of ER to the mitochondrial surface so as to facilitate inter-organelle communications. Several studies have now shown that disrupted ER-mitochondria signaling including breaking of the VAPB-PTPIP51 tethers are features of FTD/ALS and that for TDP43 and other familial genetic FTD/ALS insults, this involves activation of glycogen kinase-3 (GSK3). Such findings have prompted suggestions that correcting damage to ER-mitochondria signaling and the VAPB-PTPIP51 interaction may be broadly therapeutic. Here we provide evidence to support this notion. We show that overexpression of VAPB or PTPIP51 to enhance ER-mitochondria signaling corrects mutant TDP43 induced damage to inositol 1,4,5-trisphosphate (IP3) receptor delivery of Ca2+ to mitochondria which is a primary function of the VAPB-PTPIP51 tethers, and to synaptic function. Moreover, we show that ursodeoxycholic acid (UDCA), an FDA approved drug linked to FTD/ALS and other neurodegenerative diseases therapy and whose precise therapeutic target is unclear, corrects TDP43 linked damage to the VAPB-PTPIP51 interaction. We also show that this effect involves inhibition of TDP43 mediated activation of GSK3. Thus, correcting damage to the VAPB-PTPIP51 tethers may have therapeutic value for FTD/ALS and other age-related neurodegenerative diseases.', author = 'Andrea Markovinovic and {Martin Guerrero}, Sandra and Gabor Morotz and Shaakir Salam and {Gomez Suaga}, Patricia and Sebastien Paillusson and Jenny Greig and Younbok Lee and Jackie Mitchell and Wendy Noble and Christopher Miller', year = '2024', month = feb, day = '23', language = 'English', journal = 'Acta Neuropathologica Communications', issn = '2051-5960', publisher = 'BioMed Central', }";
    ou:openaccess "1"^^xsd:boolean;
    ou:vecesCitado "16"^^xsd:integer;
    vcard:url <https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85185963881&origin=inward>;
    dcterms:creator "Markovinovic A.";
    ou:tipoPublicacion "Article";
    a ou:Publicacion;
    dcterms:created "2024-12-01T00:00:00"^^xsd:dateTime;
    ou:eid "2-s2.0-85185963881";
    fabio:hasPublicationYear "2024";
    bibo:doi "10.1186/s40478-024-01742-x";
    ou:urlOrcid <https://kclpure.kcl.ac.uk/portal/en/publications/f26a07a6-4511-4578-a6be-1e6066db7c75>;
    vivo:identifier "2024-1010";
    ou:publicadaEnRevista <https://opendata.unex.es/recurso/ciencia-tecnologia/investigacion/revistas/Revista/2024-20919>.
<https://opendata.unex.es/recurso/educacion/universidad/personal/03301885b8214f1b43752b6676c63279-patricia-maria-gomez-suaga> ou:tienePublicacion <https://opendata.unex.es/recurso/ciencia-tecnologia/investigacion/publicaciones/Publicacion/2024-1010>.