{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Brattas PL"],"funding":["Swedish excellence project Basal Ganglia Disorders Linnaeus Consortium","Vetenskapsrådet","Kungliga Fysiografiska Sällskapet i Lund","Thorsten och Elsa Segerfalks Stiftelse","Stiftelsen Lars Hiertas Minne","Anna-Lisa Rosenberg Fund for Neurological Research","Greta och Johan Kocks stiftelser Research","Stiftelsen Olle Engkvist Byggmästare","Swedish Government Initiative for Strategic Research Areas","Crafoordska Stiftelsen","Thelma Zoéga Fund for Medical Research","Åke Wiberg Stiftelse","Stiftelsen för Strategisk Forskning","Åhlén-stiftelsen","Tore Nilsons Stiftelse för Medicinsk Forskning","Hjärnfonden"],"pagination":["1316-1329"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8204969"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(6)"],"pubmed_abstract":["Activation of macroautophagy/autophagy, a key mechanism involved in the degradation and removal of aggregated proteins, can successfully reverse Huntington disease phenotypes in various model systems. How neuronal autophagy impairments need to be considered in Huntington disease progression to achieve a therapeutic effect is currently not known. In this study, we used a mouse model of HTT (huntingtin) protein aggregation to investigate how different methods and timing of autophagy activation influence the efficacy of autophagy-activating treatment <i>in vivo</i>. We found that overexpression of human <i>TFEB</i>, a master regulator of autophagy, did not decrease mutant HTT aggregation. On the other hand, <i>Becn1</i> overexpression, an autophagic regulator that plays a key role in autophag"],"journal":["Autophagy"],"pubmed_title":["Impact of differential and time-dependent autophagy activation on therapeutic efficacy in a model of Huntington disease."],"pmcid":["PMC8204969"],"funding_grant_id":["TZ 2017-0057","N/A","20170592","FFL12-0074","# K2014-62X-22527-01-3","FO2014-0106","FO2017-0108","TZ 2018-0052","mA7/h15","M18-0044","K2014-62X-20404-08-5","2017-00505","186-655","FO2018-0058","2016-00296"],"pubmed_authors":["Madsen S","Pircs K","Brattas PL","Hersbach BA","Jakobsson J","Petri R"],"additional_accession":[]},"is_claimable":false,"name":"Impact of differential and time-dependent autophagy activation on therapeutic efficacy in a model of Huntington disease.","description":"Activation of macroautophagy/autophagy, a key mechanism involved in the degradation and removal of aggregated proteins, can successfully reverse Huntington disease phenotypes in various model systems. How neuronal autophagy impairments need to be considered in Huntington disease progression to achieve a therapeutic effect is currently not known. In this study, we used a mouse model of HTT (huntingtin) protein aggregation to investigate how different methods and timing of autophagy activation influence the efficacy of autophagy-activating treatment <i>in vivo</i>. We found that overexpression of human <i>TFEB</i>, a master regulator of autophagy, did not decrease mutant HTT aggregation. On the other hand, <i>Becn1</i> overexpression, an autophagic regulator that plays a key role in autophag","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-05-08T14:10:29.341Z","creation":"2022-02-10T16:34:04.744Z"},"accession":"S-EPMC8204969","cross_references":{"pubmed":["32374203"],"doi":["10.1080/15548627.2020.1760014"]}}