{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Marc Emmenegger"],"funding":["NOMIS Stiftung (NOMIS Foundation)","EU Horizon 2020","University of Zurich and University Hospital of Zurich","EU/EFPIA/Innovative Medicines Initiative 2 Joint Undertaking","European Research Council (ERC)","Forschungskredit University of Zurich","National Centre for Competence in Research (NCCR)","Swiss Personalized Health Network","Swiss National Science Foundation Project Grant"],"journal":["EMBO Molecular Medicine"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-SCDT-EMM-2021-14745"],"abstract":["While the initial pathology of Parkinson's disease and other ?-synucleinopathies is often confined to circumscribed brain regions, it can spread and progressively affect adjacent and distant brain locales. This process may be controlled by cellular receptors of ?-synuclein fibrils, one of which was proposed to be the LAG3 immune checkpoint molecule. Here, we analyzed the expression pattern of LAG3 in human and mouse brains. Using a variety of methods and model systems, we found no evidence for LAG3 expression by neurons. While we confirmed that LAG3 interacts with ?-synuclein fibrils, the specificity of this interaction appears limited. Moreover, overexpression of LAG3 in cultured human neural cells did not cause any worsening of ?-synuclein pathology ex vivo. The overall survival of A53T "],"repository":["biostudies-other"],"funding_grant_id":["PhysProt","51NF40-182880","2017DRI17","ETN grant 674979-Nanotrans","116060","ERC Prion2020","310030_192650"],"pubmed_authors":["Dr. Alice Kaganovich","Dr. Timo Eninger","Dr. Mathias Jucker","Ms. Therese, W. Herling","Kelvin, C Luk","Mr. Naunehal, S. Matharu","Prof. Philipp, J. Kahle","Andrés Gonzalez-Guerra","Dr. Elena De Cecco","Dr. Marian Hruska-Plochan","Mr. Daniel Heinzer","Dr. Lisa, M. Häsler","Dr. Pierre de Rossi","Ms. Melanie Barth","Dr. Nora Bengoa-Vergniory","Ms. Elena Tantardini","Prof. Adriano Aguzzi","Tuomas, P. Knowles","Mr. Matthias, M. Schneider","Prof. Magdalini Polymenidou","Dr. Ronald Melki","Merve Avar","Regina Reimann","Ms. Natalie Landeck","Dr. Mehtap Bacioglu","Dr. Rebekah, G. Langston","Dr. Simone Hornemann","Mark, R Cookson","Marc Emmenegger"],"additional_accession":[]},"is_claimable":false,"name":"LAG3 is not expressed in human and murine neurons and does not modulate ?-synucleinopathies","description":"While the initial pathology of Parkinson's disease and other ?-synucleinopathies is often confined to circumscribed brain regions, it can spread and progressively affect adjacent and distant brain locales. This process may be controlled by cellular receptors of ?-synuclein fibrils, one of which was proposed to be the LAG3 immune checkpoint molecule. Here, we analyzed the expression pattern of LAG3 in human and mouse brains. Using a variety of methods and model systems, we found no evidence for LAG3 expression by neurons. While we confirmed that LAG3 interacts with ?-synuclein fibrils, the specificity of this interaction appears limited. Moreover, overexpression of LAG3 in cultured human neural cells did not cause any worsening of ?-synuclein pathology ex vivo. The overall survival of A53T ","dates":{"release":"2021-10-14T00:00:00Z","modification":"2021-10-14T14:21:42Z","creation":"2021-10-14T14:21:42Z"},"accession":"S-SCDT-EMM-2021-14745","cross_references":{"doi":["10.15252/emmm.202114745"]}}