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Showing results (561-570 of 574) with videos related to

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JCI Insight|July 31, 2019
Antisense oligonucleotides extend survival of prion-infected miceGregory J Raymond, Hien Tran Zhao, Brent Race, et al.
Journal of Parkinson'S Disease|August 7, 2023
Outcome Measures for Disease-Modifying Trials in Parkinson's Disease: Consensus Paper by the EJS ACT-PD Multi-Arm Multi-Stage Trial InitiativeCristina Gonzalez-Robles, Rimona S Weil, Daniel van Wamelen, et al.
Scientific Reports|March 29, 2017
Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt<sup>Q111/+</sup> model of Huntington's diseaseRobert M Bragg, Sydney R Coffey, Rory M Weston, et al.
Journal of Virology|October 16, 2023
Characterization and biodistribution of under-employed gene therapy vector AAV7Samantha A Yost, Emre Firlar, Justin D Glenn, et al.
BMC Cancer|January 6, 2022
The clinical significance of adenomatous polyposis coli (APC) and catenin Beta 1 (CTNNB1) genetic aberrations in patients with melanomaGeorgia Sofia Karachaliou, Rached Alkallas, Sarah B Carroll, et al.
BMJ Open|May 29, 2021
Exenatide once weekly over 2 years as a potential disease-modifying treatment for Parkinson's disease: protocol for a multicentre, randomised, double blind, parallel group, placebo controlled, phase 3 trial: The 'Exenatide-PD3' studyNirosen Vijiaratnam, Christine Girges, Grace Auld, et al.
Human Molecular Genetics|March 24, 2017
High resolution time-course mapping of early transcriptomic, molecular and cellular phenotypes in Huntington's disease CAG knock-in mice across multiple genetic backgroundsSeth A Ament, Jocelynn R Pearl, Andrea Grindeland, et al.
Scientific Reports|February 9, 2017
Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt<sup>Q111/+</sup> model of Huntington's diseaseRobert M Bragg, Sydney R Coffey, Rory M Weston, et al.
Nucleic Acids Research|August 11, 2020
Prion protein lowering is a disease-modifying therapy across prion disease stages, strains and endpointsEric Vallabh Minikel, Hien T Zhao, Jason Le, et al.
Biorxiv : the Preprint Server for Biology|November 22, 2024
Suppression of Huntington's Disease Somatic Instability by Transcriptional Repression and Direct CAG Repeat BindingElla W Mathews, Sydney R Coffey, Annette Gärtner, et al.
Pageof 58

Showing results (561-570 of 574) with videos related to

Sort By:
Pageof 58
JCI Insight|July 31, 2019
Antisense oligonucleotides extend survival of prion-infected miceGregory J Raymond, Hien Tran Zhao, Brent Race, et al.
Journal of Parkinson'S Disease|August 7, 2023
Outcome Measures for Disease-Modifying Trials in Parkinson's Disease: Consensus Paper by the EJS ACT-PD Multi-Arm Multi-Stage Trial InitiativeCristina Gonzalez-Robles, Rimona S Weil, Daniel van Wamelen, et al.
Scientific Reports|March 29, 2017
Corrigendum: Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt<sup>Q111/+</sup> model of Huntington's diseaseRobert M Bragg, Sydney R Coffey, Rory M Weston, et al.
Journal of Virology|October 16, 2023
Characterization and biodistribution of under-employed gene therapy vector AAV7Samantha A Yost, Emre Firlar, Justin D Glenn, et al.
BMC Cancer|January 6, 2022
The clinical significance of adenomatous polyposis coli (APC) and catenin Beta 1 (CTNNB1) genetic aberrations in patients with melanomaGeorgia Sofia Karachaliou, Rached Alkallas, Sarah B Carroll, et al.
BMJ Open|May 29, 2021
Exenatide once weekly over 2 years as a potential disease-modifying treatment for Parkinson's disease: protocol for a multicentre, randomised, double blind, parallel group, placebo controlled, phase 3 trial: The 'Exenatide-PD3' studyNirosen Vijiaratnam, Christine Girges, Grace Auld, et al.
Human Molecular Genetics|March 24, 2017
High resolution time-course mapping of early transcriptomic, molecular and cellular phenotypes in Huntington's disease CAG knock-in mice across multiple genetic backgroundsSeth A Ament, Jocelynn R Pearl, Andrea Grindeland, et al.
Scientific Reports|February 9, 2017
Motivational, proteostatic and transcriptional deficits precede synapse loss, gliosis and neurodegeneration in the B6.Htt<sup>Q111/+</sup> model of Huntington's diseaseRobert M Bragg, Sydney R Coffey, Rory M Weston, et al.
Nucleic Acids Research|August 11, 2020
Prion protein lowering is a disease-modifying therapy across prion disease stages, strains and endpointsEric Vallabh Minikel, Hien T Zhao, Jason Le, et al.
Biorxiv : the Preprint Server for Biology|November 22, 2024
Suppression of Huntington's Disease Somatic Instability by Transcriptional Repression and Direct CAG Repeat BindingElla W Mathews, Sydney R Coffey, Annette Gärtner, et al.
Pageof 58