Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72
Year: 2020
Type: article
Source: Nature Neuroscience
Authors: Qiang Zhu, Jie Jiang, Tania F. Gendron, Melissa McAlonis-Downes, Lulin Jiang, Amy Taylor, Sandra Diaz Garcia, Somasish Ghosh Dastidar, Maria J. Rodriguez, Patrick King, Yongjie Zhang, Albert R. La Spada, Huaxi Xu, Leonard Petrucelli, John Ravits, Sandrine Da Cruz, Clotilde Lagier-Tourenne, Don W. Cleveland
Institutions: University of California San Diego, Ludwig Cancer Research, Emory University, Mayo Clinic in Florida, Sanford Burnham Prebys Medical Discovery Institute, Manipal Academy of Higher Education, Kasturba Medical College, Manipal, Duke University, Duke Medical Center, VIB-KU Leuven Center for Brain & Disease Research, KU Leuven, Broad Institute, Harvard University, Massachusetts General Hospital
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: G1023608167, G1739649176, Determining whether gain of toxicity from ALS/FTD-linked hexanucleotide repeat expansion synergizes with reduced C9ORF72 function to drive age-dependent ALS/FTD, Using RNA signatures for therapy development in neurodegeneration due to C9orf72 expansions, G2306569157, Storage System for High Performance Computing, G3101017460, UCSD Alzheimer's Disease Research Center P50, G4121520986, Pathophysiology of genetically defined dementia and neurodegeneration: Defining therapeutic targets and pathways, High-performance compute cluster for biomedical computing, Pathobiology of Neurodegeneration in C9ORF72 repeat expansion, G5653327095, Silencing C9or72 with rAAV Mediated RNAi, Expanding insights into FTD disease mechanisms, UCSD Shiley-Marcos Alzheimer's Disease Research Center P30, Disease Mechanism and Therapy in TDP-43 Proteinopathies and Dementias, Cancer Center Support Grant
OpenAlex ID: W3015315508