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ELAVL4, splicing,and glutamatergic dysfunction precede neuron loss in MAPT mutation cerebral organoids
Affiliation:1. Ronald M. Loeb Center for Alzheimer’s Disease, Friedman Brain Institute, Departments of Genetics and Genomic Sciences, Neuroscience, and Neurology, Icahn School of Medicine at Mount Sinai (ISMMS), New York, NY 10029, USA;2. Chemical Neurobiology Laboratory, Center for Genomic Medicine, Departments of Neurology and Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA;3. Department of Pathology, Neuropathology Brain Bank and Research Core, ISMMS, New York, NY 10029, USA;4. Neural Stem Cell Institute, Rensselaer, NY 12144, USA;5. Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA;6. Amgen Research, One Amgen Center Dr., Thousand Oaks, CA 91320, USA;7. Department of Psychiatry, Washington University in St. Louis, St. Louis, MO 63110, USA
Abstract:
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  • Keywords:frontotemporal dementia  synaptic signaling  organoids  splicing  tauopathy  autophagy  glutamatergic neurons
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