ELAVL4, splicing, and glutamatergic dysfunction precede neuron loss in MAPT mutation cerebral organoids - Bowles, Kathryn R.; Silva, M. Catarina; Whitney, Kristen; Bertucci, Taylor; Berlind, Joshua E.; Lai, Jesse D.; Garza, Jacob C.; Boles, Nathan C.; Mahali, Sidhartha; Strang, Kevin H.; Marsh, Jacob A.; Chen, Cynthia; et al. (Cell, 2021)
Keywords: autophagy; Autophagy - drug effects; Autophagy - genetics; Biomarkers - metabolism; Body Patterning - drug effects; Body Patterning - genetics; Cell Death - drug effects; Cell Line; Cerebrum - pathology; death; dementia; ELAV-Like Protein 4 - genetics; ELAVL4; frontotemporal dementia; glutamatergic neurons; glutamic acid; Glutamic Acid - metabolism; Humans; Hydrazones - pharmacology; Lysosomes - drug effects; Lysosomes - metabolism; MAPT; Morpholines - pharmacology; mutants; mutation; Mutation - genetics; neurodegenerative diseases; neurons; Neurons - drug effects; Neurons - metabolism; Neurons - pathology; organoids; Organoids - drug effects; Organoids - metabolism; Organoids - ultrastructure; Phosphorylation - drug effects; Pyrimidines - pharmacology; RNA Splicing - drug effects; RNA Splicing - genetics; RNA-binding proteins; Signal Transduction - drug effects; splicing; stem cells; Stress Granules - drug effects; Stress Granules - metabolism; Synapses - metabolism; synaptic signaling; tau Proteins - genetics; tauopathy; therapeutics; toxicity; Up-Regulation - drug effects; Up-Regulation - genetics; synaptic signaling; tauopathy; autophagy; organoids; ELAVL4; frontotemporal dementia; MAPT; splicing; glutamatergic neurons