Tau exacerbates excitotoxic brain damage in an animal model of stroke

• Main Authors: Bi, M, Gladbach, A, Van Eersel, J, Ittner, A, Przybyla, M, Van Hummel, A, Chua, S.W, Hoven, J.V.D, Lee, W.S, Müller, J, Parmar, J, Jonquieres, G.V, Stefen, H, Guccione, E, Fath, T, Housley, G.D, Klugmann, M, Ke, Y.D, Ittner, L.M
• Other Authors: BIOCHEMISTRY
• Format: Article
• Published: Nature Publishing Group 2020
• Subjects: glutamic acid; guanosine triphosphatase activating protein; mitogen activated protein kinase; Ras protein; SynGAP1 protein; tau protein; unclassified drug; Syngap1 protein, mouse; animal; brain; compartmentalization; experimental study; gene expression; inhibition; protein; stroke; toxicity; animal experiment; animal model; Article; brain damage; cerebrovascular accident; controlled study; disease exacerbation; enzyme activation; excitotoxicity; gene overexpression; middle cerebral artery occlusion; mouse; nerve cell; nonhuman; postsynaptic density; reperfusion; signal transduction; wild type; brain injury; C57BL mouse; cell culture; cerebral artery disease; complication; deficiency; disease model; gene expression profiling; genetics; human; knockout mouse; male; metabolism; procedures; synaptosome; Animalia; Mus; Animals; Brain Injuries; Cells, Cultured; Disease Models, Animal; Gene Expression Profiling; Humans; Infarction, Middle Cerebral Artery; Male; Mice, Inbred C57BL; Mice, Knockout; Neurons; ras GTPase-Activating Proteins; Signal Transduction; Stroke; Synaptosomes; tau Proteins
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/178581
• Institution: National University of Singapore

10.1038/s41467-017-00618-0