Increasing the Receptor Tyrosine Kinase EphB2 Prevents Amyloid-β-induced Depletion of Cell Surface Glutamate Receptors by a Mechanism That Requires the PDZ-binding Motif of EphB2 and Neuronal Activity
Takashi Miyamoto(Denali Therapeutics (United States)), Lennart Mucke(Gladstone Institutes)
Cited by 33
Related Papers
High-Level Neuronal Expression of Aβ<sub>1–42</sub>in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation
|Journal of Neuroscience|2000|1.9k
Network abnormalities and interneuron dysfunction in Alzheimer disease
|Nature reviews. Neuroscience|2016|1k
Neurotoxicity of Amyloid -Protein: Synaptic and Network Dysfunction
|Cold Spring Harbor Perspectives in Medicine|2012|1k
RAGE potentiates Aβ‐induced perturbation of neuronal function in transgenic mice
|The EMBO Journal|2004|327
Fibrin-targeting immunotherapy protects against neuroinflammation and neurodegeneration
|Nature Immunology|2018|210