Xenografted human iPSC-derived neurons with the familial Alzheimer's disease APP ^V717I mutation reveal dysregulated transcriptome signatures linked to synaptic function and implicate LINGO2 as a disease signaling mediator.

Autor: Qu W; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Lam M; Department of Neurology, Center for Translational and Computational Neuroimmunology, Neurological Institute, Columbia University, 710 West 168th Street, New York, NY, USA., McInvale JJ; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Mares JA; Department of Neurology, Center for Translational and Computational Neuroimmunology, Neurological Institute, Columbia University, 710 West 168th Street, New York, NY, USA., Kwon S; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Humala N; Department of Neurosurgery, Columbia University, New York, NY, USA., Mahajan A; Department of Neurosurgery, Columbia University, New York, NY, USA., Nguyen T; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Jakubiak KA; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Mun JY; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Tedesco TG; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA., Al-Dalahmah O; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Hussaini SA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA., Sproul AA; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA.; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA., Siegelin MD; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., De Jager PL; Department of Neurology, Center for Translational and Computational Neuroimmunology, Neurological Institute, Columbia University, 710 West 168th Street, New York, NY, USA.; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA., Canoll P; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA., Menon V; Department of Neurology, Center for Translational and Computational Neuroimmunology, Neurological Institute, Columbia University, 710 West 168th Street, New York, NY, USA. vm2545@cumc.columbia.edu.; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA. vm2545@cumc.columbia.edu., Hargus G; Department of Pathology and Cell Biology, Presbyterian Hospital, Columbia University, 650W 168th Street, New York, NY, USA. gh2374@cumc.columbia.edu.; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA. gh2374@cumc.columbia.edu.

Publikováno v: Acta neuropathologica [Acta Neuropathol] 2024 Jun 25; Vol. 147 (1), pp. 107. Date of Electronic Publication: 2024 Jun 25.