Jorge Ghiso
Affiliations: | Basic Medical Science | New York University, New York, NY, United States |
Area:
Pathology, Neuroscience BiologyGoogle:
"Jorge Ghiso"Mean distance: 53433
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Publications
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| Arber C, Casey JM, Crawford S, et al. (2023) Microglia produce the amyloidogenic ABri peptide in familial British dementia. Biorxiv : the Preprint Server For Biology |
| Rostagno A, Cabrera E, Lashley T, et al. (2022) N-terminally truncated Aβ4-x proteoforms and their relevance for Alzheimer's pathophysiology. Translational Neurodegeneration. 11: 30 |
| Rostagno A, Calero M, Ghiso J. (2022) Identification of Clusterin as a Major ABri- and ADan-Binding Protein Using Affinity Chromatography. Methods in Molecular Biology (Clifton, N.J.). 2466: 49-60 |
| Rostagno A, Calero M, Holton JL, et al. (2021) Association of clusterin with the BRI2-derived amyloid molecules ABri and ADan. Neurobiology of Disease. 158: 105452 |
| Alić I, Goh PA, Murray A, et al. (2021) Correction: Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene dose-sensitive AD suppressor in human brain. Molecular Psychiatry |
| Parodi-Rullán R, Ghiso J, Cabrera E, et al. (2020) Alzheimer's amyloid β heterogeneous species differentially affect brain endothelial cell viability, blood-brain barrier integrity, and angiogenesis. Aging Cell. e13258 |
| Alić I, Goh PA, Murray A, et al. (2020) Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene dose-sensitive AD suppressor in human brain. Molecular Psychiatry |
| Karkisaval AG, Rostagno A, Azimov R, et al. (2020) Ion channel formation by N-terminally truncated Aβ (4-42): Relevance for the pathogenesis of Alzheimer's disease. Nanomedicine : Nanotechnology, Biology, and Medicine. 102235 |
| Zampar S, Klafki HW, Sritharen K, et al. (2020) N-terminal heterogeneity of parenchymal and vascular amyloid-β deposits in Alzheimer's disease. Neuropathology and Applied Neurobiology |
| Sotolongo K, Ghiso J, Rostagno A. (2020) Nrf2 activation through the PI3K/GSK-3 axis protects neuronal cells from Aβ-mediated oxidative and metabolic damage. Alzheimer's Research & Therapy. 12: 13 |