Koichi Iijima
Affiliations: | Farber Institute for Neuroscience, Biochemistry and Molecular Biology | Thomas Jefferson University, Philadelphia, PA, United States |
Area:
Alzheimer's disease, energy metabolism, Drosophila neurogeneticsGoogle:
"Koichi Iijima"Mean distance: 106866
Cross-listing: Alzheimer's Tree - Chemistry Tree
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Publications
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| Iijima K, Sekiya M, Maruko-Otake A, et al. (2013) Epigenetic modifications reveal an effective use of the protein quality control system to suppress accumulation and toxicity of beta-amyloid 42 in the secretory pathway in neurons Alzheimers & Dementia. 9: 126 |
| Iijima-Ando K, Sekiya M, Suzuki E, et al. (2011) Disruption of mitochondrial transport promotes tau toxicity through Alzheimer's disease-related tau phosphorylation Alzheimers & Dementia. 7 |
| Iijima K, Gatt A, Iijima-Ando K. (2010) Tau Ser262 phosphorylation is critical for Abeta42-induced tau toxicity in a transgenic Drosophila model of Alzheimer's disease. Human Molecular Genetics. 19: 2947-57 |
| Iijima-Ando K, Zhao L, Gatt A, et al. (2010) A DNA damage-activated checkpoint kinase phosphorylates tau and enhances tau-induced neurodegeneration. Human Molecular Genetics. 19: 1930-8 |
| Iijima-Ando K, Iijima K. (2010) Transgenic Drosophila models of Alzheimer's disease and tauopathies. Brain Structure & Function. 214: 245-62 |
| Iijima K, Iijima-Ando K. (2010) Studying mechanisms underlying Aß42-induced tau toxicity in transgenic Drosophila models Alzheimers & Dementia. 6 |
| Iijima-Ando K, Hearn SA, Shenton C, et al. (2009) Mitochondrial mislocalization underlies Abeta42-induced neuronal dysfunction in a Drosophila model of Alzheimer's disease. Plos One. 4: e8310 |
| Chiang HC, Iijima K, Hakker I, et al. (2009) Distinctive roles of different beta-amyloid 42 aggregates in modulation of synaptic functions. Faseb Journal : Official Publication of the Federation of American Societies For Experimental Biology. 23: 1969-77 |
| Iijima K, Iijima-Ando K. (2008) Drosophila models of Alzheimer's amyloidosis: the challenge of dissecting the complex mechanisms of toxicity of amyloid-beta 42. Journal of Alzheimer's Disease : Jad. 15: 523-40 |
| Iijima-Ando K, Hearn SA, Granger L, et al. (2008) Overexpression of neprilysin reduces alzheimer amyloid-beta42 (Abeta42)-induced neuron loss and intraneuronal Abeta42 deposits but causes a reduction in cAMP-responsive element-binding protein-mediated transcription, age-dependent axon pathology, and premature death in Drosophila. The Journal of Biological Chemistry. 283: 19066-76 |