Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease.
By S. Oddo, A. Caccamo, M. Kitazawa, Bertrand P. Tseng, F. LaFerla. Neurobiology of Aging, 2003
1,020 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/e47ca3f068d062bb1aea69e93bcbde6edc9ee8e5
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Citations in the corpus
- Mechanisms of tau-induced neurodegeneration (2009, neutral): “Consistent with this hypothesis, both intracerebral infusion of Ab in FTDP-17 tau mutation P301L-expressing transgenic mice, as well as crossing these animals with APPTg2576 mice (APP Swedish plus London mutations), were found to exacerbate neurofibrillary pathology [54, 104] and, in the triple tran”
- The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal (2009, background): “degeneration has been seen is in the context of additional microtubule associated protein tau (MAPT) mutations (Lewis et al. 2001; Oddo et al. 2003), and in these cases, the MAPT mutations themselves lead to cell death (Lewis et al.”
- Alzheimer’s disease: experimental models and reality (2017, background): “Of all of the models reported, only the 3xTg mouse model has been widely used in AD studies and is considered the most complete transgenic mouse model of AD pathology available [108].”
- Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Triple transgenic mice with mutant APP, PS1, and tau proteins develop Aβ deposition prior to the appearance of NFT pathology (Oddo et al. 2003).”