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S5–03–01: Animal and cellular models – tau–Abeta interaction
Author(s) -
Götz Jürgen,
David Della,
Ittner Lars,
Halliday Glenda,
Shepherd Claire
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.362
Subject(s) - tau protein , neuroscience , frontotemporal dementia , genetically modified mouse , immunocytochemistry , tau pathology , tangle , biology , tauopathy , transgene , amygdala , neurofibrillary tangle , dementia , pathology , alzheimer's disease , microbiology and biotechnology , neurodegeneration , disease , medicine , gene , senile plaques , genetics , mathematics , pure mathematics
pressing c-myc and ras re-enter the cell cycle as evidenced by increasing DNA content and the expression of cyclin B1, a marker for the G2/M phase of the cell cycle. Importantly, however, and directly related to disease pathogenesis, such infected neurons also display increased levels of two specific tau changes recognized by TG3, a phospho-tau specific antibody and Alz50, a conformational epitope considered a key marker of early AD pathology. Based on these results, we propose that early elements of AD neuropathology arise due to inappropriate re-entry into the cell cycle. As such, this neuronal cell model may be extremely valuable for not only characterizing cell cycle related changes as they pertain to AD but also for the development of novel therapeutic strategies.