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- W1991145152 abstract "Abnormal tau aggregates, also known as neurofibrillary tangles (NFTs), and amyloid-beta (Aβ) plaques are pathological hallmarks of Alzheimer's disease (AD). Recent studies have shown contradictory results about the role of endogenous mouse tau in the pathological events observed in AD models. On one hand, it has been suggested that the concomitant expression of the endogenous murine tau might interfere with the disease progression and the neurodegenerative processes by delaying pathological accumulation of human mutant tau in neurons. On the other hand, other studies strongly indicate that mouse tau is a critical downstream mediator of Aβ toxicity. To clarify the role of endogenous murine tau in the pathological events that occur in AD models, we developed a novel transgenic mouse model by crossing 3xTg-AD with mtauKO mice, referred to as 3xTg-AD/mtauKO mice. This new model (3xTg-AD/mtauKO) allows us to determine the specific pathological role of murine tau. Here, we show that 3xTg-AD/mtauKO mice exhibit lower tau loads in both soluble and insoluble fractions and reduced tau hyperphosphorylation in the soluble fraction when compared with 3xTg-AD mice. These results indicate that mouse tau is hyperphosphorylated and significantly co-aggregated with human tau in 3xTg-AD mice. Interestingly, both transgenic models showed similar tau kinase activity as well as comparable Aβ pathology. Furthermore, both models exhibited equivalent cognitive dysfunction when tested on a spatial memory task. These results provide relevant insights for developing new models to better understand the link between β-amyloid and tau." @default.
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- W1991145152 date "2012-07-01" @default.
- W1991145152 modified "2023-10-18" @default.
- W1991145152 title "P3-006: Endogenous tau contributes to Alzheimer's-like tau pathology in 3xTg mice" @default.
- W1991145152 doi "https://doi.org/10.1016/j.jalz.2012.05.1224" @default.
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