Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms

By C. Andorfer, Y. Kress, Marisol Espinoza, Rohan de Silva, K. L. Tucker, Y. Barde, K. Duff, P. Davies. Journal of Neurochemistry, 2003

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Molecular mechanisms of neurodegeneration in Alzheimer's disease. (2010, background): “Tau has been targeted by reducing Tau synthesis or decreasing Tau phosphorylation with compounds such as lithium (166,167).”
Alzheimer’s disease: experimental models and reality (2017, background): “Importantly, expression of all six isoforms of human tau only results in tangle formation in mice lacking endogenous tau, showing that endogenous mouse tau inhibits the aggregation of human tau [2].”
Age-Dependent Neurofibrillary Tangle Formation, Neuron Loss, and Memory Impairment in a Mouse Model of Human Tauopathy (P301L) (2005, background): “On the other hand, mice expressing non-mutant human tau, in the absence of mouse tau, developed extensive cell death between the ages of 8 and 17 months (Andorfer et al., 2003).”
Regulation of Tau Pathology by the Microglial Fractalkine Receptor (2010, positive): “Considering that the somatodendritic accumulation of AT8+ MAPT does not occur until 3 months in the hippocampus of hTau mice (Andorfer et al., 2003), these results suggest that induction of TLR4-mediated systemic inflammation via LPS induces MAPT hyperphosphorylation in prepathological hTau mice.”
The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins. (2007, methodology): “son Laboratory and generated as previously described (29).”