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. 2006 Aug;169(2):599–616. doi: 10.2353/ajpath.2006.060002

Table 3.

Comparison of the Most Common Tau Transgenic Models and Other Models with Tauopathy

Tau transgenic models
Promoter Mutation Begin of tau brain pathology Phopho-tau in spinal cord Motor impairment Reference
PrP P301L 5 months Detectable at 5 months Yes at 6.5 months (hemizygous) 7
CamK-II (inducible tet-off) P301L 2.5 months n.d. at 2.5 months Yes at 9.5 months 9, 28
Thy1.2 P301L 3 months Detectable at 3 months Yes (muscle atrophy and weakness) 8
Thy1.2 P301S 5 months Detectable at 5 months Yes at 5 months (homozygous) 10
Thy1 G272V P301L R406W 1.5 months Detectable at 1.5 months No abnormality up to 12 months 37
CamK-II R406W 5 months Detectable at 5 months No abnormality up to 23 months 13
Thy1.2 G272V P301S 3 months Minor traces at 3 to 6 months No abnormality up to 18 months Present study
APP or PS1 and tau double/triple-transgenic models
Promoter Transgene expression Begin of tau brain pathology Phopho-tau in spinal cord Motor impairment Reference
Thy1.2 (Tau, APP), PS1-KI TauP301LxAPPswxPS1M146V 12 months No data available No data available 63
PrP (Tau), PrP(APP) TauP301LxAPPsw 6 months 3 months Yes 60
Other transgenic models with tau pathology
Promoter Targeted gene Begin of tau brain pathology Motor impairment Reference
pin1 (−/−) 2 years No 64
NSE p25 4 months No paralysis but increased spontaneous locomotor activity 65

CamK-II, Ca2+-calmodulin-dependent kinase II; KI, knockin; NSE, neuron-specific enolase; n.d., not detectable; Pin1, peptidyl-prolyl cis/trans isomerase 1; PrP, prion protein promotor; (−/−), knockout.