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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Anti-aggregant tau mutant promotes neurogenesis

Fig. 1

Expression level of the exogenous human anti-aggregant TauRDΔKPP and pro-aggregant TauRD∆K. a The anti-aggregant and pro-aggregant construct is based on the human Tau 4-repeat domain carrying the FTDP-17 mutation ΔK280 near the beginning of R2. The four repeats in the C-terminal half of Tau are highlighted in green (R1-R4). The two hexapeptide motifs at the beginning of R2 and R3 are capable of promoting aggregation by inducing ß-structure. The ΔK280 mutation promotes aggregation, and the two proline mutations inhibit it. b Luciferase activity within the brains of pups: Control (top row), expressing anti-aggregant TauRDΔKPP (middle row) or pro-aggregant TauRDΔK (bottom row) at post-natal day 8 (P8), as determined by bioluminescence (photons/sec). The control brain does not show any luciferase signal, the anti-aggregant TauRDΔKPP brain shows an intense luciferase signal (middle and right panel), ranging from 2 - 6x 107 photons per second (blue to red, see heat scale on right), predominantly in the frontal part of the brain. A similar expression pattern is seen in the pro-aggregant TauRDΔK brain at P8. c Luciferase activity monitored in slices of anti-aggregant mice from DIV10 to DIV30. The signal remains roughly constant from DIV10 to DIV20 and then declines down to ~40% at DIV25-30 (because of the aging process in the slice cultures). Data are expressed as a mean ±SEM of 4-6 slices from 10 different animals and analyzed by unpaired Student´s t-test. ** P-value <0.01. d Luciferase activity monitored in slices of pro-aggregant mice from DIV10 to DIV30. There is a similar nearly constant expression of TauRD∆K from DIV10-20, followed by a strong decline. Data are expressed as a mean ±SEM of 4-6 slices from 10 different animals and analyzed by unpaired Student´s t-test. **** P-value <0.0001

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