Figure 1From: Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease Genetic deficiency of C1q does not alter fibrillar plaque pathology in 3xTg, but kinetics of plaque deposition is increased in both 3xTg and 3xTgQ-/- backcrossed to BUB. A. Representative pictures of thioflavine staining in the subiculum area of 3xTg and 3xTgQ-/- at 16 m (scale bar: 100 um). B, C. Thioflavine quantification by image analysis in the subiculum area of the 3xTg and 3xTgQ-/- (B) or the 3xTg and 3xTgBUB and 3xTgQ-/-BUB (C) at different ages. Data points are the average of n animals +/- SE at different ages. (B) 3xTg, 3xTgQ-/- at 7 m n = 8,8; at 12 m n = 11,10; at 14 m n = 3,6; at 16 m n = 9,15; at 18 m n = 3,4. (C) 3xTg, 3xTgBUB, 3xTgQ-/-BUB at 7 m n = 3,3,5; at 10 m n = 8,3,8; at 12.5 m n = 7,7,8; 18 m n = 4,5,6. *p < 0.05 (3xTg vs 3xTgBUB) using ANOVA single factor.Back to article page