A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model
J. Clin. Invest. Rolf Postina, et al. 113:1456 doi:10.1172/JCI20864 [
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Figure 3Detection and quantitation of amyloid plaques in brains from 17- to 19-month-old (
A_
D)
APP[V717I] transgenic mice, double-transgenic
ADAM10-mo ∞
APP[V717I] mice, and
ADAM10-dn ∞
APP[V717I] mice. Immunohistochemical detection of amyloid plaques in the neocortex in paraffin-embedded sections with either antibody 6F/3D (
A) or antibody 4G8 (
B). Note that in
ADAM10-mo ∞
APP[V717I] mice, no additional plaques were detected by antibody 4G8. Arrows point to blood vessels. Scale bars: 200 ∝m. (
C and
E) Thioflavine S_stained β structures in the subiculum of either 17- to 19-month-old (
C) or 12-month-old mice (
E); scale bars: 200 ∝m. (
D) Quantitation of amyloid load in subiculum in thioflavine S_stained sections obtained from 17- to 19-month-old animals. Surface thioflavine S staining is expressed as a percentage of the total subiculum surface. Statistical analysis was performed for each genotype with the following number of animals:
APP[V717I],
n = 5;
ADAM10-mo ∞
APP[V717I],
n = 13;
ADAM10-dn ∞
APP[V717I],
n = 6. *
P < 0.05; **
P < 0.01.
