Figure 3

Exenatide does not reduce Aβ and tau pathology in 3xTg-AD mice. Immunohistochemistry was employed to detect deposits of intraneuronal Aβ (a and b) and h-tau (c and d) in brain slices from treated (n=5) and untreated (n=5) 3xTg-AD mice. Low magnification (20 × ; scale bar=100 μM) images of intraneuronal Aβ deposits in untreated (a) or treated (b) 3xTg-AD mice. Insets show a high magnification (40 × ) view of hippocampal CA1 areas (scale bar =20 μM). No differences are seen between treated and untreated mice as shown by quantification of intraneuronal Aβ loads (e). Low magnification (20 × ) images of h-tau deposits in untreated (c) or treated (d) 3xTg-AD mice. Insets show a high magnification (40 × ) view of hippocampal CA1 areas (scale bar =20 μM). No differences are seen between treated and untreated mice as shown by quantification of h-tau levels (f). Quantification of intraneuronal Aβ or h-tau levels is expressed with bar graphs of mean pixel counts for mm2± the standard deviation (S.D.)