MUTYH Actively Contributes to Microglial Activation and Impaired Neurogenesis in the Pathogenesis of Alzheimer’s Disease

Figure 5

The expression of MUTYH protein in wild-type, App^{NL-G-F/NL-G-F}, and App^{NL-G-F/NL-G-F}·Mutyh^-/- mouse brains. (a) Genotyping of wild-type, App^{NL-G-F/NL-G-F}, and App^{NL-G-F/NL-G-F}·Mutyh^-/- mice using tail DNA. Mutyh⁺ and Mutyh^- alleles were amplified using specific primer sets. Lane 1, wild type; 2 and 6, App^{NL-G-F/NL-G-F}; 3 and 7, App^{NL-G-F/NL-G-F}·Mutyh^-/-; 4, no tail DNA (negative control); and 5 and 8, Mutyh^+/- (positive control). (b) Hippocampal extracts prepared from six-month-old wild-type (Wt), App^{NL-G-F/NL-G-F} (NL-G-F), and App^{NL-G-F/NL-G-F}·Mutyh^-/- (NL-G-F·Mutyh) mice were subjected to Western blotting with the anti-MUTYH antibody. β-Actin was detected as a loading control. (c) The immunohistochemical detection of MUTYH protein in App^{NL-G-F/NL-G-F} (NL-G-F) and App^{NL-G-F/NL-G-F}·Mutyh^-/- (NL-G-F·Mutyh) mouse brains. The signal was predominantly detected in cortical (cortex), pyramidal (CA1), and granular (GCL) neurons. Cytoplasmic (i) and nuclear (ii) immunoreactivities of MUTYH were detected in the neurons of the cortex. MUTYH was also expressed in glial cells (iii). .

(a)

(b)

(c)