Can Toxoplasma gondii Pave the Road for Dementia?

Figure 3

Double-labelled immunohistochemistry in the amygdala and hippocampus for the in situ biomarker assays. (a) Immune reactivity for NF-κβ. In the infected mice: (A) marked expression of NF-κβ in amygdala containing T. gondii cysts (black arrows) (l00x), (B) nuclear and cytoplasmic expression of NF-κβ in the perivascular mononuclear inflammatory infiltrates in the amygdala (400x), and (C) high expression of NF-κβ in the hippocampus (100x). In healthy controls: hypoexpression of NF-κβ in (D) the amygdala and (E) the hippocampus (40x). (b) Immune reactivity for IGF-1R. In the infected mice: (A) hypoexpression of IGF-1R around T. gondii cyst (black arrow) and microvasculature (white arrows) in the amygdala (40x) and (B) low evidence of IGF-1R immune staining in the hippocampus (40x). In the healthy controls: (C) high expression of IGF-1R in the amygdala (100x), (D, E) perivascular expression of IGF-1R (blue arrows) (400x), and (F) marked expression of IGF-1R in the hippocampus (100x). Spearman’s rho showed that NF-κβ and IGF-1R area percentage and O.D. were in moderate negative correlations, -0.584 and -0.725, respectively.

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