A Novel Mouse Model of Alzheimer's Disease with Chronic Estrogen Deficiency Leads to Glial Cell Activation and Hypertrophy
Figure 2
Six-month-old sex-hormone-imbalanced FORKO-APPsw/PS1∆9 mice show similar plaque localization and number but difference in plaque appearance and size compared to mice coexpressing APPsw/PS1∆9 alone. (a) Six-month-old sex-hormone-imbalanced FORKO-APPsw/PS1∆9 mice show no significant changes in plaques number compared to mice coexpressing APPsw/PS1∆9 alone. APPsw/PS1∆9 and FORKO-APPsw/PS1∆9 mice were examined by immunocytochemical staining for Aβ peptide with the polyclonal antibody anti-Aβ40/42 (FCA18), anti-Aβ40 (CT40), or anti-Aβ42 (CT42). Quantification of plaques number was achieved by plaque counting on sagittal brain sections of hippocampus and cortex in APPsw/PS1Δ9 (+/+; ) and FORKO-APPsw/PS1∆9 (−/−; ). (b) Presented is anti-Aβ40/42 (FCA18) immunostaining of sagittal brain sections from APPsw/PS1∆9 (; (A), (C), and (E)) and FORKO-APPsw/PS1Δ9 (; (B), (D), and (F)). By 6 months of age, both mice strains had developed Aβ plaques in typical areas of the brain, such as ((A) and (B)) the frontal cortex, ((C) and (D)) the parietal cortex, and ((E) and (F)) the hippocampus. Note that many more relatively large and diffuse plaques are found in chimeric mice compared to those in APPsw/PS1∆9 brains. Scale bar in all panels is 20 um. ((G) and (H)) Quantification of the plaques perimeter revealed 16.67 % of large, 17.54 % of medium, and 65.79 % of small plaques in FORKO-APPsw/PS1∆9 (H) compared to 2.3 % of large plaques, 14.94 % of medium and 82.76% of small plaques in APPsw/PS1∆9 (G).
