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. 2017 May 2;8(3):257–266. doi: 10.14336/AD.2017.0112

Figure 4. Age-dependent increase of oligomeric tau and fibrillar amyloid pathology in cerebrovasculature of Tg2576 mice.

Figure 4.

(A) Representative images of brain sections from 23-month-old (top) and 3-month-old (bottom) transgenic Tg2576 mice reacted with antibodies specific for tau oligomers (T22, red) and amyloid-β (Aβ, 6E10, green). Mander’s colocalization coefficient suggests partial association of oligomeric tau and fibrillar Aβ in cerebrovasculature of 23-month-old mice. Because both T22 and Aβ immunoreactivity were absent in 3-month-old mice, a colocalization coefficient could not be computed for this group. Mean percent colocalization ± SEM are shown in the inset, which was merged without DAPI. (B) Quantitative analysis of T22-specific immunoreactivity shows increased cerebrovascular oligomeric tau deposition in 23 month-old compared to 3 month-old Tg2576 mice (**, t(19)=3.87, p=0.010). (C) Quantitative analysis of 6E10-specific immunoreactivity shows an age-dependent increase in cerebrovascular Aβ deposition in 23 month-old compared to 3 month-old mice (*, t(20)=2.62, p=0.016). n=3; 10-15 sections from each sample were analyzed for tau oligomers. All sections were positive for tau oligomers. All of the transgenic Tg2576 mice used were positive for both Abeta and tau oligomers.