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. Author manuscript; available in PMC: 2018 Jul 21.
Published in final edited form as: Circ Res. 2017 May 17;121(3):258–269. doi: 10.1161/CIRCRESAHA.117.311054

Figure 6. Deletion of CD36 or Nox2 in PVM counteracts the neurovascular dysfunction and vascular oxidative stress in Tg2576 mice.

Figure 6

Tg2576 mice receiving WT BM (WT→Tg) exhibit attenuation in CBF responses to whisker stimulation (A,B) and ACh (C) similar to those observed in Tg2576 mice not subjected to BM transplantation. Transplant of CD36−/− or Nox2−/− BM rescues the neurovascular dysfunction in Tg2576 mice (A–D), without altering brain Aβ1-40 and Aβ1-42 (E,F). *p<0.05 from WT→WT, CD36→Tg, or Nox2→Tg; ANOVA and Tukey’s test; n=5–6/group.