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[Preprint]. 2024 Feb 26:rs.3.rs-3976896. [Version 1] doi: 10.21203/rs.3.rs-3976896/v1

Figure 6. Both genetic deletion of microglial β2AR and prolonged exposure to β2AR antagonist accelerates pathology in female 5xFAD mice.

Figure 6

a Representative 20x confocal images of the ACC immunolabeled for plaque (6E10, blue), plaque-associated neuritic damage (LAMP1, green), and microglia (Iba1, magenta) in 4-month-old female 5xFAD CX3CR1-CreERT β2AR-flox without (Control, upper panels) or with tamoxifen (TAM) treatment to induce β2AR excision (β2AR deletion, lower panels) (scale bar = 200μm). b-d Ablating microglial β2AR in female 5xFAD CX3CR1-CreERT β2AR-flox mice with TAM treatment resulted in a trend toward increasing plaque load (b), significantly worsened neuritic damage (c), and microglia reactivity (d). e-g Female 5xFAD mice after treatment with ICI-118,551, a β2AR-specific antagonist, for 1 month (treatment started at 3 months) show significantly higher neuritic damage (f) but no changes in plaque load (e) and microglia reactivity (g) compared to DMSO-treated controls. n = 6–8 mice per treatment. Student t-test; *p<0.05, **p<0.01.