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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: CCR5 antagonist reduces HIV-induced amyloidogenesis, tau pathology, neurodegeneration, and blood-brain barrier alterations in HIV-infected hu-PBL-NSG mice

Fig. 7

MVC abrogated HIV-induced increased formation and accumulation of CNS GSAP and amyloid-β (Aβ), but increased plasma Aβ levels. Aβ formation in the somatosensory cortex (a) and hypothalamus region (b) were quantified by immunohistochemistry using antibodies to Aβ1–42, followed by densitometry quantification of Aβ levels in all samples: 10 random FOV (5 FOV from the somatosensory cortex and 5 FOV from the hypothalamus region) analyzed for each sample (c). Aβ levels in brain tissues were also analyzed by Western blot (d) and densitometry quantification normalized to sample’s β-actin levels (e). Both immunohistochemistry and Western blot showed no Aβ in brain tissues of animals in the PBS or MVC groups. mRNA levels of GSAP (the enzyme that catalyzes Aβ formation) in brain tissues were quantified by real-time PCR (f). Plasma Aβ1–42 were quantified by ELISA (g). For panels a, and b, images were at 40X . The four animal groups analyzed included PBS, HIV, HIV + MVC, and MVC; 9 to 11 animals in each group. #P < 0.0001, ***[(e) P = 0.0009, (f) P = 0.0008, (g) P = 0.0005]. Error bars represent SD

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