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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating PICALM at the blood-brain barrier

Fig. 3

Artesunate does not alter the levels of Aβ processing proteins and Aβ clearance enzymes in Picalm+/−; 5XFAD mice. A amyloid precursor protein (APP) abundance in cortex, B APP C-terminal fragment (APP-CTF) abundance in cortex. C β-secretase (BACE1) abundance in cortex, D soluble APP-β (sAPPβ) levels in cerebrospinal fluid (CSF), E γ–secretase activity as determined by the production of Notch intracellular domain (NICD) fragment from Notch protein, indicated by NICD abundance in cortex, F neprilysin abundance in cortex, and G insulin degrading enzyme (IDE) abundance in cortex of Picalm+/−; 5X FAD mice treated with artesunate or vehicle as in Fig. 2A. The relative abundance of proteins was normalized by the house-keeping gene glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein. Single points per mouse indicated by circles, with boxes representing mean ± SD. A-E, G n = 8 per group; F n = 7–8 per group. ns = non-significant by two-tailed t-test. Full blots for A-C, E-G shown in supp. Fig. 5

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