Figure 4 | Molecular Psychiatry

Figure 4

From: p75NTR ectodomain is a physiological neuroprotective molecule against amyloid-beta toxicity in the brain of Alzheimer’s disease

Figure 4

ECD-Fc treatment reduces amyloid-beta production via inhibition of β-site APP-cleaving enzyme expression. (a) Western blot of full length amyloid precursor protein and carboxyl-terminal fragments in brain lysates (n=8, mean±s.e.m., analysis of variance, Tukey’s test, **P<0.01). (b) Western blot of β-site APP-cleaving enzyme in brain lysates (n=8, mean±s.e.m., analysis of variance, Tukey’s test, **P<0.01). (c) Analysis of β-site APP-cleaving enzyme activity in the mouse brain (n=11 for Con, n=9 for Tre, n=8 for Pre, mean±s.e.m., analysis of variance, Tukey’s test, **P<0.01). (d) Western blot of β-site APP-cleaving enzyme and sAPPβ in the extracts of cultured primary cortical neurons from mice with Alzheimer’s disease with (AD/p75+/+) or without p75NTR gene (AD/p75−/) after treatment with different doses of Aβ42 (n=3 per dose, mean±s.e.m., analysis of variance, Tukey’s test, **P<0.01). (e) Western blot of β-site APP-cleaving enzyme in extracts of cultured primary cortical neurons from wild-type mice (p75+/+) or p75NTR knockout mice (p75−/−) after treatment with 0.3 μm Aβ42 in presence or absence of recombinant ECD-Fc (n=3 per dose, mean±s.e.m., analysis of variance, Tukey’s test, *P<0.05). scr., scramble control.

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