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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: A multifunctional therapeutic approach to disease modification in multiple familial mouse models and a novel sporadic model of Alzheimer’s disease

Fig. 2

Retention of neuroprotective activity (a-c) and the effects of NMZ treatment in APP/PS1 mice (d-h). Primary neuronal cultures treated with NMZ showed neuroprotection when exposed to 2 h OGD (a) and both low (b) and high (c) doses of Aβ oligomers. Data show mean ± S.E.M. normalized to insult and non-insult vehicle controls. Male APP/PS1 mice (n = 6–8) treated for 12 weeks with NMZ (1 mg/kg, i.p. plus 20 mg/kg/day in drinking water) demonstrated an improvement in the RAWM task (d) and reduction in levels of the pro-inflammatory marker, TNF-α, and in neurotoxic oAβ, in whole brain homogenates (e). Data show mean ± S.E.M compared to vehicle. NMZ also reduced total Aβ1–42 deposit volumes compared to vehicle control in cortex and hippocampal homogenates (f). Data show mean ± S.E.M of total deposit volume determined by fluorescent staining and were analyzed by two-tailed student’s t-test. All statistical significance is indicated by *p < 0.05, **p < 0.01, ***p < 0.001. Representative images of hippocampi and cortices with histochemical staining reveal significantly less activated microglia shown with Iba-1 (magnification: 4×, 10×, and 20× from left to right) (g) and reduced thioflavin-S staining of amyloid plaques in NMZ treatment compared to vehicle (magnification: 2× and 6×) (h)

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