Short communicationIn vitro aggregation facilitates β-amyloid peptide-(25–35)-induced amnesia in the rat
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2018, Neurobiology of Learning and MemoryCitation Excerpt :The proof-of-concept experiment used the pharmacological model induced by ICV injection of oligomerized Aβ25–35 peptide (Maurice et al., 1996). This AD-like model is widely used in pharmacological screening since it presents a high descriptive validity, a good predictive validity towards more elaborated transgenic mouse models of AD, and a short onset in the appearance of behavioural deficits and toxicity, within 1–2 weeks after peptide injection in mice and rats (Maurice et al., 1996; Delobette, Privat, & Maurice, 1997; Meunier et al., 2006; Klementiev et al., 2007; Chavant et al., 2010). Numerous aspects of the toxicity are rapidly observed, including oxidative stress, neuroinflammation, apoptosis, synaptic and cellular losses, amyloid accumulation, Tau hyperphosphorylation and activation of the related kinases.
Effect of amyloid-Β (25–35) in hyperglycemic and hyperinsulinemic rats, effects on phosphorylation and O-GlcNAcylation of tau protein
2017, NeuropeptidesCitation Excerpt :Insulin levels were determined using rat insulin ELISA kit obtained from Crystal Chem Inc. (Chicago, IL, USA). The Aβ25–35 peptide (100 μM) was dissolved in sterile water (Pike et al., 1995), and incubated at 37 °C for 24 h to favor its aggregation, before injecting into animals (Maurice et al., 1996; Delobette et al., 1997). Peptide aggregation was confirmed by light-scatter tests using Malvern Z-sizer, Grovewood Road on the peptide, which indicate 10,000,000 Da for aggregated ßA peptide based on the size calculated by the equipment Fig. 2.