The amyloid-β25–35 injection into the CA1 region of the neonatal rat hippocampus impairs the long-term memory because of an increase of nitric oxide
Section snippets
Acknowledgments
This work was supported in part by CONACYT (61205), INNN (15/06), UNAM PAPIIT IN214609 and IN212108 given to J.G. and the Laboratory of Neuropharmacology-BUAP grant (LNAB1-08) given to D.L. Thanks to Dr. Ellis Glazier for editing this English-language text.
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2014, Pharmacology and TherapeuticsCitation Excerpt :Thus, aggregated Aβ42 correlates with caspase-8 mRNA levels in the temporal region of AD-affected brains (Matsui et al., 2006) and is increased in damaged neurons (Ohyagi et al., 2000). A derivative fragment of Aβ (Aβ25–35), that is not consistently detectable in AD-affected brains but can mimic some of Aβ-related phenotypes (Diaz et al., 2010; Meunier, Leni, & Maurice, 2006), indeed promotes apoptosis in lymphocytes (Velez-Pardo, Ospina, & Jimenez del Rio, 2002) and in PC12 cells (Martin et al., 2001). This Aβ-mediated enhanced neurodegeneration also occurs in vivo in a mouse model of Alzheimer's disease (transgenic mice harboring a presenilin 1 mutation) where Aβ accumulation triggers retinal degeneration (Ning, Cui, To, Ashe, & Matsubara, 2008).
The role of NOS in the impairment of spatial memory and damaged neurons in rats injected with amyloid beta 25-35 into the temporal cortex
2011, Pharmacology Biochemistry and BehaviorCitation Excerpt :The dysfunction in the NO metabolism and the events of toxicity that this molecule enhances has been linked to neurodegeneration (Giasson et al., 2000; Stack et al., 2008), as our results have shown. Several authors have studied the effects of NO in the memory process in models of neurodegeneration, but now it appears that high amounts of nitrites could be a source of damage that promotes the nitrosative stress that enhances protein nitration and neuronal damage to cause memory impairment (Limón et al., 2009a,b; Díaz et al., 2010). The nNOS and iNOS immunoreactivity have been found over the chronic course of β-amyloid toxicity in the cortex of patients with AD (Fernández-Vizarra et al., 2004; Malinski, 2007).