NAP prevents acute cerebral oxidative stress and protects against long-term brain injury and cognitive impairment in a model of neonatal hypoxia–ischemia

Mechanisms of Neuroprotection from Hypoxia-Ischemia (HI) Brain Injury by Up-regulation of Cytoglobin (CYGB) in a Neonatal Rat Model

“…As compared with the adult brain, the immature brain is highly susceptible to oxidative stress because of its high concentration of unsaturated fatty acids, rate of oxygen consumption, and availability of redox-active iron but poorly developed scavenging systems (48). Therefore, oxidative stress is thought to be one of the major factors that induce neuronal cell death in the immature brain (49). In this study, MDA and SOD activity were measured to confirm the antioxidant role of CYGB in vivo.…”

Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges

“…Many papers have investigated the behavioral outcomes of Rice–Vannucci injury in adult rodents. This model gives rise to well documented behavioral phenotypes including: impaired spatial learning and memory (Balduini et al, 2000, 2001; Ikeda et al, 2001; Wang et al, 2002; Arteni et al, 2003; Pereira et al, 2007; Cai et al, 2009; Greggio et al, 2011; Hill et al, 2012; Zheng and Weiss, 2013; Alexander et al, 2014; Gillani et al, 2015); impaired motor function as assessed by rotarod test, open field and motor reflexes (Barth and Stanfield, 1990; Jansen and Low, 1996a,b; Jansen et al, 1997; Balduini et al, 2000, 2001; Tomimatsu et al, 2002; Ådén et al, 2003; Lubics et al, 2005; Pazaiti et al, 2009; Im et al, 2010; Nijboer et al, 2010; Karalis et al, 2011; Chen et al, 2012; Ruiz et al, 2012; Sanches et al, 2012; Zheng et al, 2012; Xiong et al, 2013; Alexander et al, 2014; Gillani et al, 2014, 2015; Kim et al, 2014; Zhang Q. et al, 2014; Park D. et al, 2015; Park W.S. et al, 2015); sensory processing abnormalities (Alexander et al, 2014); and other cognitive phenotypes, such as reduced attention (Buwalda et al, 1995; Martin et al, 1997; Sanches et al, 2013; Perera et al, 2014; Miguel et al, 2015).…”

Mitochondrial Abnormalities in Alzheimer’s Disease

“…NAP has been shown to reduce tau hyperphosphorylation and Aβ accumulation in both in vitro and in vivo AD models, and also benefit cognitive test performance in some of these models (Gozes & Divinski, 2004; Matsuoka et al, 2007; Matsuoka et al, 2008; Shiryaev et al, 2009; Vulih-Shultzman et al, 2007). Although its biological effects remain to be fully investigated (Shiryaev et al, 2011), based on encouraging preclinical data and an apparent lack of toxicity NAP is now being tested in persons with AD and other disorders of the CNS (Greggio et al, 2011; Idan-Feldman et al, 2011; Javitt et al, 2011). A recent phase IIa clinical study reported that intranasal NAP improved memory performance in patients with an amnestic MCI syndrome, a frequent an AD precursor state (Gozes et al, 2009).…”