The development of a novel mouse model of transient global cerebral ischemia

Nicotinamide mononucleotide inhibits post-ischemic NAD+ degradation and dramatically ameliorates brain damage following global cerebral ischemia

“…However, the protective effect of anesthetics was observed only at short, 3 days recovery period (Elsersy et al, 2004), for discussion see (Onken et al, 2012). Furthermore, our model gives rise to similar extends of CA1 damage as observed in commonly used models of mouse forebrain ischemia (Hua et al, 2006; Zhen and Dore, 2007, Yonekura et al, 2004, Panahian et al, 1996). Additionally, it is unlikely that the NMN protective effect was due to increased intra-ischemic isoflurane levels since both vehicle and NMN treated animals were subjected to the same isoflurane protocol.…”

Impaired gait pattern as a sensitive tool to assess hypoxic brain damage in a novel mouse model of atherosclerotic plaque rupture

“…We investigated the neurons of the parietal cortex and could detect clear signs of hypoxic damage, such as eosinophilic cytoplasm and pyknotic nuclei. These results were confirmed by other studies in which the mechanisms and effects of cerebral ischemia were investigated [11,12]. We were also able to find a correlation between the percentage of pyknotic neurons and track width, which confirms the relevance of these measurements as a marker for hypoxic brain damage.…”

Ischemic Postconditioning Protects Against Global Cerebral Ischemia/Reperfusion-Induced Injury in Rats

“…11,24,25 Neuron loss increases with reperfusion time, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive neurons can be seen only 1 day after reperfusion. 26 Some studies have demonstrated that this neuron death is, at least in part, caused by apoptosis.…”