Metabolic brain disease
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Uremic encephalopathy is a severe complication of renal failure. The underlying pathogenesis is unknown although several mechanisms have been suggested. Renal failure causes oxidative stress leading to cardiovascular complications. ⋯ In conclusion, our results indicate that AKI leads to oxidative stress in the brain, especially in the hippocampus and in the frontal cortex. This kidney-brain crosstalk mediated by increased oxidative stress might explain some of the symptoms of uremic encephalopathy. The causes and consequences of oxidative damage observed in the brain during AKI remain to be elucidated.
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Metabolic brain disease · Jun 2018
Meta AnalysisAssociation between PDE4D rs966221 polymorphism and risk of ischemic stroke: a systematic review and meta-analysis.
PDE4D polymorphism (SNP83/rs966221) was reported to be associated with the susceptibility to ischemic stroke (IS), however, the results were inconclusive. An electronic search of Embase, PubMed, CNKI and Wan Fang Date was performed to identify relevant studies published throughout April 2017. A total of 26 studies were enrolled in the analysis. ⋯ In conclusion, our meta-analysis demonstrated that the SNP83 polymorphism in the PDE4D gene might contribute to IS susceptibility especially in Asian populations. Whereas the relationship of the polymorphism to the disease in Caucasian population was still in controversial. In future, additional well designed studies with larger sample sizes are still required to further elucidate this association.
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Metabolic brain disease · Jun 2018
Vanillic acid attenuates cerebral hyperemia, blood-brain barrier disruption and anxiety-like behaviors in rats following transient bilateral common carotid occlusion and reperfusion.
Transient bilateral common carotid artery occlusion (tBCCAO), followed by reperfusion, is a model of transient global hypoperfusion. In the present study we aimed to investigate the probable effects of Vanillic acid (VA) on some physiological parameters including cerebral hyperemia, blood-brain barrier (BBB) disruption, anxiety behaviors and neurological deficits induced by bilateral occlusion of the common carotid arteries and reperfusion (BCCAO/R) in rats. Rats were randomly divided into four groups; Sham, BCCAO/R, VA and VA+ BCCAO/R. ⋯ Further, VA attenuated reactive hyperemia and BBB disruption in BCCAO/R rats compared with untreated rats (p < 0.01). To our knowledge, this study is the first to reveal VA could attenuate reactive hyperemia and improve BBB disruption following BCCAO/R, and could improve neurological scores and anxiety like behaviors in this model of cerebral hypoperfusion. These results suggest that VA could be a promising pretreatment agent in cerebral hypoperfusion.