Researchers observed that CA activates the Keap1/Nrf2 transcripti

Researchers observed that CA activates the Keap1/Nrf2 transcriptional factor, thereby protecting neurons from oxidative stress and excitotoxicity. In cerebrocortical cultures, CA-biotin accumulates in nonneuronal cells at low concentrations and in neurons at higher concentrations. Furthermore, based on the fact that CA can transfer into the brain, a single intraperitoneal injection blog of sinaling pathways of CA (1mg/kg) 1h prior to MCAO (middle cerebral artery occlusion) protects the brain against the toxic effects of the ischemia/reperfusion [11].In addition to the antioxidant activity of carnosic acid [22], it has been reported to have several other beneficial effects, including chemoprotective effects in the presence of carcinogens, suppression of metalloproteinase-1 mRNA expression which is induced by UVA irradiation[23], anti-inflammatory effect [24], and neurotrophic activities [25].

Furthermore, Ninomiya et al. (2004) showed that oral administration of CA at a dose of 20mg/kg/day for 14 days suppressed the increased epididymal fat and body weight gain in high fat diet-fed mice [26]. Additionally, CA can protect photoreceptors against light-induced oxidative damage and retinal dysfunction [27].In this study, due to the passive shock avoidance learning test results, there is a 90.3% increase in the mean score of the A�� + CA group as compared to the A�� group. The results of the short-term spatial memory test demonstrated a 39% increase in the mean score in the A�� + CA group as compared to the A�� group.5.

ConclusionTaken together, it is suggested that the administration of CA could significantly improve short-term spatial and learning memory scores following their impairment by A�� toxicity. This protective role may be due to the antioxidant, anti-inflammatory, and neurotrophic activities of CA. Therefore, CA may be considered as a chemopreventive agent against neurodegenerative disorders like Alzheimer’s disease.Conflict of InterestsThe authors declare that there is no conflict of interests regarding the publication of this paper.AcknowledgmentsThis work was supported by a grant from Iran University of Medical Sciences (Chancellor for Research and also Cellular & Molecular Research Center), Tehran, Iran.
Human herpesvirus 6 (HHV-6) infection is common and has a worldwide distribution.

Recently, HHV-6A and HHV-6B have been reclassified Dacomitinib into two distinct species based on different biological features (genetic, antigenic, and cell tropism) and disease associations: HHV-6A, with still unknown disease association, and HHV-6B, the etiologic agent of roseola (exanthem subitum), a childhood benign febrile disease.In the recent years, several reports have provided important information linking HHV-6A/B to autoimmune diseases (AD) including multiple sclerosis [1�C7], autoimmune connective tissue diseases [8�C11], and Hashimoto’s thyroiditis [12].

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