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Objective: To evaluate the neuroprotective effect of ashwagandha extract against aluminum chloride-induced neurotoxicity in rats. Methods: Rats were divided into control, aluminum-intoxicated rats treated daily with aluminum trichloride (AlCl3) (100 mg/kg, orally) for 30 d and aluminum-intoxicated animals protected by receiving daily ashwagandha extract (200 mg/kg, orally) one hour before AlCl3 administration for 30 d. Levels of lipid peroxidation, nitric oxide, reduced glutathione and tumor necrosis factor-α were measured in the cortex, hippocampus and striatum. In addition, the activities of Na+, K+, ATPase and acetylcholinesterase were determined in the three studied brain regions. Results: Aluminum increased the levels of lipid peroxidation and nitric oxide in the cortex, hippocampus and striatum and decreased the reduced glutathione level in the hippocampus and striatum. In rats protected with ashwagandha extract, non significant changes were observed in lipid peroxidation, nitric oxide and reduced glutathione. In addition, ashwagandha extracts prevented the increased activity of acetylcholinesterase and Na+, K+, ATPase induced by AlCl3 in the cortex, hippocampus and striatum. The present findings also showed that the significant increase in tumor necrosis factor-α induced by AlCl3 in the cortex and hippocampus was prevented by ashwagandha extract. Conclusions: The present results suggest that ashwagandha extract possesses antioxidant and anti-inflammatory effects against aluminum neurotoxicity. In addition, ashwagandha extract could prevent the decline in cholinergic activity by maintaining normal acetylcholinesterase activity. The later effect could recommend the use of ashwagandha as a memory enhancer.

Microtia is a congenital anomaly that is found with different prevalence among various populations. The exact etiology of ear anomalies is still unknown. We describe a new additional family with this rare disorder; Johnson-McMillin syndrome (JMS) where mother, son, and distant grandmother have multiple features of JMS in the form of microtia, facial asymmetry, ear malformation, hearing defect, and hypotrichosis. Variable presentations in this family could be referred to phenotype variation supporting an autosomal dominant pattern of inheritance. We observed that the mother was very sad and suffered from feelings of guilt. We found that she had isolated herself from family and community out of fear of being stigmatized and hurt. We concluded that the occurrence of microtia is of public health importance, adhering to traditional marriage customs in Egypt increases women's risk of giving birth to a disabled child, yet the mothers are blamed and shamed for their children's birth defects by their husbands, families, and communities, while the fathers are not stigmatized.