ABSTRACT
Autism spectrum disorders are complex developmental disorders with increasing incidence and poorly understood etiology. Imbalance of amino acids profoundly influences brain function, and is thought to be one of the key players in the pathophysiology of autism. This study aimed to measure the plasma amino acid profiles of 20 Egyptian and 20 Saudi autistic patients in comparison to matching healthy controls to clarify the role of impaired amino acid concentrations in the etiology of autism. Plasma amino acids profiles were measured using high performance liquid chromatography. While plasma levels of glutamic, aspartic, and glycine recorded the most significant percentage elevated amino acids, glutamine, asparagine, arginine, tyrosine and isoleucine recorded the most remarkable percentage decrease in autistic patients from both populations compared to controls. Among the calculated relative values, only acidic/basic, and glutamate/glutamine ratios were significantly higher in autistics compared to controls. Non-essential/essential and glucogenic/ketogenic ratios were unaltered in autistics compared to controls. Increased plasma glutamate/glutamine ratio, together with increased glycine, arginine, aspartate, aspargine levels, and acidic/basic amino acid ratio can serve as a predictive tools for the early detection of autism. These findings suggest that glu-tamatergic abnormalities in the brain may be associated with the pathobiology of autism
Subject(s)
Autistic Disorder , Glutamic Acid , GlutamineABSTRACT
Background: Patients with Parkinson's disease (PD) show a dramatic increase in their brain iron content has suggested the role of iron in degeneration of dopaminergic nigrostriatal neurons in PD. Several studies have described the association of high dietary iron and PD. However; the role of iron the pathogenesis of PD is still hotly debated. Objective: The purpose of this study was to investigate the effects of L-glutamate; oxyferriscorbone (OFC) and L-Deprenyl on parkinsonian syndrome (PS) in rats. Methods: This study was performed on 244 male non-strain rats (250-270g;-10 wk old). By intranigral bilateral administration of 1-Methyl-4-phenylpyridinium ion (MPP+) (10?g/2?/l into each side) and 6-hydroxydopamine (6-OHDA) (12?g/3?l; Sigma; into each side ) in rats was induced the dopamine deficient model of PS (DDPS) and the cholinergic model (ChPS) in rats produced by intracaudate injection of acetylcholine (5?g/2?l each side ) with neostigmine (1?g/1?l each side). These models were then used to investigate the effects of L-glutamate; OFC and L-Deprenyl on PS and the electric activity (EA) of the sensorimotor cortex; caudate nuclei; ventrolateral nuclei of the thalami; and substantia nigra in rats. Results: Intracaudate injection of L-glutamate (100?g/3?l; into each side) enhanced bradykinesia; rigidity and produced a weak tremor in the DDPS. This effect was more pronounced in ageing (12 months) rats and in some of them; we observed orofacial dyskinesia. In the ChPS; L-glutamate enhanced tremor and bradykinesia. The single and repeated injection of OFC (5; 7; 5; 15 and 20 mg/rat; intraperitioneally; i.p.) did not produce a statistically significant change of PS in both models. L-deprenyl (5; 10 and 20 mg/kg; i.p.) dose-dependently reduced bradykinesia and rigidity in the DDPS; whereas increased tremor and failed to decrease bradykinesia and rigidity in the ChPS. Conclusion: This study indicates that glutamate aggravates PS in both models. OFC does not have any effect on PS. Deprenyl has antiparkinsonian effect in the DDPS; but not in the ChPS