Abstract
BackgroundThere is evidence that impaired metabolism play an important role in the etiology of many neuropsychiatric disorders. Although this has not been investigated to date, several recent studies proposed that nitrogen metabolism-related parameters may have a pathophysiological role in autism.MethodsThe study enrolled 20 Saudi boys with autism aged 4 to 12 years and 20 healthy controls matched for age and gender. Levels of creatine, urea, ammonia, gamma-aminobutyric acid (GABA), glutamate:glutamine (Glu:Gln) ratio, and enzymatic activities of glutamate dehydrogenase, 5'-nucleotidase, and adenosine deaminase (ADA) were determined in plasma samples from both groups.ResultsWe found a significant elevation of creatine, 5'-nucleotidase, GABA, and glutamic acid and a significant decrease in the enzymatic activity of ADA and glutamine level in patients with autism compared with healthy controls. The most significant variation between the two groups was found in the Glu:Gln ratio.ConclusionA raised Glu:Gln ratio together with positive correlations in creatine, GABA, and 5'-nucleotidase levels could contribute to the pathophysiology of autism, and might be useful diagnostic markers. The mechanism through which these parameters might be related to autism is discussed in detail.
Highlights
There is evidence that impaired metabolism play an important role in the etiology of many neuropsychiatric disorders
There was a 43% increase in gamma-aminobutyric acid (GABA) in patients with autism compared with controls (Figure 2)
There was a marked increase in the Glu:Gln ratio, with all (20/20; 100%) of patients with autism having ratios greater than 1.25, whereas all the controls had ratios of less than 0.55; overall, there was an increase of 196.18% increase in the Glu:Gln ratio in patients with autism compared with controls (Figure 2)
Summary
There is evidence that impaired metabolism play an important role in the etiology of many neuropsychiatric disorders. This has not been investigated to date, several recent studies proposed that nitrogen metabolism-related parameters may have a pathophysiological role in autism. Autism is a complex disorder that is heterogeneous in nature, with varying degrees of severity, and for which no specific biological marker has been identified. The core deficits may fall in the similar domains, no two people with autism have exactly the same profile. Such a wide range of clinical features makes the diagnosis and treatment of autism very challenging. A role for mild mitochondrial dysfunction in autism has been suggested [4,5,6]
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