scholarly journals Role of NAD+, Oxidative Stress, and Tryptophan Metabolism in Autism Spectrum Disorders

2013 ◽  
Vol 6s1 ◽  
pp. IJTR.S11355 ◽  
Author(s):  
Musthafa Mohamed Essa ◽  
Selvaraju Subash ◽  
Nady Braidy ◽  
Samir Al-Adawi ◽  
Chai K Lim ◽  
...  

Autism spectrum disorder (ASD) is a pervasive neuro-developmental disorder characterized by impaired social interaction, reduced/absent verbal and non-verbal communication, and repetitive behavior during early childhood. The etiology of this developmental disorder is poorly understood, and no biomarkers have been identified. Identification of novel biochemical markers related to autism would be advantageous for earlier clinical diagnosis and intervention. Studies suggest that oxidative stress-induced mechanisms and reduced antioxidant defense, mitochondrial dysfunction, and impaired energy metabolism (NAD+, NADH, ATP, pyruvate, and lactate), are major causes of ASD. This review provides renewed insight regarding current autism research related to oxidative stress, mitochondrial dysfunction, and altered tryptophan metabolism in ASD.

Author(s):  
Shanna L. Burke ◽  
Jessica Cobb ◽  
Rumi Agarwal ◽  
Marlaina Maddux ◽  
Marcus S. Cooke

Abstract Growing interest in the pathogenesis of autism spectrum disorders (ASDs) and other intellectual and developmental disabilities (IDD) has led to emerging evidence implicating a role for oxidative stress. However, understanding the strength of this association is made challenging by the use of a variety of purported biomarkers of oxidative stress, many of which have either uncertain specificity or flawed methods of analysis. This review aims to address this issue, which is widespread in the ASD and IDD literature, by providing readers with information concerning the strengths and limitations of the choice and analysis of biomarkers of oxidative stress. We highlight that biomarkers and assays should be specific, sensitive, reproducible, precise, robust, and chosen with careful consideration. Future studies should be sufficiently powered and address sample collection, processing, and storage which are, additionally, poorly considered, sources of bad practice, and potential errors. Only with these issues considered, will the data lead to conclusions as to the precise role of oxidative stress in ASDs and IDD.


2016 ◽  
Vol 22 (18) ◽  
pp. 2650-2656 ◽  
Author(s):  
Noelia Diaz-Morales ◽  
Susana Rovira-Llopis ◽  
Irene Escribano-Lopez ◽  
Celia Bañuls ◽  
Sandra Lopez-Domenech ◽  
...  

2021 ◽  
Vol 168 ◽  
pp. 138-145
Author(s):  
Yuan-Mei Wang ◽  
Ming-Yue Qiu ◽  
Qing Liu ◽  
Huang Tang ◽  
Hong-Feng Gu

2020 ◽  
Vol 83 (6) ◽  
pp. AB11
Author(s):  
Amanda Kuan ◽  
Sai Yee Chuah ◽  
Yun Sheng Yip ◽  
Nguan Soon Tan ◽  
Tien Guan Steven Thng

2016 ◽  
Vol 19 (2) ◽  
pp. 17-22 ◽  
Author(s):  
H Onay ◽  
D Kacamak ◽  
AN Kavasoglu ◽  
B Akgun ◽  
M Yalcinli ◽  
...  

AbstractThe aim of this study was to identify the sequence mutations in the Neurexin 1 (NRXN1) gene that has been considered as one of the strong candidate genes. A total of 30 children and adolescents (aged 3-18) with non syndromic autism were enrolled this study. Sequencing of the coding exons and the exon-intron boundaries of the NRXN1 gene was performed. Two known mutations were described in two different cases. Heterozygous S14L was determined in one patient and heterozygous L748I was determined in another patient. The S14L and L748I mutations have been described in the patients with autism before. Both of these mutations were inherited from their father. In this study, two of 30 (6.7%) autism spectrum disorder (ASD) patients carrying NRXN1 gene mutations were detected. It indicates that variants in the NRXN1 gene might confer a risk of developing nonsyndromic ASD. However, due to the reduced penetrance in the gene, the causal role of the NRXN1 gene mutations must be evaluated carefully in all cases.


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