Autism Spectrum Disorders
|MedDra Level:||[ ]|
- Twenty-seven of their 313 metabolites in faeces and serum were also different, and of the 313, two – 5-aminovaleric acid (5AV) and taurine – were also present in lower quantities. These two molecules are neurotransmitter agonists: their molecular structures resemble that of the GABA and glycine neurotransmitters, and they interfere with the latter’s functions.” As it happens, both GABA and glycine, help the brain develop normally.
And when the scientists injected the mice with 5AV and taurine, the rodents developed ASD-like symptoms. Ergo, bacteria probably interfere with brain functions using these molecules. (1)
- Members of the C. histolyticum group are recognized toxin-producers and may contribute towards gut dysfunction, with their metabolic products also exerting systemic effects.
- Strategies to reduce clostridial population levels harboured by ASD patients or to improve their gut microflora profile through dietary modulation may help to alleviate gut disorders common in such patients. (3)
- L. reuteri produces a metabolite that activates the vagus nerve to promote oxytocin, the cuddle hormone.This hormone then turns on the brain reward center for social behavior. Impeding the message at any point along this relay from bacteria to metabolite to vagus nerve to oxytocin receptors impairs the animals sociability (4)
- Blood of mice with autism symptoms had levels of a chemical called 4-ethylphenylsulphate (4EPS) that were 46 times higher than that of the control group. This substance is structurally similar to a chemical called para-cresol that is elevated in people with autism .
- When the researchers injected 4EPS into wild-type mice, they started behaving like the untreated autistic mice - obsessively repeating some behaviours and squeaking differently when greeting other mice. (5)
- ASD mice were fed with Bacteroides fragilis, a gut microbe with positive effects on the immune system, the abundance of 34% of these metabolites changed back, gut barrier integrity was improved, the gut-microbiome was restored to a non-ASD state, and ASD-related behavioral abnormalities were ameliorated. In addition, a 46-fold increase of 4-ethylphenylsulfate (4-EPS) in the serum of MIA offspring returned to normal levels.
-A second metabolite elevated in the MIA serum, and normalized by treatment with B. fragilis, was indolepyruvate. Indolepyruvate is generated by microbial tryptophan catabolism and is related to indolyl-3-acryloylglycine, another human autism marker. Indolepyruvate elevation could be linked to increased serum levels of serotonin, yet another human autism biomarker.
- Application of the B. fragilis probiotic, increased many other metabolites including N-acetylserine, which the authors hypothesize may provide protection against some ASD symptoms. (6)
- Bifidobacterium, Blautia, Dialister, Prevotella, Veillonella, and Turicibacter were consistently decreased, while Lactobacillus, Bacteroides, Desulfovibrio, and Clostridium were increased in patients with ASD relative to HCs in certain studies. (7)
- Specifically, Bacteroidetes, Bacteroides, and Parabacteroides were decreased in oASD mice, with an increase in Akkermansia, Sutterella, and Lachnospiraceae, as has been reported in humans.
- Both the Bacteroides spp. (b20cd_Bacteroides) and P. merdae (4ae7e_Parabacteroides) correlated with reduced repetitive behavior and increased social behavior.
- E. tayi (02b40_Lachnospiraceae) showed the opposite effects, as it correlated with increased repetitive behavior and social interaction deficits
- P. merdae, were more abundant in ASD individuals from human.
- L. reuteri produces a metabolite that activates the vagus nerve to promote oxytocin, the cuddle hormone.This hormone then turns on the brain reward center for social behavior. Impeding the message at any point along this relay from bacteria to metabolite to vagus nerve to oxytocin receptors impairs the animals sociability.
- [1.1] Fecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specified  
- [1.2] Differences in fecal microbial metabolites and microbiota of children with autism spectrum disorders  
- [1.3] Gastrointestinal microbiota in children with autism in Slovakia.  
- [1.4] Gastrointestinal flora and gastrointestinal status in children with autism-comparisons to typical children and correlation with autism severity  
- [1.5] Gut microbial dysbiosis in Indian children with autism spectrum disorders  
- [1.6] Pyrosequencing study of fecal microflora of autistic and control children  
- [1.7] Reduced incidence of Prevotella and other fermenters in intestinal microflora of autistic children  
- [1.8] Gastrointestinal microflora studies in late-onset autism  
- [1.9] Increased abundance of Sutterella spp. and Ruminococcus torques in feces of children with autism spectrum disorder  
- [1.10] Application of novel PCR-based methods for detection, quantitation, and phylogenetic characterization of Sutterella species in intestinal biopsy samples from children with autism and gastrointestinal disturbances  
- [1.11] Real-time PCR quantitation of Clostridia in feces of autistic children  
- [1.12] Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children  
- [1.13] Human Gut Microbiota from Autism Spectrum Disorder Promote Behavioral Symptoms in Mice  [Research] 
- [1.14] Supplements, worms and stool: How families are trying to game the gut to treat autism traits  [Report]