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Alternative Autism
Published in Michael Fitzpatrick, Mmr And Autism, 2004
The quest for an auto-immune mechanism in autism, perhaps linked to an infectious agent, received a boost in the late 1990s with the emergence of the concept of ‘Pandas’ (paediatric auto-immune neuro-developmental disorder associated with streptococcal infection) (Kurlan 1998). Cases of Tourette’s syndrome (characterised by multiple involuntary motor and vocal tics, notably taking the form of obscenities) sometimes occur, or worsen, following throat infections with the bacterium streptococcus. The discovery that some affected individuals had developed antibodies to specific areas of the brain implicated in movement disorders led to the hypothesis that anti-streptococcal antibodies cross-react with brain targets to produce localised neuronal damage, causing the characteristic features of Tourette’s. There are some parallels with autism: both conditions have a significant genetic component, and both have in the past been explained in psychogenic terms. A similar mechanism has been suggested to explain the onset of obsessional compulsive disorder in children, in whom it is often associated with tics (it also commonly co-exists with Tourette’s) (Murphy, Pichichero 2002). Although the ‘Pandas’ concept remains controversial, early studies of treatment with intravenous immunoglobulin (IVIG) have been reported as ‘promising for the highly selected patient’ (Perlmutter et al 1999, Singer 1999). However, it has been recommended that this treatment should be given only as part of controlled double-blind trials and should not yet be considered ‘ready for routine use’ (Singer 1999:1138).
Altered gut microbial profile is associated with abnormal metabolism activity of Autism Spectrum Disorder
Published in Gut Microbes, 2020
Zhou Dan, Xuhua Mao, Qisha Liu, Mengchen Guo, Yaoyao Zhuang, Zhi Liu, Kun Chen, Junyu Chen, Rui Xu, Junming Tang, Lianhong Qin, Bing Gu, Kangjian Liu, Chuan Su, Faming Zhang, Yankai Xia, Zhibin Hu, Xingyin Liu
The equilibrium between reduced and oxidized forms of glutathione (GSH and GSSG, respectively) is the primary determinant of intracellular redox status,54 which may play an essential role in this pathogenesis of ASD.55 Systemic deficits of glutathione and cysteine in ASD have been reported by Frustaci et al.56 Consistent with this finding, the current study found that the level of the intermediate product, Methylselenocysteine Se-oxide and 3-(Uracil-1-yl)-L-alanine from intermediate derivative of L-alanine were elevated in ASD group, which may further lead to a decrease in selenocysteine and the abnormal reaction of glutathione. Gut microbes in the gastrointestinal tract compete for nutrient resources in the usual symbiotic way; however, gut dysbiosis may interfere with nutrient resources. Thus, the current study suggested constipated ASD may be related to the failure of gastrointestinal epithelium to absorb antioxidant nutrients such as cysteine or selenocysteine. Recently, Wang et al. reported that alterations in the gut glutamate metabolism were associated with changes in gut microbiota composition in ASD children,57 but the differential metabolites shown in the Wang et al. study showed no difference between the ASD and TD groups of the current study, which imply the complexity of the pathological mechanism of ASD. These inconsistent and altered metabolites also reflect the limitation of the analysis method, since fecal metabolism analysis does not fully reveal the true metabolic state of the host. Thus, future studies that focus on the associated analysis of the urine metabolism with fecal microbiota metabolites are suggested to better understand the metabolite role in the pathological mechanism of autism.