1998
DOI: 10.1016/s0306-9877(98)90107-4
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Autism and clostridium tetani

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Cited by 184 publications
(126 citation statements)
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References 80 publications
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“…Disruptions in the gut microbiota may be one common thread linking these two disparate systems. For instance, intestinal colonization by the anerobic bacteria, Clostridium tetani, was postulated to increase the risk and severity of ASD; however, this past work did not test for a direct linkage (Bolte, 1998). These bacteria produce a neurotoxin that may reach the brain via the vagus nerve.…”
Section: Human Epidemiologic Studies Linking Gut Dysbiosis and Asdmentioning
confidence: 97%
“…Disruptions in the gut microbiota may be one common thread linking these two disparate systems. For instance, intestinal colonization by the anerobic bacteria, Clostridium tetani, was postulated to increase the risk and severity of ASD; however, this past work did not test for a direct linkage (Bolte, 1998). These bacteria produce a neurotoxin that may reach the brain via the vagus nerve.…”
Section: Human Epidemiologic Studies Linking Gut Dysbiosis and Asdmentioning
confidence: 97%
“…Numerous theories have been proposed regarding the aetiology of ASDs (including pathogenesis), yet the condition remains poorly understood. Recent studies have correlated gut dysfunction with ASD group and suggested a possible role of the gastrointestinal (GI) microflora in symptomatology and/or severity of symptoms in autistic children (Shaw et al, 1995;Bolte, 1998). However, the evidence is rather speculative, as little is known on the gut flora of ASD sufferers compared with that of healthy controls.…”
Section: Introductionmentioning
confidence: 99%
“…The case of Rab3A indicates a probable tangible medical benefit from a systematic analysis of the proteolytic susceptibility of other SNARE proteins to the clostridial NTs. Certain cases of autism, a non-fatal neurological disorder, were recently postulated to be caused by subacute chronic infection by clostridial species and tetanus NT (Bolte, 1998;Finegold et al, 2002). If this is correct, it follows that the familiar acute spastic or flaccid paralysis does not ensue because, perhaps, the NT protease acts at site(s) other than NMJ and CNS (the well recognized sites of action of the NT protease), by gaining entry in an as yet unknown way, on the familiar or other protein substrates.…”
mentioning
confidence: 99%