Serotonin and amino acid content in platelets of autistic children

Rolf, L. H.; Haarmann, F Y; Grotemeyer, K.-H.; Kehrer, Hans E.

doi:10.1111/j.1600-0447.1993.tb03378.x

Cited by 106 publications

(74 citation statements)

References 13 publications

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“…97,98 Serotonin has wide-ranging effects on physiological processes in the nervous, GI, and immune systems. Antibodies directed against serotonin receptors have also been reported in ASD, 62,99 suggesting that the availability of serotonin may be different in ASD.…”

Section: Neurotransmittersmentioning

confidence: 99%

Immune Dysfunction in Autism: A Pathway to Treatment

2010

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Summary: Autism is a complex and clinically heterogeneous disorder with a spectrum of symptoms. Clinicians, schools, and service agencies worldwide have reported a dramatic increase in the number of children identified with autism. Despite expanding research, the etiology and underlying biological processes of autism remain poorly understood, and the relative contribution from genetic, epigenetic, and environmental factors remains unclear. Although autism affects primarily brain function (especially affect, social functioning, and cognition), it is unknown to what extent other organs and systems are disrupted. Published findings have identified widespread changes in the immune systems of children with autism, at both systemic and cellular levels. Brain specimens from autism subjects exhibit signs of active, ongoing inflammation, as well as alterations in gene pathways associated with immune signaling and immune function. Moreover, many genetic studies have indicated a link between autism and genes that are relevant to both the nervous system and the immune system. Alterations in these pathways can affect function in both systems. Together, these reports suggest that autism may in fact be a systemic disorder with connections to abnormal immune responses. Such immune system dysfunction may represent novel targets for treatment. A better understanding of the involvement of the immune response in autism, and of how early brain development is altered, may have important therapeutic implications.

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Section: Neurotransmittersmentioning

confidence: 99%

Immune Dysfunction in Autism: A Pathway to Treatment

2010

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“…17 Finally, disturbed glutamate concentrations have been reported in autistic patients compared to controls, with high levels in plasma 18 and low levels in platelets. 19 In the present study, we present the complete genomic structure of the human GluR6 gene, including new isoforms, linkage/association analyses in autistic subjects and the nucleotide variations present in the gene. These studies support the hypothesis that GluR6 may be a susceptibility gene for autism.…”

Section: Introductionmentioning

confidence: 99%

Linkage and association of the glutamate receptor 6 gene with autism

Jamain¹,

Betancur

Quach³

et al. 2002

Mol Psychiatry

286

184

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A genome scan was previously performed and pointed to chromosome 6q21 as a candidate region for autism. This region contains the glutamate receptor 6 (GluR6 or GRIK2) gene, a functional candidate for the syndrome. Glutamate is the principal excitatory neurotransmitter in the brain and is directly involved in cognitive functions such as memory and learning. We used two different approaches, the affected sib-pair (ASP) method and the transmission disequilibrium test (TDT), to investigate the linkage and association between GluR6 and autism. The ASP method, conducted with additional markers on the 51 original families and in eight new sibling pairs, showed a significant excess of allele sharing, generating an elevated multipoint maximum LOD score (ASPEX MLS = 3.28). TDT analysis, performed in the ASP families and in an independent data set of 107 parent-offspring trios, indicated a significant maternal transmission disequilibrium (TDTall P = 0.0004). Furthermore, TDT analysis (with only one affected proband per family) showed significant association between GluR6 and autism (TDT association P = 0.008). In contrast to maternal transmission, paternal transmission of GluR6 alleles was as expected in the absence of linkage, suggesting a maternal effect such as imprinting. Mutation screening was performed in 33 affected individuals, revealing several nucleotide polymorphisms (SNPs), including one amino acid change (M867I) in a highly conserved domain of the intracytoplasmic C-terminal region of the protein. This change is found in 8% of the autistic subjects and in 4% of the control population and seems to be more maternally transmitted than expected to autistic males (P = 0.007). Taken together, these data suggest that GluR6 is in linkage disequilibrium with autism. Molecular Psychiatry Molecular Psychiatry (2002) 7, 302-310.

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“…Blood plasma glutamate levels have been found to be increased (Hassan et al, 2013) and platelet levels of its precursor glutamine, decreased (Rolf, Haarmann, Grotemeyer, & Kehrer, 1993) in participants with ASD compared to neurotypical controls. Similarly, whilst Dhossche et al (2002) reported higher blood plasma GABA levels in children with ASD, decreased platelet levels of GABA have also been reported (Rolf et al, 1993).…”

Section: Blood Measurementmentioning

confidence: 99%

Measuring neural excitation and inhibition in autism: Different approaches, different findings and different interpretations

2016

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The balance of neural excitation and inhibition (E/I balance) is often hypothesised to be altered in autism spectrum disorder (ASD). One widely held view is that excitation levels are elevated relative to inhibition in ASD. Understanding whether, and how, E/I balance may be altered in ASD is important given the recent interest in trialling pharmacological interventions for ASD which target inhibitory neurotransmitter function.Here we provide a critical review of evidence for E/I balance in ASD. We conclude that data from a number of domains provides support for alteration in excitation and inhibitory neurotransmission in ASD, but when considered collectively, the available literature provide little evidence to support claims for either a net increase in excitation or a net increase in inhibition. Strengths and limitations of available techniques are considered, and directions for future research discussed.3

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Serotonin and amino acid content in platelets of autistic children

Cited by 106 publications

References 13 publications

Immune Dysfunction in Autism: A Pathway to Treatment

Immune Dysfunction in Autism: A Pathway to Treatment

Linkage and association of the glutamate receptor 6 gene with autism

Measuring neural excitation and inhibition in autism: Different approaches, different findings and different interpretations

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