ArticleTranslational psychiatry2021
Decreased phenol sulfotransferase activities associated with hyperserotonemia in autism spectrum disorders.
Article in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Miscompartmentalization of microbiota-derived TMAO is a reversible driver in autism spectrum disorder.iScience · 2026Article
- The autism-linked gut microbial metabolite p-cresol inhibits host catecholamine biosynthesizing enzymes to elicit social deficits.Communications biology · 2025Article
- Elevated Microbially-Derived Metabolites in Autism: A Possible Diagnostic Screening Test for a Distinct ASD Phenotype.Research square · 2025Article
- Gut-brain-immune axis implications for mental health and disease.Molecular and cellular biochemistry · 2025Review
- Autoantibody profiling of autism spectrum disorder patients with monoamine oxidase a deficiency.Brain, behavior, & immunity - health · 2025Article
- Biogenic Amine Metabolism and Its Genetic Variations in Autism Spectrum Disorder: A Comprehensive Overview.Biomolecules · 2025Review
- Review of Elevated Para-Cresol in Autism and Possible Impact on Symptoms.International journal of molecular sciences · 2025Review
- RFW captures species-level metagenomic functions by integrating genome annotation information.Cell reports methods · 2024Article
- Evaluating the Role of Susceptibility Inducing Cofactors and of Acetaminophen in the Etiology of Autism Spectrum Disorder.Life (Basel, Switzerland) · 2024Article
- A Systematic Review on Autism and Hyperserotonemia: State-of-the-Art, Limitations, and Future Directions.Brain sciences · 2024Review
- Acetaminophen causes neurodevelopmental injury in susceptible babies and children: no valid rationale for controversy.Clinical and experimental pediatrics · 2024Article
- Impact of IDO activation and alterations in the kynurenine pathway on hyperserotonemia, NADTranslational psychiatry · 2023Article
- Review
- Biallelic variants in the SLC13A1 sulfate transporter gene cause hyposulfatemia with a mild spondylo-epi-metaphyseal dysplasia.Clinical genetics · 2023Article
- Multivariate Analysis of Metabolomic and Nutritional Profiles among Children with Autism Spectrum Disorder.Journal of personalized medicine · 2022Article
- Low plasma serotonin linked to higher nigral iron in Parkinson's disease.Scientific reports · 2021Article
- Rare Opportunities for Insights Into Serotonergic Contributions to Brain and Bowel Disorders: Studies of the SERT Ala56 Mouse.Frontiers in cellular neuroscience · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperserotonemia is the most replicated biochemical abnormality associated with autism spectrum disorders (ASD). However, previous studies of serotonin synthesis, catabolism, and transport have not elucidated the mechanisms underlying this hyperserotonemia. Here we investigated serotonin sulfation by phenol sulfotransferases (PST) in blood samples from 97 individuals with ASD and their first-degree relatives (138 parents and 56 siblings), compared with 106 controls. We report a deficient activity of both PST isoforms (M and P) in platelets from individuals with ASD (35% and 78% of patients, respectively), confirmed in autoptic tissues (9 pineal gland samples from individuals with ASD-an important source of serotonin). Platelet PST-M deficiency was strongly associated with hyperserotonemia in individuals with ASD. We then explore genetic or pharmacologic modulation of PST activities in mice: variations of PST activities were associated with marked variations of blood serotonin, demonstrating the influence of the sulfation pathway on serotonemia. We also conducted in 1645 individuals an extensive study of SULT1A genes, encoding PST and mapping at highly polymorphic 16p11.2 locus, which did not reveal an association between copy number or single nucleotide variations and PST activity, blood serotonin or the risk of ASD. In contrast, our broader assessment of sulfation metabolism in ASD showed impairments of other sulfation-related markers, including inorganic sulfate, heparan-sulfate, and heparin sulfate-sulfotransferase. Our study proposes for the first time a compelling mechanism for hyperserotonemia, in a context of global impairment of sulfation metabolism in ASD.
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