Serotonin and serotonin transporter levels in autistic children

Abdulamir, Haidar A.; Abdul‐Rasheed, Omar F.; Abdulghani, Emad A.

doi:10.15537/smj.2018.5.21751

Cited by 62 publications

(38 citation statements)

References 32 publications

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“…Half a century ago, elevated whole blood 5-HT (hyperserotonemia) was the first molecular phenomenon found in a subset of ASD subjects, today associated with 25-30% of cases. The fact that hyperserotonemia is not detected in every autistic case is consistent with the correlation of this feature with ASD severity (Abdulamir et al, 2018) and also reveals individual variations in the biological inner management of disturbances impacting the 5-HT system. Along this line, it is worth knowing first that the level of 5-HT contained in blood platelets does not reflect its synaptic concentration.…”

Section: Pivotal Role Of Serotoninsupporting

confidence: 78%

Paradoxical Effects of a Cytokine and an Anticonvulsant Strengthen the Epigenetic/Enzymatic Avenue for Autism Research

Béroule¹

2020

Front. Cell. Neurosci.

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Maternal exposure to the valproate short-chain fatty acid (SCFA) during pregnancy is known to possibly induce autism spectrum disorders (ASDs) in the offspring. By contrast, case studies have evidenced positive outcomes of this anticonvulsant drug in children with severe autism. Interestingly, the same paradoxical pattern applies to the IL-17a inflammatory cytokine involved in the immune system regulation. Such joint apparent contradictions can be overcome by pointing out that, among their respective signaling pathways, valproate and IL-17a share an enhancement of the “ type A monoamine oxidase ” (MAOA) enzyme carried by the X chromosome. In the Guided Propagation (GP) model of autism, such enzymatic rise triggers a prenatal epigenetic downregulation, which, without possible X-inactivation , and when coinciding with genetic expression variants of other brain enzymes, results in the delayed onset of autistic symptoms. The underlying imbalance of synaptic monoamines, serotonin in the first place, would reflect a mismatch between the environment to which the brain metabolism was prepared during gestation and the postnatal actual surroundings. Following a prenatal exposure to molecules that significantly elicit the MAOA gene expression, a daily treatment with the same metabolic impact would tend to recreate the fetal environment and contribute to rebalance monoamines, thus allowing proper neural circuits to gradually develop, provided behavioral re-education. Given the multifaceted other players than MAOA that are involved in the regulation of serotonin levels, potential compensatory effects are surveyed, which may underlie the autism heterogeneity. This explanatory framework opens up prospects regarding autism prevention and treatment, strikingly in line with current advances along the gut microbiome–brain axis.

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Section: Pivotal Role Of Serotoninsupporting

confidence: 78%

Paradoxical Effects of a Cytokine and an Anticonvulsant Strengthen the Epigenetic/Enzymatic Avenue for Autism Research

Béroule¹

2020

Front. Cell. Neurosci.

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“…We found a correlation between gut serotonin levels with neurodevelopment scores of ASD children, while serotonin and N-feruloyl serotonin levels were positively correlated with sensory subscales of ABC. Many researches have indicated that the blood levels of serotonin are correlated with autism severity [36]. A Balanced amount of enteric serotonin is bene cial to the functioning of the intestine, nervous system, and gut-brain axis, while excess serotonin may play a harmful role in the progression of ASD.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Gut Vitamins and Amino Acids Metabolism are Associated with Symptoms and Neurodevelopment of Children with Autism Spectrum Disorders

Zhu

Hua

Yang

et al. 2020

Preprint

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Background Accumulated evidence have supported metabolic disturbance may be associated with the pathogenesis of autism spectrum disorders (ASD). Despite abnormalities of some shared metabolic pathways, specific differential compounds are inconsistent in studies, which made a challenge to elucidate the role of metabolism in the mechanism of ASD. Besides, few researches have assessed the correlation between gut metabolites with symptoms of ASD. Objectives The present study aimed to evaluate the gut metabolomic profiles of children with ASD and to analyze potential interaction between gut metabolites with symptoms and neurodevelopment of ASD children. Methods In this cross-sectional case-control study, 120 aged 2–6 years ASD children and 60 sex and age matched typically developing (TD) children were included. Autistic symptoms were assessed with the Autism Behavior Checklist (ABC), Childhood Autism Rating Scale (CARS), and the Social Responsiveness Scale (SRS). Neurodevelopment was assessed with the Gesell Developmental Scale (GDS). Fecal samples were analyzed by untargeted liquid chromatography-mass spectrometry (LC-MS) methods, then systematic bioinformatic analyses were performed to characterize the gut metabolomic profiles of ASD and TD children. The correlations between metabolites and clinical assessment scores were assessed using Spearman correlation. Results ASD children exhibit gut metabolism perturbation compared with TD children. A total of 96 differential metabolites between the ASD and TD groups were identified, with 35 increased and 61 decreased in ASD group. The metabolic disturbance of ASD involved in multiple vitamins and amino acids metabolism pathways, with the strongest enrichment identified for tryptophan metabolism, retinol metabolism, cysteine and methionine metabolism, and vitamin digestion and absorption. The imbalanced gut metabolites are significantly correlated to symptoms and neurodevelopment of ASD children. Limitations This cross-sectional study revealed a correlation, but do not allow to prove causation of symptoms and gut metabolites outcome. The disease specificity of the metabolomic disturbance need to be evaluated in future studies.Conclusions ASD children have altered gut metabolite profiles compared with TD children, which mainly involved in multiple vitamins and amino acids metabolism pathways. Notably, vitamins metabolism abnormalities may play roles in the disturbance of amino acids metabolism. Imbalanced gut metabolites are related to symptoms and neurodevelopment of ASD children. Our findings provided an improved understanding of perturbations of metabolome networks in ASD.

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“…Elevated blood serotonin (5-HT) levels, and serotonin transporter (SERT) consistently recorded in individuals with ASD [16].…”

Section: Biomarker For Autism Gives Hope For Future Autism Treatmentmentioning

confidence: 99%

Review in Autism and Epilepsy

AlKhateeb¹,

Aldhalaan²

2021

Epilepsy - Update on Classification, Etiologies, Instrumental Diagnosis and Treatment

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Autism is a neurodevelopmental disorder of undefined etiology characterized by social, communication deficits, and restricted interests/repetitive or isolated behaviors. The determination of autism is made in early life as the patients create unusual or decreased social interaction and communication, together with stereotypic movement. In most patients, a delay in verbal and nonverbal communication is watched, whereas a few patients never accomplish valuable language. Patients with autism and epilepsy may develop any type of seizure and maybe all type of seizures. Interestingly, not absolutely understood relationship between each and a lot of research in progress concerning these relations. In patients with autism, some they do not develop seizures; however, abnormal paroxysmal electroencephalographic "EEG" activity can be seen in up to 30%. For that reason, important investigation of patients with autistic spectrum disorders, and any kids with language regression, should always include sleep recording EEG in order to exclude acquired epileptic aphasia (Landau-Kleffner syndrome). The complex relationship between autism and epilepsy provides a bridge to further knowledge of shared neuronal networks for both the autisms and the epilepsies We review the literature to elucidate the relationships between epilepsy and autism.

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Serotonin and serotonin transporter levels in autistic children

Cited by 62 publications

References 32 publications

Paradoxical Effects of a Cytokine and an Anticonvulsant Strengthen the Epigenetic/Enzymatic Avenue for Autism Research

Paradoxical Effects of a Cytokine and an Anticonvulsant Strengthen the Epigenetic/Enzymatic Avenue for Autism Research

Alterations in Gut Vitamins and Amino Acids Metabolism are Associated with Symptoms and Neurodevelopment of Children with Autism Spectrum Disorders

Review in Autism and Epilepsy

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