ArticleLife (Basel, Switzerland)2023
Neuron-Specific Enolase (NSE) as a Biomarker for Autistic Spectrum Disease (ASD).
Article in Life (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06756711 (Combination of Supplements for Treating Autistic Spectrum Disorder), which is not on this map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Combination of Supplements for Treating Autistic Spectrum Disorder
Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Autologous cord bloodWorld journal of clinical pediatrics · 2025Trial
- Association between serum cytokine and neuron-specific enolase levels and the core symptoms of autism spectrum disorder.IBRO neuroscience reports · 2026Article
- A Biochemical Analysis of LINC00896 RNA in Cortex Neuronal Cells and Its Possible Connection to the Development of Autism.Journal of nucleic acids · 2026Article
- An impaired glycolysis induces ATP deficiency and reduced cell respiration in stem cells of patients with autism spectrum disorders.Scientific reports · 2025Article
- Neuron-specific enolase in patients with acute and chronic schizophrenia, diversity of approaches: marker of neuronal death, neurodegeneration or neurodevelopmental theory in schizophrenia? a single-center case-control study.Frontiers in psychiatry · 2025Article
- Evaluating the Role of Susceptibility Inducing Cofactors and of Acetaminophen in the Etiology of Autism Spectrum Disorder.Life (Basel, Switzerland) · 2024Article
- Research progress of neuron-specific enolase in cognitive disorder: a mini review.Frontiers in human neuroscience · 2024Review
- Neuroplasticity of children in autism spectrum disorder.Frontiers in psychiatry · 2024Review
- The Dangers of Acetaminophen for Neurodevelopment Outweigh Scant Evidence for Long-Term Benefits.Children (Basel, Switzerland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autistic spectrum disease (ASD) is an increasingly common diagnosis nowadays with a prevalence of 1-2% in most countries. Its complex causality-a combination of genetic, immune, metabolic, and environmental factors-is translated into pleiomorphic developmental disorders of various severity, which have two main aspects in common: repetitive, restrictive behaviors and difficulties in social interaction varying from awkward habits and verbalization to a complete lack of interest for the outside world. The wide variety of ASD causes also makes it very difficult to find a common denominator-a disease biomarker and medication-and currently, there is no commonly used diagnostic and therapeutic strategy besides clinical evaluation and psychotherapy. In the CORDUS clinical study, we have administered autologous cord blood to ASD kids who had little or no improvement after other treatments and searched for a biomarker which could help predict the degree of improvement in each patient. We have found that the neuron-specific enolase (NSE) was elevated above the normal clinical range (less than 16.3 ng/mL) in the vast majority of ASD kids tested in our study (40 of 41, or 97.5%). This finding opens up a new direction for diagnostic confirmation, dynamic evaluation, and therapeutic intervention for ASD kids.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.