ReviewMolecular diagnosis & therapy2020
The Role of Lipidomics in Autism Spectrum Disorder.
Review in Molecular diagnosis & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Ceruloplasmin deficiency drives a fusiform-centric lipid-myelin pathology underlying a visual subtype in autism.Molecular psychiatry · 2026Article
- Prenatal targeted maternal pregnancy metabolomic profiles, child emotional and behavioral problems, and autism related traits in the NYU CHES cohort.Molecular psychiatry · 2026Article
- Plasma sterol profiling in autism spectrum disorder: insights from cerebrotendinous xanthomatosis screening and beyond.Metabolic brain disease · 2026Article
- Longitudinal metabolome profiling from pregnancy through childhood and risk of neurodevelopmental disorders at age 10.Nature communications · 2026Article
- The relationship between functional brain connectivity and neuroinflammatory processes-new insights into the pathomechanisms of ASD.Frontiers in neuroscience · 2026Review
- Lipidomic Signatures in Pediatric Metabolic Disorders.Metabolites · 2025Review
- Exploring Causal Associations Between Plasma Metabolites and Autism Spectrum Disorder.Alpha psychiatry · 2025Article
- Autism Spectrum Disorder: What Do We Know and Where Do We Go?Brain sciences · 2025Review
- From Genetics to Function: the Role of ABCA12 in Autism Neurobiology.Journal of molecular neuroscience : MN · 2025Review
- Gangliosides and Cholesterol: Dual Regulators of Neuronal Membrane Framework in Autism Spectrum Disorder.International journal of molecular sciences · 2025Review
- Prostaglandins: Biological Action, Therapeutic Aspects, and Pathophysiology of Autism Spectrum Disorders.Current issues in molecular biology · 2025Review
- Article
- Involvement of sphingosine-1-phosphate receptor 1 in pain insensitivity in a BTBR mouse model of autism spectrum disorder.BMC medicine · 2024Article
- Milk Fat Globule Membranes for Mental Health across the Human Lifespan.Foods (Basel, Switzerland) · 2024Review
- Article
- Cord Blood Metabolite Profiles and Their Association with Autistic Traits in Childhood.Metabolites · 2023Article
- The expanding organelle lipidomes: current knowledge and challenges.Cellular and molecular life sciences : CMLS · 2023Review
- The Potency of Goat Milk in Reducing the Induced Neurotoxic Effects of Valproic Acid in Rat Pups as a Rodent Model of Autism Spectrum Disorder.Metabolites · 2023Article
- Proteomic-Based Approach Reveals the Involvement of Apolipoprotein A-I in Related Phenotypes of Autism Spectrum Disorder in the BTBR Mouse Model.International journal of molecular sciences · 2022Article
- Protective Mechanism ofFoods (Basel, Switzerland) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a complex neurodevelopmental syndrome commonly diagnosed in early childhood; it is usually characterized by impairment in reciprocal communication and speech, repetitive behaviors, and social withdrawal with loss in communication skills. Its development may be affected by a variety of environmental and genetic factors. Trained physicians diagnose and evaluate the severity of ASD based on clinical evaluations of observed behaviors. As such, this approach is inevitably dependent on the expertise and subjective assessment of those administering the clinical evaluations. There is a need to identify objective biological markers associated with diagnosis or clinical severity of the disorder. Several important issues and concerns exist regarding the diagnostic competence of the many abnormal plasma metabolites produced in the different biochemical pathways evaluated in individuals with ASD. The search for high-performing bio-analytes to diagnose and follow-up ASD development is still a major target in medicine. Dysregulation in the oxidative stress response and proinflammatory processes are major etiological causes of ASD pathogenesis. Furthermore, dicarboxylic acid metabolites, cholesterol-related metabolites, phospholipid-related metabolites, and lipid transporters and mediators are impaired in different pathological conditions that have a role in the ASD etiology. A mechanism may exist by which pro-oxidant environmental stressors and abnormal metabolites regulate clinical manifestations and development of ASD.
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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.