ArticleThe international journal of neuropsychopharmacology2013
Monoamine oxidase A and A/B knockout mice display autistic-like features.
Article in The international journal of neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Redox System Dysfunction as a Key Mechanism in Autism Spectrum Disorder Pathogenesis.International journal of molecular sciences · 2025Review
- Rescaling of Point Charges as a Way to Improve the Simple-to-Use Electrostatic Embedding Scheme Developed to Explore Enzyme Activity with QM-Oriented Software.Journal of chemical information and modeling · 2025Article
- Autoantibody profiling of autism spectrum disorder patients with monoamine oxidase a deficiency.Brain, behavior, & immunity - health · 2025Article
- Modulating autism spectrum disorder pathophysiology using a trace amine-focused approach: targeting the gut.Molecular medicine (Cambridge, Mass.) · 2025Review
- Theranostic Near-Infrared Monoamine Oxidase Inhibitor (NMI) Protein Binding Interactions with MAOA and Albumin.Pharmaceutical research · 2025Article
- Early Postnatal Pharmacological Intervention Rescues the Disruption of Developmental Connectivity in MAO-A KO Mice.Neuroscience bulletin · 2025Article
- Unveiling the role of phytochemicals in autism spectrum disorder by employing network pharmacology and molecular dynamics simulation.Metabolic brain disease · 2024Article
- Maternal LPS Exposure Enhances the 5-HT Level in the Prefrontal Cortex of Autism-like Young Offspring.Brain sciences · 2023Article
- Deletion of monoamine oxidase A in a prostate cancer model enhances anti-tumor immunity through reduced immune suppression.Biochemical and biophysical research communications · 2022Article
- Top2a promotes the development of social behavior via PRC2 and H3K27me3.Science advances · 2022Article
- Abnormal brain development of monoamine oxidase mutant zebrafish and impaired social interaction of heterozygous fish.Disease models & mechanisms · 2022Article
- Combined Antagonism of 5-HTPharmaceuticals (Basel, Switzerland) · 2022Article
- Harmane Potentiates Nicotine Reinforcement Through MAO-A Inhibition at the Dose Related to Cigarette Smoking.Frontiers in molecular neuroscience · 2022Article
- Monoamine Oxidase Inhibition by Plant-Derived β-Carbolines; Implications for the Psychopharmacology of Tobacco and Ayahuasca.Frontiers in pharmacology · 2022Review
- Anhedonia and Hyperhedonia in Autism and Related Neurodevelopmental Disorders.Current topics in behavioral neurosciences · 2022Article
- Systemic enhancement of serotonin signaling reverses social deficits in multiple mouse models for ASD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Prenatal THC Does Not Affect Female Mesolimbic Dopaminergic System in Preadolescent Rats.International journal of molecular sciences · 2021Article
- Biological Timing and Neurodevelopmental Disorders: A Role for Circadian Dysfunction in Autism Spectrum Disorders.Frontiers in neuroscience · 2021Review
- The role of monoamine oxidase A in the neurobiology of aggressive, antisocial, and violent behavior: A tale of mice and men.Progress in neurobiology · 2020Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Converging lines of evidence show that a sizable subset of autism-spectrum disorders (ASDs) is characterized by increased blood levels of serotonin (5-hydroxytryptamine, 5-HT), yet the mechanistic link between these two phenomena remains unclear. The enzymatic degradation of brain 5-HT is mainly mediated by monoamine oxidase (MAO)A and, in the absence of this enzyme, by its cognate isoenzyme MAOB. MAOA and A/B knockout (KO) mice display high 5-HT levels, particularly during early developmental stages. Here we show that both mutant lines exhibit numerous behavioural hallmarks of ASDs, such as social and communication impairments, perseverative and stereotypical responses, behavioural inflexibility, as well as subtle tactile and motor deficits. Furthermore, both MAOA and A/B KO mice displayed neuropathological alterations reminiscent of typical ASD features, including reduced thickness of the corpus callosum, increased dendritic arborization of pyramidal neurons in the prefrontal cortex and disrupted microarchitecture of the cerebellum. The severity of repetitive responses and neuropathological aberrances was generally greater in MAOA/B KO animals. These findings suggest that the neurochemical imbalances induced by MAOA deficiency (either by itself or in conjunction with lack of MAOB) may result in an array of abnormalities similar to those observed in ASDs. Thus, MAOA and A/B KO mice may afford valuable models to help elucidate the neurobiological bases of these disorders and related neurodevelopmental problems.
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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 OpenQuestion graph.