Autism-related Research Digest

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Biomedical research, treatable look-alikes, and medical treatments for ASD.

516 articles · page 1 / 104

  1. Gut microbes

    Nutritional regulation of gut-brain immune crosstalk across the lifespan.

    Zhou, Yulin; Del Toro, Sebastian; Zeng, Melody Y

    The gut-brain immune axis integrates microbial, immune, and neural signals to regulate neurodevelopment, homeostasis, and disease susceptibility. Early-life nutrition, particularly human milk oligosaccharides, shapes beneficial microbiota composition, enhances hippocampal plasticity, promotes anti-inflammatory microglia polarization, and fosters immune tolerance. Gut microbiota-derived metabolites, including short-chain fatty acids, tryptophan derivatives and secondary bile acids, regulate microglia maturation, astrocyte function, T cell differentiation, neurotransmitter production, and vagus nerve signaling. These processes influence synaptic pruning, neurogenesis, and neuroinflammation. Adaptive immune cells in the central nervous system, notably meningeal and infiltrating CD4 T cells, further connect peripheral immunity to neuronal responses through cytokines, such as IL-4, IFNγ, and IL-17A. Nutritional imbalances may exacerbate disease-associated microglia and pathogenic T cell activity in Multiple Sclerosis, Alzheimer's disease, and autism spectrum disorders. In aging, diet helps mitigate "inflammaging" by countering metabolic shifts in microglia and lymphocytes. This review examines how nutrition modulates bidirectional gut-brain immune crosstalk across the lifespan.

    • ASD
    • Metabolic & Mitochondrial
    • Neuroinflammation & Immune
    • Gut & Microbiome
    • Synaptic & Neurotransmitter
    • Dietary intervention
  2. Gut microbes

    Nutritional regulation of gut-brain immune crosstalk across the lifespan.

    Zhou, Yulin; Del Toro, Sebastian; Zeng, Melody Y

    The gut-brain immune axis integrates microbial, immune, and neural signals to regulate neurodevelopment, homeostasis, and disease susceptibility. Early-life nutrition, particularly human milk oligosaccharides, shapes beneficial microbiota composition, enhances hippocampal plasticity, promotes anti-inflammatory microglia polarization, and fosters immune tolerance. Gut microbiota-derived metabolites, including short-chain fatty acids, tryptophan derivatives and secondary bile acids, regulate microglia maturation, astrocyte function, T cell differentiation, neurotransmitter production, and vagus nerve signaling. These processes influence synaptic pruning, neurogenesis, and neuroinflammation. Adaptive immune cells in the central nervous system, notably meningeal and infiltrating CD4 T cells, further connect peripheral immunity to neuronal responses through cytokines, such as IL-4, IFNγ, and IL-17A. Nutritional imbalances may exacerbate disease-associated microglia and pathogenic T cell activity in Multiple Sclerosis, Alzheimer's disease, and autism spectrum disorders. In aging, diet helps mitigate "inflammaging" by countering metabolic shifts in microglia and lymphocytes. This review examines how nutrition modulates bidirectional gut-brain immune crosstalk across the lifespan.

    • ASD
    • Metabolic & Mitochondrial
    • Neuroinflammation & Immune
    • Gut & Microbiome
    • Synaptic & Neurotransmitter
    • Dietary intervention
  3. Brain, behavior, & immunity - health

    Neurocognitive sequelae following seronegative anti-NMDA receptor encephalitis with ovarian teratoma in a pediatric patient: A six-year follow-up case report.

    Dalvi-Garcia, Felipe; de Salles Fonseca Carvalho, Iolanda; de Almeida, Julia Valeriano; Pereira Costa, Roozemeria; Caldeira da Silva, Ligia et al.

    Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the commonest form of autoimmune encephalitis of childhood. However, little information is captured with formal neuropsychological testing. When the pre-illness history is incomplete, it is also hard to judge how much of the residual picture reflects the encephalitis itself rather than an earlier neurodevelopmental vulnerability. We describe the case of an adopted girl who became acutely unwell at 11 years of age, with a rapid neuropsychiatric deterioration, seizures and abnormal movements. A mature ovarian teratoma was found and removed, and the clinical course, serial EEGs and response to immunotherapy supported a diagnosis of probable anti-NMDAR encephalitis. Serum and cerebrospinal fluid (CSF) antibodies were negative, although the samples were taken late and after treatment had begun. She was managed with corticosteroids and intravenous immunoglobulin. Six years on, formal testing showed largely intact verbal comprehension but clear weaknesses in executive function, attention, processing speed and verbal memory. She met criteria for autism spectrum disorder; overall cognitive ability was in the low average range. This case shows how a paraneoplastic, immune-mediated insult to the developing brain can leave a lasting cognitive mark, how easily seronegative disease is missed, and why it is often neuropsychological assessment, rather than imaging, that reveals the residual burden.

    • ASD
    • Neurodevelopmental delay
    • Treatable similar conditions
    • Neuroinflammation & Immune
    • Biomarkers & Diagnosis
  4. Chembiochem : a European journal of chemical biology

    Functional Heterogeneity of the Autism Spectrum Disorder-Associated Gut Microbial Ecosystem Revealed by Fecal Lipopolysaccharides and Bacterial Proteomic Profiling.

    De Chiara, Stefania; Di Somma, Angela; Mazziotti, Valentina; Coppola, Serena; Oglio, Franca et al.

    The etiology of pediatric autism spectrum disorder (ASD) has been increasingly linked to alterations in the gut-brain axis, highlighting the intricate bidirectional communication between gut microbiota and central nervous system. The molecular mechanisms of this communication are poorly understood. Here we investigated whether ASD-associated gut microbiota could exhibit altered inflammatory molecular outputs by integrating chemistry-driven profiling of fecal lipopolysaccharides (LPS), functional bacterial proteomics, and neuroimmune cellular assays. Structural analyses revealed that LPS from non-autistic healthy donors (NASD) displayed highly conserved carbohydrate and lipid A signatures dominated by hypo-acylated mono-phosphorylated species typically associated with immunomodulatory Bacteroides-derived LPS. In contrast, LPS from ASD children exhibited increased structural heterogeneity. These molecular alterations were functionally reflected in human HMC3 microglial cells, where ASD-derived fecal LPS induced stronger IL-6 and IL-8 release compared with NASD-derived LPS, indicating enhanced neuroinflammatory potential. Functional proteomic profiling disclosed broadly comparable microbial compositions but marked metabolic divergence. These findings suggest that gut microbiota in ASD children are associated with a functionally heterogeneous microbial ecosystem characterized by altered immunostimulatory molecular outputs despite the absence of massive taxonomic shifts, with potential relevance for neuroimmune dysregulation.

    • ASD
    • Metabolic & Mitochondrial
    • Neuroinflammation & Immune
    • Gut & Microbiome
  5. Nutrients

    Ketogenic Dietary Therapies and β-Hydroxybutyrate as Modulators of Mitochondrial Function: From Molecular Mechanisms to Clinical Translation

    Ji-Hoon Na, Young-Mock Lee

    Ketogenic dietary therapies (KDTs) have been used for a century in drug-resistant epilepsy, and β-hydroxybutyrate (BHB), the major ketone body, is recognized as a signaling metabolite. This review examines how KDTs and BHB modulate mitochondrial function and evaluates evidence supporting these mechanisms. BHB is oxidized through D-β-hydroxybutyrate dehydrogenase 1 and succinyl-CoA:3-oxoacid-CoA transferase and alters redox balance and oxidative phosphorylation. It also inhibits class I histone deacetylases, serves as the substrate for lysine β-hydroxybutyrylation, activates hydroxycarboxylic acid receptor 2, and blocks the NLR family pyrin domain-containing 3 inflammasome. These pathways influence redox defense, organelle quality, and inflammation. However, ketogenic feeding suppresses mitochondrial one-carbon metabolism and some signaling effects occur only at BHB concentrations exceeding those typically achieved through dietary ketosis. Clinical benefits are best established in drug-resistant epilepsy and appear genotype-dependent in primary mitochondrial disease, with potential benefit in mitochondrial DNA (mtDNA) variant carriers but possible harm in DNA polymerase gamma-related disease and mtDNA deletion myopathy. Outside neurology, human evidence includes a hemodynamic response to infused 3-hydroxybutyrate in heart failure, sustained glycemic improvement in non-randomized diabetes cohorts, and small trials in psychiatric and oncological populations. Most clinical studies have not directly measured mitochondrial outcomes. Proposed mitochondrial mechanisms of KDTs and BHB remain plausible but are not established explanations for clinical benefit. Genotype-stratified trials, ketone exposure assessment, and direct measurement of mitochondrial variables in patients are needed.

    • Treatable similar conditions
    • Metabolic & Mitochondrial
    • Dietary intervention