ArticleCerebral cortex (New York, N.Y. : 1991)2024
Quantitative proteomics of dorsolateral prefrontal cortex reveals an early pattern of synaptic dysmaturation in children with idiopathic autism.
Article in Cerebral cortex (New York, N.Y. : 1991), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Peripheral blood mononuclear cell proteomic profiling reveals cytoskeletal- and chromatin-associated protein signatures in autism spectrum disorder.Brain, behavior, & immunity - health · 2026Article
- Modulation of Homer1 EVH1 domain internal dynamics by putative autism-associated mutations.FEBS letters · 2026Article
- A patient-derived mouse model reproduces molecular, neurological, and sleep symptoms of SHINE syndrome.Human molecular genetics · 2026Article
- Alteration in hippocampal mitochondria ultrastructure and cholesterol accumulation linked to mitochondrial dysfunction in the valproic acid rat model of autism spectrum disorders.Psychopharmacology · 2026Article
- Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- GABAFrontiers in pharmacology · 2026Review
- Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.Frontiers in synaptic neuroscience · 2026Review
- Article
- Roles of NRXN1 in neuropsychiatric disorders: from genetic lesion to molecular mechanism.Frontiers in neuroscience · 2026Review
- Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism.Journal of visualized experiments : JoVE · 2025Article
- Impaired Aggrephagy, Interrupted Vesicular Trafficking, and Cellular Stress, Lead to Protein Aggregation, and Synaptic Dysfunction in Cerebellum of Children and Adults with Idiopathic Autism.Cerebellum (London, England) · 2025Article
- A Refined Approach to Isolate Interneurons for High-Validity Epigenetic Studies in Human Brain Tissue.Methods and protocols · 2025Article
- Prefrontal Blood Flow Activity During Drawing Intervention in School-Age Children with Autism: An fNIRS Hyperscanning Study.Brain sciences · 2025Article
- Heterogeneity and convergence across seven neuroimaging modalities: a review of the autism spectrum disorder literature.Frontiers in psychiatry · 2024Review
- A most important gift: the critical role of postmortem brain tissue in autism science.Frontiers in neurology · 2024Article
Corrections and comments
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5 authors.
Funding
Abstract
Autism spectrum disorder (ASD) is a developmental disorder with a rising prevalence and unknown etiology presenting with deficits in cognition and abnormal behavior. We hypothesized that the investigation of the synaptic component of prefrontal cortex may provide proteomic signatures that may identify the biological underpinnings of cognitive deficits in childhood ASD. Subcellular fractions of synaptosomes from prefrontal cortices of age-, brain area-, and postmortem-interval-matched samples from children and adults with idiopathic ASD vs. controls were subjected to HPLC-tandem mass spectrometry. Analysis of data revealed the enrichment of ASD risk genes that participate in slow maturation of the postsynaptic density (PSD) structure and function during early brain development. Proteomic analysis revealed down regulation of PSD-related proteins including AMPA and NMDA receptors, GRM3, DLG4, olfactomedins, Shank1-3, Homer1, CaMK2α, NRXN1, NLGN2, Drebrin1, ARHGAP32, and Dock9 in children with autism (FDR-adjusted P < 0.05). In contrast, PSD-related alterations were less severe or unchanged in adult individuals with ASD. Network analyses revealed glutamate receptor abnormalities. Overall, the proteomic data support the concept that idiopathic autism is a synaptopathy involving PSD-related ASD risk genes. Interruption in evolutionarily conserved slow maturation of the PSD complex in prefrontal cortex may lead to the development of ASD in a susceptible individual.
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