ArticleMolecular psychiatry2022
Altered canonical and striatal-frontal resting state functional connectivity in children with pathogenic variants in the Ras/mitogen-activated protein kinase pathway.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Social Communication in Ras Pathway Disorders: A Comprehensive Review From Genetics to Behavior in Neurofibromatosis Type 1 and Noonan Syndrome.Biological psychiatry · 2025Pooled it
- Transdiagnostic similarities and distinctions in brain networks associated with autistic social impairments: a prospective cohort study.Molecular autism · 2025Article
- A familial modeling framework for advancing precision medicine for children with neuropsychiatric disorders.Developmental medicine and child neurology · 2025Article
- Transdiagnostic similarities and distinctions in brain networks associated with ASD symptoms: A prospective cohort study.medRxiv : the preprint server for health sciences · 2025Article
- Executive and Social Functioning in Children and Adolescents With Noonan Syndromes: Cognition and Behavior.JAACAP open · 2025Article
- Subcortical shape alterations in children with Noonan syndrome spectrum: insights into genotype-phenotype associations.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Moderation between resting-state connectivity and brain amyloid levels on speed of cognitive and physical function in older adults: Evidence for network-based cognitive reserve.Aperture neuro · 2025Article
- Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury.Neural regeneration research · 2023Article
- Neuropsychiatric phenotypes in children with Noonan syndrome.Developmental medicine and child neurology · 2023Article
- Novel effects of Ras-MAPK pathogenic variants on the developing human brain and their link to gene expression and inhibition abilities.Translational psychiatry · 2023Article
- Aberrant Cortical Layer Development of Brain Organoids Derived from Noonan Syndrome-iPSCs.International journal of molecular sciences · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mounting evidence supports the role of the Ras/mitogen-activated protein kinase (Ras/MAPK) pathway in neurodevelopmental disorders. Here, the authors used a genetics-first approach to examine how Ras/MAPK pathogenic variants affect the functional organization of the brain and cognitive phenotypes including weaknesses in attention and inhibition. Functional MRI was used to examine resting state functional connectivity (RSFC) in association with Ras/MAPK pathogenic variants in children with Noonan syndrome (NS). Participants (age 4-12 years) included 39 children with NS (mean age 8.44, SD = 2.20, 25 females) and 49 typically developing (TD) children (mean age 9.02, SD = 9.02, 33 females). Twenty-eight children in the NS group and 46 in the TD group had usable MRI data and were included in final analyses. The results indicated significant hyperconnectivity for the NS group within canonical visual, ventral attention, left frontoparietal and limbic networks (p < 0.05 FWE). Higher connectivity within canonical left frontoparietal and limbic networks positively correlated with cognitive function within the NS but not the TD group. Further, the NS group demonstrated significant group differences in seed-based striatal-frontal connectivity (Z > 2.6, p < 0.05 FWE). Hyperconnectivity within canonical brain networks may represent an intermediary phenotype between Ras/MAPK pathogenic variants and cognitive phenotypes, including weaknesses in attention and inhibition. Altered striatal-frontal connectivity corresponds with smaller striatal volume and altered white matter connectivity previously documented in children with NS. These results may indicate delayed maturation and compensatory mechanisms and they are important for understanding the pathophysiology underlying cognitive phenotypes in NS and in the broader population of children with neurodevelopmental disorders.
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