ArticleCerebral cortex (New York, N.Y. : 1991)2018
Dysfunctional Autism Risk Genes Cause Circuit-Specific Connectivity Deficits With Distinct Developmental Trajectories.
Article in Cerebral cortex (New York, N.Y. : 1991), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- A systematic review of the relationship between magnetic resonance imaging based resting-state and structural networks in the rodent brain.Frontiers in neuroscience · 2023Pooled it
- Microglial TDP-43 mediates myelin refinement and represses Tyrobp cryptic exon inclusion in mice.Nature neuroscience · 2026Article
- Imaging brain development in a KCNQ2-developmental and epileptic encephalopathy mouse model: identifying early biomarkers for functional and structural brain changes.EBioMedicine · 2025Article
- A common computational and neural anomaly across mouse models of autism.Nature neuroscience · 2025Article
- Intermittent Fasting Enhances Motor Coordination Through Myelin Preservation in Aged Mice.Aging cell · 2025Article
- Transient CSF1R inhibition ameliorates behavioral deficits in Cntnap2 knockout and valproic acid-exposed mouse models of autism.Journal of neuroinflammation · 2024Article
- Local and long-range input balance: A framework for investigating frontal cognitive circuit maturation in health and disease.Science advances · 2024Review
- CDKL5 sculpts functional callosal connectivity to promote cognitive flexibility.Molecular psychiatry · 2024Article
- The mouse motor system contains multiple premotor areas and partially follows human organizational principles.Cell reports · 2024Article
- Low Plasma Levels of Contactin-Associated Protein-Like 2 in Children with Autism Spectrum Disorder: Links to Neural Development.Neuropsychiatric disease and treatment · 2024Article
- Mapping and comparing fMRI connectivity networks across species.Communications biology · 2023Review
- Resting-State Functional MRI and PET Imaging as Noninvasive Tools to Study (Ab)Normal Neurodevelopment in Humans and Rodents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Cortex-restricted deletion of Foxp1 impairs barrel formation and induces aberrant tactile responses in a mouse model of autism.Molecular autism · 2023Article
- Sexual dimorphism in the social behaviour of Cntnap2-null mice correlates with disrupted synaptic connectivity and increased microglial activity in the anterior cingulate cortex.Communications biology · 2023Article
- CNTNAP2 Protein Is Degraded by the Ubiquitin-Proteasome System and the Macroautophagy-Lysosome Pathway.Molecular neurobiology · 2023Article
- Differential impacts ofFrontiers in neuroscience · 2023Article
- mTOR-Dependent Spine Dynamics in Autism.Frontiers in molecular neuroscience · 2022Review
- Brain mapping across 16 autism mouse models reveals a spectrum of functional connectivity subtypes.Molecular psychiatry · 2021Article
- Prenatal interleukin 6 elevation increases glutamatergic synapse density and disrupts hippocampal connectivity in offspring.Immunity · 2021Article
- Experience-dependent weakening of callosal synaptic connections in the absence of postsynaptic FMRP.eLife · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Autism spectrum disorders (ASD) are a set of complex neurodevelopmental disorders for which there is currently no targeted therapeutic approach. It is thought that alterations of genes regulating migration and synapse formation during development affect neural circuit formation and result in aberrant connectivity within distinct circuits that underlie abnormal behaviors. However, it is unknown whether deviant developmental trajectories are circuit-specific for a given autism risk-gene. We used MRI to probe changes in functional and structural connectivity from childhood to adulthood in Fragile-X (Fmr1-/y) and contactin-associated (CNTNAP2-/-) knockout mice. Young Fmr1-/y mice (30 days postnatal) presented with a robust hypoconnectivity phenotype in corticocortico and corticostriatal circuits in areas associated with sensory information processing, which was maintained until adulthood. Conversely, only small differences in hippocampal and striatal areas were present during early postnatal development in CNTNAP2-/- mice, while major connectivity deficits in prefrontal and limbic pathways developed between adolescence and adulthood. These findings are supported by viral tracing and electron micrograph approaches and define 2 clearly distinct connectivity endophenotypes within the autism spectrum. We conclude that the genetic background of ASD strongly influences which circuits are most affected, the nature of the phenotype, and the developmental time course of the associated changes.
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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.