ArticleJCI insight2017
Association of impaired neuronal migration with cognitive deficits in extremely preterm infants.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 33 citations in OpenAlex.
- Early soluble LOX-1, cerebral perfusion, and intrauterine inflammation in very and extremely preterm infants.Pediatric research · 2026Observational
- Group-based trajectory modelling and interpretable machine learning to identify factors associated with neurodevelopmental trajectories in preterm infants.BMC pediatrics · 2026Article
- Evaluation of kidney injury and metabolomic analysis in adulthood in a non-obese hyperglycemic female mouse model after birth with low birthweight.BMC nephrology · 2025Article
- Aging aggravates cognitive dysfunction in spontaneously hypertensive rats by inducing cerebral microvascular endothelial dysfunction.PloS one · 2025Article
- Trauma context exerts intergenerational effects on child mental health via DNA methylation.Epigenetics · 2024Article
- Efficacy of Human Recombinant Growth Hormone in Females of a Non-Obese Hyperglycemic Mouse Model after Birth with Low Birth Weight.International journal of molecular sciences · 2024Article
- Cortical Layer Markers Expression and Increased Synaptic Density in Interstitial Neurons of the White Matter from Drug-Resistant Epilepsy Patients.Brain sciences · 2023Article
- A Unique "Reversed" Migration of Neurons in the Developing Claustrum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Developmental Brain Injury and Social Determinants of Health: Opportunities to Combine Preclinical Models for Mechanistic Insights into Recovery.Developmental neuroscience · 2023Review
- A Simplified Paradigm of Late Gestation Transient Prenatal Hypoxia to Investigate Functional and Structural Outcomes from a Developmental Hypoxic Insult.Bio-protocol · 2022Article
- A Non-Obese Hyperglycemic Mouse Model that Develops after Birth with Low Birthweight.Biomedicines · 2022Article
- Phosphorylation of Focal Adhesion Kinase at Y925: Role in Glia-Dependent and Independent Migration through Regulating Cofilin and N-Cadherin.Molecular neurobiology · 2022Article
- Lack of placental neurosteroid alters cortical development and female somatosensory function.Frontiers in endocrinology · 2022Article
- Deficits in Seizure Threshold and Other Behaviors in Adult Mice without Gross Neuroanatomic Injury after Late Gestation Transient Prenatal Hypoxia.Developmental neuroscience · 2022Article
- Article
- Cortical morphology at birth reflects spatiotemporal patterns of gene expression in the fetal human brain.PLoS biology · 2020Article
- Synthetic PreImplantation Factor (sPIF) reduces inflammation and prevents preterm birth.PloS one · 2020Article
- A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis.Journal of visualized experiments : JoVE · 2018Article
- Preterm Birth Causes Decreased Postnatal Neurogenesis: A Novel Mechanism Underlying Adverse Neurodevelopmental Outcomes.Pediatrics international : official journal of the Japan Pediatric SocietyReview
Corrections and comments
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Authors and funding
27 authors at 10 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many extremely preterm infants (born before 28 gestational weeks [GWs]) develop cognitive impairment in later life, although the underlying pathogenesis is not yet completely understood. Our examinations of the developing human neocortex confirmed that neuronal migration continues beyond 23 GWs, the gestational week at which extremely preterm infants have live births. We observed larger numbers of ectopic neurons in the white matter of the neocortex in human extremely preterm infants with brain injury and hypothesized that altered neuronal migration may be associated with cognitive impairment in later life. To confirm whether preterm brain injury affects neuronal migration, we produced brain damage in mouse embryos by occluding the maternal uterine arteries. The mice showed delayed neuronal migration, ectopic neurons in the white matter, altered neuronal alignment, and abnormal corticocortical axonal wiring. Similar to human extremely preterm infants with brain injury, the surviving mice exhibited cognitive deficits. Activation of the affected medial prefrontal cortices of the surviving mice improved working memory deficits, indicating that decreased neuronal activity caused the cognitive deficits. These findings suggest that altered neuronal migration altered by brain injury might contribute to the subsequent development of cognitive impairment in extremely preterm infants.
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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.