ReviewAnnual review of pathology2019
Malformations of Cerebral Cortex Development: Molecules and Mechanisms.
Review in Annual review of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 116 citations in OpenAlex.
- Loss of Zmiz1 in Mice Leads to Impaired Cortical Development and Autistic-Like Behaviors.Biological psychiatry · 2026Article
- Minor Physical Anomalies and Congenital Malformations Among Children with Psychotic Symptoms: An Exploratory Descriptive Study with Illustrative Clinical Cases.Brain sciences · 2026Article
- Prenatal (1-3)IGF-1 Treatment Is Ineffective and Behaviorally Detrimental in a Rat Model of Cortical Malformation.Brain and behavior · 2026Article
- Drospondin, a glial glycoprotein with similarities to human Reelin/F-spondin, contributes toProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Stem cells in organogenesis and regeneration.Stem cell research & therapy · 2026Review
- Prenatal Diagnosis of Malformations of Cortical Development: A Review of Genetic and Imaging Advances.Biomedicines · 2026Review
- Genetic landscape and phenotypic correlations of lissencephaly: prenatal and postnatal insights.Brain communications · 2026Article
- Beyond mTOR: Unraveling the Complex Pathophysiology and Signaling Pathways in Focal Cortical Dysplasia.Molecular neurobiology · 2025Review
- Article
- Ablation of dysmorphic neurons is a safe and effective treatment for focal cortical dysplasia II.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- A pathogenic NR2F1 gene variant disrupts transcriptional activity and causes severe neurodevelopmental delay in Bosch-Boonstra-Schaaf syndrome.Hereditas · 2025Article
- Personalized Human Astrocyte-Derived Region-Specific Forebrain Organoids Recapitulate Endogenous Pathological Features of Focal Cortical Dysplasia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Brain malformation, neurodevelopmental disorder and epilepsy in a case of two rare genetic diseases: overlapping phenotype.Neurogenetics · 2024Article
- Role of Maternal Immune Factors in Neuroimmunology of Brain Development.Molecular neurobiology · 2024Review
- Cobblestone lissencephaly (Type II), clinical, and neuroimaging: A case report and literature review.Radiology case reports · 2024Article
- Article
- Altered expression of the Plexin-B2 system in tuberous sclerosis complex and focal cortical dysplasia IIb lesions.Histology and histopathology · 2024Article
- MSL2 variants lead to a neurodevelopmental syndrome with lack of coordination, epilepsy, specific dysmorphisms, and a distinct episignature.American journal of human genetics · 2024Article
- Loss of protein tyrosine phosphatase receptor delta PTPRD increases the number of cortical neurons, impairs synaptic function and induces autistic-like behaviors in adult mice.Biological research · 2024Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Malformations of cortical development encompass heterogeneous groups of structural brain anomalies associated with complex neurodevelopmental disorders and diverse genetic and nongenetic etiologies. Recent progress in understanding the genetic basis of brain malformations has been driven by extraordinary advances in DNA sequencing technologies. For example, somatic mosaic mutations that activate mammalian target of rapamycin signaling in cortical progenitor cells during development are now recognized as the cause of hemimegalencephaly and some types of focal cortical dysplasia. In addition, research on brain development has begun to reveal the cellular and molecular bases of cortical gyrification and axon pathway formation, providing better understanding of disorders involving these processes. New neuroimaging techniques with improved resolution have enhanced our ability to characterize subtle malformations, such as those associated with intellectual disability and autism. In this review, we broadly discuss cortical malformations and focus on several for which genetic etiologies have elucidated pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.