ReviewFrontiers in neuroscience2015
Genotype-phenotype correlation in neuronal migration disorders and cortical dysplasias.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 55 citations in OpenAlex.
- When the Cytoskeleton Fails: Primary Structural Defects Underlying Disorders with Neurological Involvement.International journal of molecular sciences · 2026Review
- The Value of Transvaginal Neurosonography in the Detection of Fetal Ganglionic Eminence Abnormalities.Life (Basel, Switzerland) · 2026Review
- Neurabin I haploinsufficiency disrupts ion channel regulation and synaptic maturation in human cortical neurons in neurodevelopmental disorders.Molecular psychiatry · 2026Article
- Proteasomal activation ameliorates neuronal phenotypes linked to FBXO11-deficiency.HGG advances · 2025Article
- Efficacy and tolerability of celastrol and edaravone in the multiple-hit rat model of infantile spasms.Epilepsy & behavior : E&B · 2025Article
- Compromised transcription-mRNA export factor THOC2 causes R-loop accumulation, DNA damage and adverse neurodevelopment.Nature communications · 2024Article
- PCDH12 loss results in premature neuronal differentiation and impeded migration in a cortical organoid model.Cell reports · 2023Article
- The fetal brain: migration and gyration anomalies - pre- and postnatal correlations.Pediatric radiology · 2023Article
- Malformation of the Cortical Development Associated with Severe Clusters of Epileptic Seizures.Veterinary sciences · 2022Article
- Loss of ARHGAP15 affects the directional control of migrating interneurons in the embryonic cortex and increases susceptibility to epilepsy.Frontiers in cell and developmental biology · 2022Article
- Modeling epileptic spasms during infancy: Are we heading for the treatment yet?Pharmacology & therapeutics · 2020Review
- Pathogenic variants inCold Spring Harbor molecular case studies · 2020Article
- Developmental brain abnormalities and acute encephalopathy in a patient with myopathy with extrapyramidal signs secondary to pathogenic variants in MICU1.JIMD reports · 2020Article
- Generation and analysis of novel Reln-deleted mouse model corresponding to exonic Reln deletion in schizophrenia.Psychiatry and clinical neurosciences · 2020Article
- Article
- NovelHuman genome variation · 2020Article
- Dynein activating adaptor BICD2 controls radial migration of upper-layer cortical neurons in vivo.Acta neuropathologica communications · 2019Article
- Review
- β-Tubulinopathy caused by a mutation of the TUBB2B gene: magnetic resonance imaging findings of the brain.The neuroradiology journal · 2019Article
- Multiple Functions of KBP in Neural Development Underlie Brain Anomalies in Goldberg-Shprintzen Syndrome.Frontiers in molecular neuroscience · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal migration disorders are human (or animal) diseases that result from a disruption in the normal movement of neurons from their original birth site to their final destination during early development. As a consequence, the neurons remain somewhere along their migratory route, their location depending on the pathological mechanism and its severity. The neurons form characteristic abnormalities, which are morphologically classified into several types, such as lissencephaly, heterotopia, and cobblestone dysplasia. Polymicrogyria is classified as a group of malformations that appear secondary to post-migration development; however, recent findings of the underlying molecular mechanisms reveal overlapping processes in the neuronal migration and post-migration development stages. Mutations of many genes are involved in neuronal migration disorders, such as LIS1 and DCX in classical lissencephaly spectrum, TUBA1A in microlissencephaly with agenesis of the corpus callosum, and RELN and VLDLR in lissencephaly with cerebellar hypoplasia. ARX is of particular interest from basic and clinical perspectives because it is critically involved in tangential migration of GABAergic interneurons in the forebrain and its mutations cause a variety of phenotypes ranging from hydranencephaly or lissencephaly to early-onset epileptic encephalopathies, including Ohtahara syndrome and infantile spasms or intellectual disability with no brain malformations. The recent advances in gene and genome analysis technologies will enable the genetic basis of neuronal migration disorders to be unraveled, which, in turn, will facilitate genotype-phenotype correlations to be determined.
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.