ArticleBrain pathology (Zurich, Switzerland)2015
Homozygous Deletion of the LGI1 Gene in Mice Leads to Developmental Abnormalities Resulting in Cortical Dysplasia.
Article in Brain pathology (Zurich, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 18 citations in OpenAlex.
- A novel LGI1 mutation causing autosomal dominant lateral temporal lobe epilepsy confirmed by a precise knock-in mouse model.CNS neuroscience & therapeutics · 2022Article
- The LGI1 protein: molecular structure, physiological functions and disruption-related seizures.Cellular and molecular life sciences : CMLS · 2021Review
- Celecoxib Ameliorates Seizure Susceptibility in Autosomal Dominant Lateral Temporal Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Leucine-Rich Glioma Inactivated 1 Promotes Oligodendrocyte Differentiation and Myelination via TSC-mTOR Signaling.Frontiers in molecular neuroscience · 2018Article
- YM155 inhibits topoisomerase function.Anti-cancer drugs · 2017Article
- Cornu Ammonis Regions-Antecedents of Cortical Layers?Frontiers in neuroanatomy · 2017Review
- Autoimmune synaptopathies.Nature reviews. Neuroscience · 2016Review
- The LGI1-ADAM22 protein complex directs synapse maturation through regulation of PSD-95 function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
LGI1 mutations lead to an autosomal dominant form of epilepsy. Lgi1 mutant null mice develop seizures and show abnormal neuronal excitability. A fine structure analysis of the cortex in these mice demonstrated a subtle cortical dysplasia, preferentially affecting layers II-IV, associated with increased Foxp2 and Cux1-expressing neurons leading to blurring of the cortical layers. The hypercellularity observed in the null cortex resulted from an admixture of highly branched mature pyramidal neurons with short and poorly aligned axons as revealed by Golgi staining and immature small neurons with branched disoriented dendrites with reduced spine density and undersized, morphologically altered and round-headed spines. In vitro, hippocampal neurons revealed poor neurite outgrowth in null mice as well as reduced synapse formation. Electron microscopy demonstrated reduced spine-localized asymmetric (axospinous) synapses with postsynaptic densities and vesicle-loaded synapses in the mutant null cortex. The overall pathology in the null mice suggested cortical dyslamination most likely because of mislocalization of late-born neurons, with an admixture of those carrying suboptimally developed axons and dendrites with reduced functional synapses with normal neurons. Our study suggests that LGI1 has a role in regulating cortical development, which is increasingly becoming recognized as one of the causes of idiopathic epilepsy.
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.