Evidence map›Paper›PMID 19701204›Full record

ArticleNature medicine2009

Arrested maturation of excitatory synapses in autosomal dominant lateral temporal lobe epilepsy.

Yu-Dong Zhou, Sanghoon Lee, Zhe Jin, Moriah Wright, Stephen E P Smith, Matthew P Anderson

Open access · greenAbstract read
In one paragraph

Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 185 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. LGI1 Autoantibodies Enhance Synaptic Transmission by Presynaptic KNeurology(R) neuroimmunology & neuroinflammation · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Rescue of Normal Excitability in LGI1-Deficient Epileptic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Genes · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Review

36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Yu-Dong ZhouDepartments of Neurology and Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Sanghoon Lee
Zhe Jin
Moriah Wright
Stephen E P Smith
Matthew P Anderson
Harvard University · USBeth Israel Deaconess Medical Center · USCenter for Systems Biology · USTufts University · US

Funding

Role of LGI1 in Autosomal Dominant Lateral Temporal Lobe EpilepsyR01NS057444 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ANDERSON, MATTHEW P · 2008 to 2011
$1.3M
Engineering the Mouse Nervous System To Decipher Network Mechanisms of EpilepsyK02NS054674 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ANDERSON, MATTHEW P · 2006 to 2010
$974k
Modeling Childhhood Absence Epilepsy in MiceR03NS052521 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ANDERSON, MATTHEW P · 2005 to 2006
$168k
NINDS NIH HHS K02 NS054674NINDS NIH HHS K02 NS054674-03NINDS NIH HHS R01 NS057444NINDS NIH HHS R03 NS052521
6 · The paper itself

Abstract

A subset of central glutamatergic synapses are coordinately pruned and matured by unresolved mechanisms during postnatal development. We report that the human epilepsy gene LGI1, encoding leucine-rich, glioma-inactivated protein-1 and mutated in autosomal dominant lateral temporal lobe epilepsy (ADLTE), mediates this process in hippocampus. We created transgenic mice either expressing a truncated mutant LGI1 (835delC) found in ADLTE or overexpressing a wild-type LGI1. We discovered that the normal postnatal maturation of presynaptic and postsynaptic functions was arrested by the 835delC mutant LGI1, and contrastingly, was magnified by excess wild-type LGI1. Concurrently, mutant LGI1 inhibited dendritic pruning and increased the spine density to markedly increase excitatory synaptic transmission. Inhibitory transmission, by contrast, was unaffected. Furthermore, mutant LGI1 promoted epileptiform discharge in vitro and kindling epileptogenesis in vivo with partial gamma-aminobutyric acid(A) (GABA(A)) receptor blockade. Thus, LGI1 represents a human gene mutated to promote epilepsy through impaired postnatal development of glutamatergic circuits.

Indexed as

AnimalsEpilepsy, Temporal LobeGene Expression Regulation, DevelopmentalGenes, DominantHumansIntracellular Signaling Peptides and ProteinsMiceMice, TransgenicMutationProteinsReceptors, GABA-BSynapsesTransgenesIntracellular Signaling Peptides and ProteinsLGI1 protein, humanLgi1 protein, mouseProteinsReceptors, GABA-B

Identifiers

PMID19701204
PMCPMC2759408
OpenAlexW2051240384

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.