Evidence map›Paper›PMID 18505356›Full record

ReviewExpert review of neurotherapeutics2008

Stabilizing dendritic structure as a novel therapeutic approach for epilepsy.

Michael Wong

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of neurotherapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Bistable Firing Pattern in a Neural Network Model.Frontiers in computational neuroscience · 2019
    Article
  8. The calcineurin inhibitor Ascomicin interferes with the early stage of the epileptogenic process induced by Latrunculin A microperfusion in rat hippocampus.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    Article
  9. Article
  10. Brief seizures cause dendritic injury.Neurobiology of disease · 2012
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Michael WongDepartment of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. wong_m@wustl.edu.
Washington University in St. Louis · US

Funding

MECHANISMS OF BRAIN DYSFUNCTION IN TUBEROUS SCLEROSISR01NS056872 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2006 to 2019
$4.0M
Rapid seizure-induced changes in dendritic spinesK02NS045583 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2003 to 2007
$714k
NINDS NIH HHS K02 NS045583NINDS NIH HHS K02NS045583NINDS NIH HHS R01 NS056872NINDS NIH HHS R01NS056872
6 · The paper itself

Abstract

People with epilepsy often experience long-term cognitive dysfunction and other neurological deficits, including memory loss, learning disabilities and neurobehavioral disorders, which may exhibit a progressive course correlating with worsening seizure control. Furthermore, a third of epilepsy patients have seizures that are intractable to all available treatments. Thus, novel therapies for seizures and the neurological comorbidities of epilepsy are desperately needed. As most current treatments are merely symptomatic therapies that suppress seizures, epilepsy researchers have recently realized the critical need for novel therapeutic strategies targeting the underlying mechanisms of epileptogenesis and seizure-related brain injury. Yet, to date, few such antiepileptogenic therapies have emerged or are even in developmental stages. Although many seizure medications modulate the functional or physiological activity of neurons, the methods for stabilizing the structure of neurons are relatively unexplored therapeutic strategies for epilepsy. Human pathological studies and animal models of epilepsy demonstrate obvious structural abnormalities in dendrites of neurons, which could contribute to neuronal dysfunction, epileptogenesis and cognitive/neurological deficits in epilepsy patients. This dendritic injury may be caused by activity-dependent breakdown of cytoskeletal elements, such as actin. Mechanistically targeted approaches to limit seizure-related structural changes in dendrites may represent a novel therapeutic strategy for treating epilepsy and its complications.

Indexed as

EpilepsyAnimalsBrainDendritesHumans

Identifiers

PMID18505356
PMCPMC3935512
OpenAlexW2032694193

What OpenQuestion holds

Textmetadata
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.