Evidence map›Paper›PMID 19850449›Full record

ReviewEpilepsy research2010

Mitochondria, oxidative stress, and temporal lobe epilepsy.

Simon Waldbaum, Manisha Patel

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Epilepsy research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 2 pooled it
8.2field-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

156 citing papers in PubMed, 2 syntheses or guidelines pooled it, 337 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Causal correlation between seizure activity and brain damage.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

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

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

2 authors at 1 institution in 1 country.

Simon WaldbaumDepartment of Pharmaceutical Sciences, University of Colorado Denver School of Pharmacy, Aurora, 80045, USA.
Manisha Patel
University of Colorado Denver · US

Funding

SUPEROXIDE RADICALS IN SEIZURE-INDUCED NEURONAL DEATHR01NS039587 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2000 to 2019
$5.9M
NINDS NIH HHS R01 NS039587PHS HHS R01 NSO39587
6 · The paper itself

Abstract

Mitochondrial oxidative stress and dysfunction are contributing factors to various neurological disorders. Recently, there has been increasing evidence supporting the association between mitochondrial oxidative stress and epilepsy. Although certain inherited epilepsies are associated with mitochondrial dysfunction, little is known about its role in acquired epilepsies such as temporal lobe epilepsy (TLE). Mitochondrial oxidative stress and dysfunction are emerging as key factors that not only result from seizures, but may also contribute to epileptogenesis. The occurrence of epilepsy increases with age, and mitochondrial oxidative stress is a leading mechanism of aging and age-related degenerative disease, suggesting a further involvement of mitochondrial dysfunction in seizure generation. Mitochondria have critical cellular functions that influence neuronal excitability including production of adenosine triphosphate (ATP), fatty acid oxidation, control of apoptosis and necrosis, regulation of amino acid cycling, neurotransmitter biosynthesis, and regulation of cytosolic Ca(2+) homeostasis. Mitochondria are the primary site of reactive oxygen species (ROS) production making them uniquely vulnerable to oxidative stress and damage which can further affect cellular macromolecule function, the ability of the electron transport chain to produce ATP, antioxidant defenses, mitochondrial DNA stability, and synaptic glutamate homeostasis. Oxidative damage to one or more of these cellular targets may affect neuronal excitability and increase seizure susceptibility. The specific targeting of mitochondrial oxidative stress, dysfunction, and bioenergetics with pharmacological and non-pharmacological treatments may be a novel avenue for attenuating epileptogenesis.

Indexed as

AnimalsAntioxidantsDNA, MitochondrialElectron Transport Complex IEpilepsy, Temporal LobeGlutamic AcidHumansIon ChannelsLipidsMitochondriaModels, BiologicalNeuronsOxidation-ReductionOxidative StressAntioxidantsDNA, MitochondrialElectron Transport Complex IGlutamic AcidIon ChannelsLipids

Identifiers

PMID19850449
PMCPMC3236664
OpenAlexW2045243715

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.