CoChat
Sign Up
Cited by 508

Epilepsy and brain inflammation

Vezzani, Annamaria, Aronica, Eleonora, Mazarati, Andrey, Pittman, Quentin J.·2013·Experimental Neurology
DOI 10.1016/j.expneurol.2011.09.033
Open this paper in CoChat — free account

Abstract

During the last decade, experimental research has demonstrated a prominent role of glial cells, activated in brain by various injuries, in the mechanisms of seizure precipitation and recurrence. In particular, alterations in the phenotype and function of activated astrocytes and microglial cells have been described in experimental and human epileptic tissue, including modifications in potassium and water channels, alterations of glutamine/glutamate cycle, changes in glutamate receptor expression and transporters, release of neuromodulatory molecules (e.g. gliotransmitters, neurotrophic factors), and induction of molecules involved in inflammatory processes (e.g. cytokines, chemokines, prostaglandins, complement factors, cell adhesion molecules) (Seifert et al., 2006; Vezzani et al., 2011; Wetherington et al., 2008). In particular, brain injury or proconvulsant events can activate microglia and astrocytes to release a number of proinflammatory mediators, thus initiating a cascade of inflammatory processes in brain tissue. Proinflammatory molecules can alter neuronal excitability and affect the physiological functions of glia by paracrine or autocrine actions, thus perturbing the glioneuronal communications. In experimental models, these changes contribute to decreasing the threshold to seizures and may compromise neuronal survival (Riazi et al., 2010; Vezzani et al., 2008). In this context, understanding which are the soluble mediators and the molecular mechanisms crucially in…

Integrity signals

Registry

Crossref · 10.1016/j.expneurol.2011.09.033

Cites

11 of 11 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Inflammation is relevant in the pathophysiology of epilepsy.

    “During the last decade, both experimental and clinical studies have demonstrated the relevance of inflammation in the pathophysiology of epilepsy (for reviews see [1]–[3].”

    From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [2]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Vezzani, A., Aronica, E., Mazarati, A., & Pittman, Q. J.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2013-06
Volume
244
Pages
11-21
ISSN
0014-4886
DOI
10.1016/j.expneurol.2011.09.033
Cited by
508
References
11
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review