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Jan A. Gorter

Researcher at University of Amsterdam

Publications -  144
Citations -  11267

Jan A. Gorter is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Epileptogenesis & Epilepsy. The author has an hindex of 56, co-authored 140 publications receiving 10253 citations. Previous affiliations of Jan A. Gorter include Albert Einstein College of Medicine.

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Blood–brain barrier leakage may lead to progression of temporal lobe epilepsy

TL;DR: The findings indicate that BBB leakage occurs during epileptogenesis and the chronic epileptic phase and suggest that this can contribute to the progression of epilepsy.
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The GluR2 (GluR-B) hypothesis: Ca2+-permeable AMPA receptors in neurological disorders

TL;DR: Observations suggest that downregulation of gluR2 gene expression may serve as a 'molecular switch' leading to the formation of Ca(2+)-permeable AMPA receptors and enhanced toxicity of endogenous glutamate following a neurological insult.
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Potential New Antiepileptogenic Targets Indicated by Microarray Analysis in a Rat Model for Temporal Lobe Epilepsy

TL;DR: The targeting of specific genes that are involved in these biological processes may be a promising strategy to slow down or prevent the progression of epilepsy, especially genes related to the immune response.
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MicroRNA-146a: a key regulator of astrocyte-mediated inflammatory response.

TL;DR: Observations indicate that in response to inflammatory cues, miR-146a was induced as a negative-feedback regulator of the astrocyte-mediated inflammatory response and suggests that this miR may represent a novel target for therapeutic strategies.
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Global Ischemia Induces Downregulation of Glur2 mRNA and Increases AMPA Receptor-Mediated Ca2+ Influx in Hippocampal CA1 Neurons of Gerbil

TL;DR: It is suggested that “switching off” GluR2 expression in CAI after an ischemic insult is translated into formation of new AMPA receptors lacking the GLUR2 subunit, which increases AMPA-receptor-mediated Ca2+ entry in response to endogenous glutamate and enhances glutamate pathogenicity in this region.