The influence of neuropathology on brain inflammation in human and experimental temporal lobe epilepsy

M.W. Aalbers; K. Rijkers; H.J.M. Majoie; J.T. Dings; O.E.M.G. Schijns; S. Schipper; M.H. de Baets; A. Kessels; J.S.H. Vles; G. Hoogland

doi:10.1016/j.jneuroim.2014.03.016

The influence of neuropathology on brain inflammation in human and experimental temporal lobe epilepsy

M.W. Aalbers^*, K. Rijkers, H.J.M. Majoie, J.T. Dings, O.E.M.G. Schijns, S. Schipper, M.H. de Baets, A. Kessels, J.S.H. Vles, G. Hoogland

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

It is unclear to what extent neuropathological changes contribute to brain inflammation observed in temporal lobe epilepsy (TLE). Here, we compared cytokine levels between histopathologically-confirmed sclerotic hippocampi and histopathologically-confirmed normal hippocampi from TLE patients. We analyzed a similar cytokine panel in the hippocampi of amygdala-kindled rats and we evaluated neuropathological changes by immunohistochemistry. In TLE patients, cytokine levels were not significantly different between sclerotic and nonsclerotic hippocampi. Though kindling resulted in increased astrocyte activation, cytokine levels and microglia activation were unchanged. These results suggest that the chronic epileptic state in TLE can also occur in the absence of intracerebral inflammation.

Original language	English
Pages (from-to)	36-42
Journal	Journal of Neuroimmunology
Volume	271
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2014.03.016
Publication status	Published - 1 Jan 2014

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10.1016/j.jneuroim.2014.03.016

Cite this

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title = "The influence of neuropathology on brain inflammation in human and experimental temporal lobe epilepsy",

abstract = "It is unclear to what extent neuropathological changes contribute to brain inflammation observed in temporal lobe epilepsy (TLE). Here, we compared cytokine levels between histopathologically-confirmed sclerotic hippocampi and histopathologically-confirmed normal hippocampi from TLE patients. We analyzed a similar cytokine panel in the hippocampi of amygdala-kindled rats and we evaluated neuropathological changes by immunohistochemistry. In TLE patients, cytokine levels were not significantly different between sclerotic and nonsclerotic hippocampi. Though kindling resulted in increased astrocyte activation, cytokine levels and microglia activation were unchanged. These results suggest that the chronic epileptic state in TLE can also occur in the absence of intracerebral inflammation. ",

author = "M.W. Aalbers and K. Rijkers and H.J.M. Majoie and J.T. Dings and O.E.M.G. Schijns and S. Schipper and {de Baets}, M.H. and A. Kessels and J.S.H. Vles and G. Hoogland",

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T1 - The influence of neuropathology on brain inflammation in human and experimental temporal lobe epilepsy

AU - Aalbers, M.W.

AU - Rijkers, K.

AU - Majoie, H.J.M.

AU - Dings, J.T.

AU - Schijns, O.E.M.G.

AU - Schipper, S.

AU - de Baets, M.H.

AU - Kessels, A.

AU - Vles, J.S.H.

AU - Hoogland, G.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - It is unclear to what extent neuropathological changes contribute to brain inflammation observed in temporal lobe epilepsy (TLE). Here, we compared cytokine levels between histopathologically-confirmed sclerotic hippocampi and histopathologically-confirmed normal hippocampi from TLE patients. We analyzed a similar cytokine panel in the hippocampi of amygdala-kindled rats and we evaluated neuropathological changes by immunohistochemistry. In TLE patients, cytokine levels were not significantly different between sclerotic and nonsclerotic hippocampi. Though kindling resulted in increased astrocyte activation, cytokine levels and microglia activation were unchanged. These results suggest that the chronic epileptic state in TLE can also occur in the absence of intracerebral inflammation.

AB - It is unclear to what extent neuropathological changes contribute to brain inflammation observed in temporal lobe epilepsy (TLE). Here, we compared cytokine levels between histopathologically-confirmed sclerotic hippocampi and histopathologically-confirmed normal hippocampi from TLE patients. We analyzed a similar cytokine panel in the hippocampi of amygdala-kindled rats and we evaluated neuropathological changes by immunohistochemistry. In TLE patients, cytokine levels were not significantly different between sclerotic and nonsclerotic hippocampi. Though kindling resulted in increased astrocyte activation, cytokine levels and microglia activation were unchanged. These results suggest that the chronic epileptic state in TLE can also occur in the absence of intracerebral inflammation.

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DO - 10.1016/j.jneuroim.2014.03.016

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C2 - 24746448

SN - 0165-5728

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