Journal ArticleDOI
Interleukin-6 deficiency reduces the brain inflammatory response and increases oxidative stress and neurodegeneration after kainic acid-induced seizures.
TLDR
It is demonstrated that interleukin-6 deficiency increases neuronal injury and impairs the inflammatory response after kainic acid-induced seizures, and that reactive astrogliosis and microgliosis were reduced, while morphological hippocampal damage, oxidative stress and apoptotic neuronal death were increased.About:
This article is published in Neuroscience.The article was published on 2001-02-14. It has received 149 citations till now. The article focuses on the topics: Kainic acid & Oxidative stress.read more
Citations
More filters
Journal ArticleDOI
Interleukin-6, a major cytokine in the central nervous system.
TL;DR: Its expression is affected in several of the main brain diseases, and animal models strongly suggest that IL-6 could have a role in the observed neuropathology and that therefore it is a clear target of strategic therapies.
Journal ArticleDOI
The neuropoietic cytokine family in development, plasticity, disease and injury
TL;DR: This work has shown that neuropoietic cytokines, well known for their role in the control of neuronal, glial and immune responses to injury or disease, have yet more functions, as key modulators of synaptic plasticity and of various behaviours.
Journal ArticleDOI
Roles of the metallothionein family of proteins in the central nervous system
TL;DR: The biology of the MT family is reviewed in the context of their expression and functional roles in the central nervous system, both in normal brain physiology, as well as in pathophysiological states.
Journal ArticleDOI
Neuronal and glial pathological changes during epileptogenesis in the mouse pilocarpine model.
Karin Borges,Marla Gearing,Dayna L. McDermott,Amy B. Smith,Antoine G. Almonte,Bruce H. Wainer,Raymond Dingledine +6 more
TL;DR: Major neuropathological changes not previously studied in the rodent pilocarpine model include widespread microglial activation, delayed thalamic axonal death, and persistent NPY upregulation in mossy fibers, together revealing extensive and persistent glial as well as neuronal pathology.
Journal ArticleDOI
Interleukin-6, a mental cytokine.
Anneleen Spooren,Krzysztof Kolmus,Guy Laureys,R Clinckers,Jacques De Keyser,Guy Haegeman,Sarah Gerlo +6 more
TL;DR: It is evident that IL-6 has a dichotomic action in the CNS, displaying neurotrophic properties on the one hand, and detrimental actions on the other, in agreement with its central role in neuroinflammation, which evolved as a beneficial process, aimed at maintaining tissue homeostasis, but which can become malignant when exaggerated.
References
More filters
Journal ArticleDOI
Microglia: a sensor for pathological events in the CNS
TL;DR: An understanding of intercellular signalling pathways for microglia proliferation and activation could form a rational basis for targeted intervention on glial reactions to injuries in the CNS.
Journal ArticleDOI
Impaired immune and acute-phase responses in interleukin-6-deficient mice
Manfred Kopf,Heinz Baumann,Giulia Freer,Marina A. Freudenberg,Marinus C. Lamers,Tadamitsu Kishimoto,Rolf M. Zinkernagel,Horst Bluethmann,Georges Köhler +8 more
TL;DR: It is concluded that IL-6 production induced by injury or infection is an important in vivo SOS signal which coordinates activities of liver cells, macrophages and lymphocytes.
Journal ArticleDOI
Limbic seizure and brain damage produced by kainic acid: Mechanisms and relevance to human temporal lobe epilepsy
TL;DR: This work has shown that kainate-like endotoxins pose a novel threat to the integrity of the immune system through their role as a “spatially aggregating substance” in the response of epilepsy.
Journal ArticleDOI
Molecular profile of reactive astrocytes—Implications for their role in neurologic disease
Michael Eddleston,Lennart Mucke +1 more
TL;DR: A summary of molecules whose levels of expression differentiate activated from resting astrocytes is provided and it becomes apparent that reactive astroCytes may benefit the injured nervous system by participating in diverse biological processes.
Journal ArticleDOI
Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury.
Andrew G. Reaume,Jeffrey L. Elliott,Eric K. Hoffman,Neil W. Kowall,Neil W. Kowall,Robert J. Ferrante,Robert J. Ferrante,Donald R Siwek,Donald R Siwek,Heide M. Wilcox,Dorothy G. Flood,M. Flint Beal,Robert H. Brown,Richard W. Scott,William D. Snider +14 more
TL;DR: The creation and characterization of mice completely deficient for SOD1 indicate that Cu/Zn SOD is not necessary for normal motor neuron development and function but is required under physiologically stressful conditions following injury.