Advances in the development of biomarkers for epilepsy DOI
Asla Pitkänen, Wolfgang Löscher, Annamaria Vezzani

et al.

The Lancet Neurology, Journal Year: 2016, Volume and Issue: 15(8), P. 843 - 856

Published: June 6, 2016

Language: Английский

Epilepsy and brain inflammation DOI
Annamaria Vezzani, Eleonora Aronica, Andréy Mazarati

et al.

Experimental Neurology, Journal Year: 2011, Volume and Issue: 244, P. 11 - 21

Published: Oct. 2, 2011

Language: Английский

Citations

546

Neurogenic neuroinflammation: inflammatory CNS reactions in response to neuronal activity DOI

Dimitris N. Xanthos,

Jürgen Sandkühler

Nature reviews. Neuroscience, Journal Year: 2013, Volume and Issue: 15(1), P. 43 - 53

Published: Nov. 27, 2013

Language: Английский

Citations

525

Glial responses to implanted electrodes in the brain DOI
Joseph W. Salatino, Kip A. Ludwig, Takashi D.Y. Kozai

et al.

Nature Biomedical Engineering, Journal Year: 2017, Volume and Issue: 1(11), P. 862 - 877

Published: Nov. 3, 2017

Language: Английский

Citations

503

Review: Hippocampal sclerosis in epilepsy: a neuropathology review DOI Creative Commons
Maria Thom

Neuropathology and Applied Neurobiology, Journal Year: 2014, Volume and Issue: 40(5), P. 520 - 543

Published: April 25, 2014

Hippocampal sclerosis (HS) is a common pathology encountered in mesial temporal lobe epilepsy (MTLE) as well other syndromes and both surgical post-mortem practice. The 2013 International League Against Epilepsy (ILAE) classification segregates HS into typical (type 1) atypical 2 3) groups, based on the histological patterns of subfield neuronal loss gliosis. In addition, granule cell reorganization alterations interneuronal populations, neuropeptide fibre networks mossy sprouting are distinctive features associated with epilepsies; they can be useful diagnostic aids to discriminate from causes HS, highlighting potential mechanisms hippocampal epileptogenesis. cause remains elusive may multifactorial; contribution febrile seizures, genetic susceptibility, inflammatory neurodevelopmental factors discussed. Post-mortem research an addition studies samples, has added advantage enabling study wider network changes long-term effects comorbidities. It likely that heterogeneous aspects its cause, epileptogenetic mechanisms, response medical treatments. Future neuropathological will contribute better recognition understanding these clinical patho-aetiological subtypes HS.

Language: Английский

Citations

502

The impact of microglial activation on blood-brain barrier in brain diseases DOI Creative Commons
Anna Carolina Carvalho da Fonseca, Diana Matias, Celina García

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2014, Volume and Issue: 8

Published: Nov. 3, 2014

The blood-brain barrier (BBB), constituted by an extensive network of endothelial cells together with neurons and glial cells, including microglia, forms the neurovascular unit. crosstalk between these guarantees a proper environment for brain function. In this context, changes in endothelium-microglia interactions are associated variety inflammation-related diseases brain, where BBB permeability is compromised. Increasing evidences indicate that activated microglia modulate expression tight junctions, which essential integrity On other hand, endothelium can regulate state microglial activation. Here, we review recent advances provide insights into vascular system such as infectious/inflammatory diseases, epilepsy, ischemic stroke neurodegenerative disorders.

Language: Английский

Citations

498

The role of inflammation in epileptogenesis DOI
Annamaria Vezzani, Alon Friedman, Raymond Dingledine

et al.

Neuropharmacology, Journal Year: 2012, Volume and Issue: 69, P. 16 - 24

Published: April 13, 2012

Language: Английский

Citations

451

Silencing microRNA-134 produces neuroprotective and prolonged seizure-suppressive effects DOI
Eva M. Jiménez‐Mateos, Tobías Engel, Paula Merino-Serráis

et al.

Nature Medicine, Journal Year: 2012, Volume and Issue: 18(7), P. 1087 - 1094

Published: June 10, 2012

Language: Английский

Citations

443

Neuronal Hyperactivity Recruits Microglial Processes via Neuronal NMDA Receptors and Microglial P2Y12 Receptors after Status Epilepticus DOI Open Access
Ukpong B. Eyo, Jing Peng,

Przemyslaw Swiatkowski

et al.

Journal of Neuroscience, Journal Year: 2014, Volume and Issue: 34(32), P. 10528 - 10540

Published: Aug. 6, 2014

Microglia are highly dynamic immune cells of the CNS and their dynamism is proposed to be regulated by neuronal activities. However, mechanisms underlying regulation microglial have not been determined. Here, we found an increased number primary processes in hippocampus during KA-induced seizure activity. Consistently, global glutamate induced robust process extension toward neurons both brain slices intact in vivo. The mechanism glutamate-induced involves activation NMDA receptors, calcium influx, subsequent ATP release, response through P2Y12 receptors. Seizure-induced increases numbers were also dependent on receptor activation. Finally, that KO mice exhibited reduced seizure-induced worsened behaviors. Our results elucidate molecular microglia–neuron communication may potentially neuroprotective epileptic brain.

Language: Английский

Citations

416

Cytokines and brain excitability DOI

Michael A. Galic,

Kiarash Riazi, Quentin J. Pittman

et al.

Frontiers in Neuroendocrinology, Journal Year: 2011, Volume and Issue: 33(1), P. 116 - 125

Published: Dec. 27, 2011

Language: Английский

Citations

397

Depression: an inflammatory illness?: Figure 1 DOI Open Access
Rajeev Krishnadas, Jonathan Cavanagh

Journal of Neurology Neurosurgery & Psychiatry, Journal Year: 2012, Volume and Issue: 83(5), P. 495 - 502

Published: March 15, 2012

Major depressive disorder (MDD) is associated with significant morbidity and mortality. Findings from preclinical clinical studies suggest that psychiatric illnesses, particularly MDD, are inflammatory processes. While it unlikely MDD a primary ‘inflammatory’ disorder, there now evidence to inflammation may play subtle role in the pathophysiology of MDD. Most links comes three observations: (a) one-third those major depression show elevated peripheral biomarkers, even absence medical illness; (b) illnesses greater rates MDD; (c) patients treated cytokines at risk developing illness. We know brain not an immune privileged organ. Inflammatory mediators have been found affect various substrates thought be important aetiopathogenesis including altered monoamine glutamate neurotransmission, glucocorticoid receptor resistance adult hippocampal neurogenesis. At higher level, signalling patterns, cognition production constellation symptoms, termed ‘sickness behaviour’. Inflammation therefore aetiology depression, least ‘cohort’ vulnerable individuals. only act as precipitating factor pushes person into but also perpetuating pose obstacle recovery. More importantly, markers aid diagnosis prediction treatment response, leading possibility tailored treatments, thereby allowing stratification what remains heterogenous disorder.

Language: Английский

Citations

376