Seizure-Induced Oxidative Stress in Temporal Lobe Epilepsy

BioMed Research International, Journal Year: 2015, Volume and Issue: 2015, P. 1 - 20

Published: Jan. 1, 2015

An insult to the brain (such as first seizure) causes excitotoxicity, neuroinflammation, and production of reactive oxygen/nitrogen species (ROS/RNS). ROS RNS produced during status epilepticus (SE) overwhelm mitochondrial natural antioxidant defense mechanism. This leads dysfunction damage DNA. in turn affects synthesis various enzyme complexes that are involved electron transport chain. Resultant effects occur epileptogenesis include lipid peroxidation, gliosis, hippocampal neurodegeneration, reorganization neural networks, hypersynchronicity. These factors predispose spontaneous recurrent seizures (SRS), which ultimately establish into temporal lobe epilepsy (TLE). review discusses some these issues. Though antiepileptic drugs (AEDs) beneficial control/suppress seizures, their long term usage has been shown increase ROS/RNS animal models human patients. In established TLE, be harmful they can susceptibility SRS. Further, this paper, we briefly data from TLE patients on adverse medications plausible ameliorating antioxidants an adjunct therapy.

Language: Английский

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Stratification of astrocytes in healthy and diseased brain

Brain Pathology, Journal Year: 2017, Volume and Issue: 27(5), P. 629 - 644

Published: Aug. 13, 2017

Abstract Astrocytes, a subtype of glial cells, come in variety forms and functions. However, overarching role these cell is the homeostasis brain, be that regulation ions, neurotransmitters, metabolism or neuronal synaptic networks. Loss represents underlying cause all brain disorders. Thus, astrocytes are likely involved most if not pathologies. We tabulate astroglial homeostatic functions along with pathological condition arise from dysfunction cells. Classification presented emphasis on evolutionary trails, morphological appearance numerical preponderance. note that, even though mammalian species share some common features, human appear to largest complex studied thus far. It then an imperative develop humanized models study pathologies, which perhaps abundantly clear case glioblastoma multiforme.

Language: Английский

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Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons

Molecular Neurodegeneration, Journal Year: 2016, Volume and Issue: 11(1)

Published: May 12, 2016

Despite the clear physical association between activated astrocytes and amyloid-β (Aβ) plaques, importance of their therapeutic potential in Alzheimer's disease remain elusive. Soluble Aβ aggregates, such as protofibrils, have been suggested to be responsible for widespread neuronal cell death disease, but mechanisms behind this unclear. Moreover, ineffective degradation is great interest when it comes development progression neurodegeneration. Based on our previous results that are extremely slow degrading phagocytosed material, we hypothesized may an important player these processes. Hence, aim study was clarify role clearance, spreading toxicity Aβ. To examine pathology, added protofibrils a co-culture system primary neurons glia. Our data demonstrates rapidly engulf large amounts then store, rather than degrade ingested material. The incomplete digestion high intracellular load toxic, partly N-terminally truncated severe lysosomal dysfunction. secretion microvesicles containing Aβ, induce apoptosis cortical neurons. Taken together, suggest play central by accumulating toxic species.

Language: Английский

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Chronic stress followed by social isolation promotes depressive-like behaviour, alters microglial and astrocyte biology and reduces hippocampal neurogenesis in male mice

Brain Behavior and Immunity, Journal Year: 2020, Volume and Issue: 91, P. 24 - 47

Published: Aug. 2, 2020

Language: Английский

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Reactive astrocytes undergo M1 microglia/macrohpages-induced necroptosis in spinal cord injury

Molecular Neurodegeneration, Journal Year: 2016, Volume and Issue: 11(1)

Published: Feb. 3, 2016

A unique feature of the pathological change after spinal cord injury (SCI) is progressive enlargement lesion area, which usually results in cavity formation and accompanied by reactive astrogliosis chronic inflammation. Reactive astrocytes line cavity, walling off core from normal tissue, are thought to play multiple important roles SCI. The contribution cell death, particularly apoptosis neurons oligodendrocytes during process cavitation has been extensively studied. However, how eliminated following SCI remains largely unclear. By immunohistochemistry, vivo propidium iodide (PI)-labeling electron microscopic examination, here we reported that mice, died receptor-interacting protein 3 mixed lineage kinase domain-like (RIP3/MLKL) mediated necroptosis, rather than or autophagy. Inhibiting 1 (RIP1) depleting RIP3 not only significantly attenuated astrocyte death but also rescued neurotrophic function astrocytes. astrocytic expression necroptotic markers followed polarization M1 microglia/macrophages Depleting transplantation macrophages could reduce increase necroptosis Further, inflammatory responsive genes Toll-like receptor 4 (TLR4) myeloid differentiation primary response gene 88 (MyD88) induced In vitro antagonizing MyD88 alleviate microglia/macrophages-induced death. Finally, our data showed human, TLR4/MyD88 were co-expressed injured, cord. Taken together, these reveal SCI, undergo partially through TLR/MyD88 signaling, suggest inhibiting may be beneficial for preventing secondary

Language: Английский

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