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1. Full Text Apoptotic mechanisms after cerebral ischemia
by Broughton, Brad R.S and Reutens, David C and Sobey, Christopher G
Stroke, ISSN 0039-2499, 05/2009, Volume 40, Issue 5, pp. e331 - e339
Background and Purpose-Traditionally, cell death after cerebral ischemia was considered to be exclusively necrotic in nature, but research over the past decade... 
Cytochrome c | Fas receptor | Stroke | Caspases | Penumbra | MITOCHONDRIAL CYTOCHROME-C | POLY(ADP-RIBOSE) POLYMERASE | ARTERY OCCLUSION | BRAIN-INJURY | TRANSIENT FOCAL ISCHEMIA | NEURONAL CELL-DEATH | SUBSEQUENT DNA FRAGMENTATION | stroke | OXYGEN-GLUCOSE DEPRIVATION | NUCLEAR TRANSLOCATION | CLINICAL NEUROLOGY | penumbra | TRANSGENIC MICE PROTECTS | PERIPHERAL VASCULAR DISEASE | cytochrome c | caspases | Caspases - physiology | Animals | Reactive Oxygen Species - metabolism | Calcium Channels - metabolism | Calcium - metabolism | Humans | Brain Ischemia - pathology | Apoptosis Regulatory Proteins - physiology | fas Receptor - physiology | Apoptosis - physiology | DNA Damage | Receptors, Tumor Necrosis Factor - physiology
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2. Full Text Postischemic treatment of neonatal cerebral ischemia should target autophagy
by Puyal, Julien and Vaslin, Anne and Mottier, Vincent and Clarke, Peter G.H
Annals of Neurology, ISSN 0364-5134, 09/2009, Volume 66, Issue 3, pp. 378 - 389
Objective To evaluate the contributions of autophagic, necrotic, and apoptotic cell death mechanisms after neonatal cerebral ischemia and hence define the most... 
APOPTOSIS | HYPOXIA-ISCHEMIA | KAINIC ACID | RAT-BRAIN | TRANSIENT ISCHEMIA | FOCAL ISCHEMIA | UP-REGULATION | CATHEPSINS B | NEUROSCIENCES | CLINICAL NEUROLOGY | DELAYED NEURONAL DEATH | CELL-DEATH | Immunohistochemistry | Neurons - pathology | Neuroprotective Agents | Apoptosis - drug effects | Injections, Intraventricular | Brain Ischemia - metabolism | Male | Autophagy - physiology | Necrosis - pathology | Autophagy - drug effects | Brain - metabolism | Caspases - metabolism | Adenine - therapeutic use | Lysosomes - pathology | Cell Death - drug effects | Ischemic Attack, Transient - metabolism | Neurons - drug effects | Ischemic Attack, Transient - pathology | Phagosomes - drug effects | Animals, Newborn | Lysosomes - drug effects | Adenine - analogs & derivatives | Ischemic Attack, Transient - drug therapy | Phagosomes - metabolism | Rats | Necrosis - metabolism | Adenine - pharmacology | Microscopy, Electron | Caspase Inhibitors | Phagosomes - pathology | Rats, Sprague-Dawley | Necrosis - prevention & control | Adenine - administration & dosage | Brain - drug effects | Animals | Cell Death - physiology | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Brain - pathology | Apoptosis - physiology
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3. Full Text Purinergic signalling in brain ischemia
by Pedata, Felicita and Dettori, Ilaria and Coppi, Elisabetta and Melani, Alessia and Fusco, Irene and Corradetti, Renato and Pugliese, Anna Maria
Neuropharmacology, ISSN 0028-3908, 05/2016, Volume 104, pp. 105 - 130
Ischemia is a multifactorial pathology characterized by different events evolving in the time. After ischemia a primary damage due to the early massive... 
Adenosine | Cerebral ischemia | Oxygen glucose deprivation | P1 receptors | ATP | P2 receptors | ACTIVATED PROTEIN-KINASE | IN-VITRO ISCHEMIA | FOCAL CEREBRAL-ISCHEMIA | PREVENTS ATP EXCITOTOXICITY | ADENOSINE A(2A) RECEPTOR | GLUTAMATERGIC NERVE-TERMINALS | NEUROSCIENCES | OXYGEN-GLUCOSE DEPRIVATION | EXCITATORY AMINO-ACIDS | TUMOR-NECROSIS-FACTOR | TRANSIENT FOREBRAIN ISCHEMIA | PHARMACOLOGY & PHARMACY | Animals | Signal Transduction | Adenosine Triphosphate - metabolism | Encephalitis - metabolism | Humans | Receptors, Purinergic P2 - metabolism | Adenosine - metabolism | Brain Ischemia - metabolism | Purinergic P2 Receptor Antagonists - pharmacology | Receptors, Purinergic P1 - metabolism | Purinergic P1 Receptor Antagonists - pharmacology | Brain | Brain damage | Glutamate | Injuries | Glucose | Dextrose
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4. Full Text Neuroprotective mechanisms of hypothermia in brain ischaemia
by Yenari, Midori A and Han, Hyung Soo
Nature Reviews Neuroscience, ISSN 1471-003X, 04/2012, Volume 13, Issue 4, pp. 267 - 278
Cooling can reduce primary injury and prevent secondary injury to the brain after insults in certain clinical settings and in animal models of brain insult.... 
TO-MODERATE HYPOTHERMIA | WHOLE-BODY HYPOTHERMIA | ASPHYXIAL CARDIAC-ARREST | THERAPEUTIC HYPOTHERMIA | FOCAL CEREBRAL-ISCHEMIA | MILD HYPOTHERMIA | FACTOR-KAPPA-B | NECROSIS-FACTOR-ALPHA | SIGNAL-REGULATED KINASE | NEUROSCIENCES | RNA-BINDING PROTEIN | Brain - physiopathology | Brain Ischemia - therapy | Humans | Hypothermia, Induced - methods | Brain Ischemia - pathology | Brain - pathology | Brain Ischemia - physiopathology | Prevention | Physiological aspects | Brain | Research | Ischemia | Hypothermia
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5. Full Text Molecular Mechanisms of Ischemia–Reperfusion Injury in Brain: Pivotal Role of the Mitochondrial Membrane Potential in Reactive Oxygen Species Generation
by Sanderson, Thomas H and Sanderson, Thomas H and Reynolds, Christian A and Reynolds, Christian A and Kumar, Rita and Kumar, Rita and Przyklenk, Karin and Przyklenk, Karin and Hüttemann, Maik and Hüttemann, Maik
Molecular Neurobiology, ISSN 0893-7648, 2/2013, Volume 47, Issue 1, pp. 9 - 23
Stroke and circulatory arrest cause interferences in blood flow to the brain that result in considerable tissue damage. The primary method to reduce or prevent... 
Neurology | Brain | Neurosciences | Reactive oxygen species | Mitochondria | Biomedicine | Reperfusion | Ischemia | Oxidative phosphorylation | Neurobiology | Cell Biology | OXIDATIVE-PHOSPHORYLATION | FOCAL CEREBRAL-ISCHEMIA | NEURONAL CELL-DEATH | RAT-LIVER MITOCHONDRIA | NEUROSCIENCES | ELECTRON-TRANSPORT CHAIN | CYTOCHROME-C-OXIDASE | TRANSIENT FOREBRAIN ISCHEMIA | UNCOUPLING PROTEIN-2 | SUPEROXIDE-DISMUTASE | PHOSPHORYLATED IN-VIVO | Animals | Reactive Oxygen Species - metabolism | Reperfusion Injury - pathology | Models, Biological | Humans | Brain Ischemia - pathology | Membrane Potential, Mitochondrial | Brain Ischemia - metabolism | Reperfusion Injury - metabolism | Cytoprotection | Proteins | Medical colleges | Analysis | Emergency medicine | Physiological aspects | Mitochondrial DNA | Reperfusion injury | Membranes | Brain damage | Molecular biology | Reactive Oxygen Species | Oxidative Phosphorylation
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6. Full Text Astrocyte metabolism and signaling during brain ischemia
by Rossi, David J and Brady, James D and Mohr, Claudia
Nature Neuroscience, ISSN 1097-6256, 11/2007, Volume 10, Issue 11, pp. 1377 - 1386
Brain ischemia results from cardiac arrest, stroke or head trauma. These conditions can cause severe brain damage and are a leading cause of death and... 
GLUTAMATE TRANSPORTER GLT-1 | CULTURED RAT ASTROCYTES | FOCAL CEREBRAL-ISCHEMIA | VESICULAR GLUTAMATE | IN-VIVO | SYNAPTIC-TRANSMISSION | SIMULATED ISCHEMIA | GAP-JUNCTION HEMICHANNELS | NEUROSCIENCES | EXCITATORY AMINO-ACIDS | CELL-DEATH | Animals | Models, Biological | Humans | Brain Ischemia - pathology | Brain Ischemia - metabolism | Signal Transduction - physiology | Brain Ischemia - physiopathology | Astrocytes - metabolism | Cerebral ischemia | Astrocytes | Cellular control mechanisms | Neural transmission | Regulation | Research | Risk factors
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7. Full Text Astrocyte‐enriched miR‐29a targets PUMA and reduces neuronal vulnerability to forebrain ischemia
by Ouyang, Yi‐Bing and Xu, Lijun and Lu, Yu and Sun, Xiaoyun and Yue, Sibiao and Xiong, Xiao‐Xing and Giffard, Rona G
Glia, ISSN 0894-1491, 11/2013, Volume 61, Issue 11, pp. 1784 - 1794
Following transient forebrain ischemia, astrocytes play a key role in determining whether or not neurons in the hippocampal CA1 sector go on to die in a... 
PUMA | microRNA | astrocyte | MicroRNA | Astrocyte | APOPTOSIS | MEDIATOR | TRANSIENT FOCAL ISCHEMIA | NEUROSCIENCES | CELL-DEATH | OVEREXPRESSION | INHIBITION |