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Brain Pathology, ISSN 1015-6305, 03/2019, Volume 29, Issue 2, pp. 263 - 277
Although the mechanisms underlying prion propagation and infectivity are now well established, the processes accounting for prion toxicity and pathogenesis... 
mitogen‐activated protein kinase (MAPK) | antibody | neurotoxicity | cell culture | neurodegeneration | dendrite | prion | spine | ionic current | synapse | transgenic mouse | glutamate | mitogen-activated protein kinase (MAPK) | PROTEIN | PATHOLOGY | A-BETA OLIGOMERS | CLINICAL NEUROLOGY | PRP | SCRAPIE | IN-VITRO | OCTAREPEAT DOMAIN | TERMINAL DOMAIN | NEUROSCIENCES | DENDRITIC SPINES | DISEASE | SYNAPSE LOSS | Cell Line | Neurons - pathology | Phosphorylation | Prion Diseases - genetics | Prions - genetics | N-Methylaspartate - metabolism | Signal Transduction | Humans | Cells, Cultured | Hippocampus - pathology | alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid - metabolism | Prions - toxicity | Animals | Dendritic Spines - pathology | Brain - pathology | p38 Mitogen-Activated Protein Kinases - metabolism | PrPC Proteins - metabolism | PrPC Proteins - genetics | Prion Diseases - metabolism | Viral antibodies | Prions | Analysis | Antibodies | Genetic engineering | Glutamate | Mitogens | Cell culture | Target recognition | Propagation | Glutamic acid receptors (ionotropic) | Toxicity | Pathogenesis | Gene deletion | α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors | Dendritic spines | Signal transduction | Receptors | Neurotoxicity | Clonal deletion | α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid | Actin | Infectivity | Prion protein | Collapse | Transgenic mice | MAP kinase | N-Methyl-D-aspartic acid receptors | Epitopes | Molecular modelling | Morphology | Cytoskeleton | Mutation | Hippocampus
Journal Article
Pflügers Archiv - European Journal of Physiology, ISSN 0031-6768, 7/2010, Volume 460, Issue 2, pp. 525 - 542
Glutamate excitotoxicity is a hypothesis that states excessive glutamate causes neuronal dysfunction and degeneration. As glutamate is a major excitatory... 
TRP channel | Sodium–calcium exchange | Biomedicine | Human Physiology | Calcium | Neuroprotective drugs | Excitotoxicity | Neuronal cell death | Glutamate | NMDA receptor | Free radical | Gap junction | Sodium-calcium exchange | APOPTOSIS-INDUCING FACTOR | PRESYNAPTIC KAINATE RECEPTORS | PHYSIOLOGY | NITRIC-OXIDE SYNTHASE | ANEURYSMAL SUBARACHNOID HEMORRHAGE | FOCAL CEREBRAL-ISCHEMIA | CULTURED CORTICAL-NEURONS | INTRACELLULAR ZINC RELEASE | TRAUMATIC BRAIN-INJURY | MANGANESE-SUPEROXIDE-DISMUTASE | METHYL-D-ASPARTATE | Caspases - physiology | Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors | Receptors, Kainic Acid | Calcium - metabolism | Humans | Nerve Degeneration - physiopathology | Receptors, Metabotropic Glutamate - physiology | Calpain - physiology | Zinc - physiology | Free Radicals - metabolism | Sodium-Calcium Exchanger - therapeutic use | Free Radical Scavengers - therapeutic use | Hypothalamus - drug effects | Glutamic Acid - adverse effects | Receptors, AMPA - physiology | Glutamic Acid - physiology | Nitric Oxide - physiology | Receptors, N-Methyl-D-Aspartate - physiology | Antioxidants - therapeutic use | Animals | Neurodegenerative Diseases - physiopathology | Cell Death - physiology | Neurotoxicity Syndromes - physiopathology | Receptors, Glutamate - physiology | Receptors, AMPA - antagonists & inhibitors | Methyl aspartate | Brain | Nervous system diseases | Multiple sclerosis | Parkinson's disease | Neurons | Cell death | Physiological aspects | Injuries | Index Medicus
Journal Article
Neurobiology of Disease, ISSN 0969-9961, 2006, Volume 25, Issue 2, pp. 360 - 366
Abstract The idea that the environmental toxin β- N -methylamino- l -alanine (BMAA) is involved in neurodegenerative diseases on Guam has risen and fallen over... 
Neurology | NMDA | Oxidative stress | BMAA | Alzheimer's disease | Apoptosis | Necrosis | NEURODEGENERATIVE DISEASE | apoptosis | AMYOTROPHIC-LATERAL-SCLEROSIS | NEUROSCIENCES | CELL-DEATH | CYANOBACTERIAL NEUROTOXINS | GLUTAMATE RECEPTORS | AMINO-ACID | necrosis | CORTICAL CULTURES | D-ASPARTATE | PARKINSONISM-DEMENTIA | oxidative stress | Amino Acids, Diamino - toxicity | Receptors, Metabotropic Glutamate - drug effects | Neurons - pathology | Oxidative Stress - physiology | Cerebral Cortex - pathology | Nerve Degeneration - physiopathology | Receptors, N-Methyl-D-Aspartate - metabolism | Receptors, Metabotropic Glutamate - metabolism | Hazardous Substances - toxicity | Cerebral Cortex - metabolism | Nerve Degeneration - chemically induced | Nerve Degeneration - metabolism | Brain - metabolism | Receptor, Metabotropic Glutamate 5 | Neurons - metabolism | Cerebral Cortex - drug effects | Neurons - drug effects | Receptors, N-Methyl-D-Aspartate - drug effects | Brain - physiopathology | Cells, Cultured | Neurotoxins - toxicity | Neurodegenerative Diseases - metabolism | Brain - drug effects | Patch-Clamp Techniques | Animals | Excitatory Amino Acid Agonists - toxicity | Neurodegenerative Diseases - chemically induced | Neurodegenerative Diseases - physiopathology | Mice | Oxidative Stress - drug effects | Alzheimer’s disease
Journal Article
Journal Article