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Journal of Neuroscience, ISSN 0270-6474, 05/2012, Volume 32, Issue 22, pp. 7585 - 7593
Parkinson's disease (PD) is characterized pathologically by the formation of ubiquitin and alpha-synuclein (alpha-syn)-containing inclusions (Lewy bodies),... 
CELLS | CLEARANCE | PROTEIN | PROTEASOME | NEURODEGENERATION | DEGRADATION | MICE | MACROAUTOPHAGY | NEUROSCIENCES | LEWY BODY DISEASES | PARKINSONS-DISEASE | Dendrites - pathology | Tyrosine 3-Monooxygenase - metabolism | Nestin | Chromatography, High Pressure Liquid - methods | Presynaptic Terminals - pathology | Microtubule-Associated Proteins - genetics | Dopaminergic Neurons - pathology | Embryo, Mammalian | Microtubule-Associated Proteins - metabolism | Ubiquitin - metabolism | Autophagy - physiology | Presynaptic Terminals - ultrastructure | Intermediate Filament Proteins - genetics | Autophagy - genetics | Microtubule-Associated Proteins - deficiency | Dopamine - metabolism | Disease Models, Animal | Fibroblasts - metabolism | Gene Expression Regulation - genetics | Cells, Cultured | Mice, Transgenic | Ephrin-B1 - metabolism | Nerve Tissue Proteins - genetics | Nerve Degeneration - pathology | Nerve Tissue Proteins - metabolism | Motor Activity - genetics | Tyrosine 3-Monooxygenase - genetics | Autophagy-Related Protein 7 | Inclusion Bodies - genetics | Animals | Autophagy-Related Protein 5 | Brain - pathology | Inclusion Bodies - pathology | Presynaptic Terminals - metabolism | Mice | Movement Disorders - genetics | Nerve Degeneration - etiology | Intermediate Filament Proteins - metabolism | alpha-Synuclein - metabolism | Index Medicus
Journal Article
Journal Article
Advances in Experimental Medicine and Biology, ISSN 0065-2598, 2018, Volume 1074, pp. 351 - 357
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 09/2011, Volume 194, Issue 5, pp. 751 - 764
The c-Jun N-terminal kinase (JNK) signaling pathway is essential for neuronal degeneration in multiple contexts but also regulates neuronal homeostasis. It... 
PROGRAMMED CELL-DEATH | SIGNALING PATHWAY | N-TERMINAL KINASE | WALLERIAN DEGENERATION | SYMPATHETIC NEURONS | ACTIVATED PROTEIN-KINASES | C-JUN | MICROTUBULE DYNAMICS | MICE LACKING | NERVE GROWTH-FACTOR | CELL BIOLOGY | RNA, Small Interfering - genetics | Caspase 9 - metabolism | Central Nervous System - metabolism | Apoptosis - drug effects | Homeodomain Proteins - metabolism | Caspase 3 - metabolism | Central Nervous System - pathology | Axons - physiology | Ganglia, Spinal - cytology | Central Nervous System - embryology | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Protein Kinase Inhibitors - pharmacokinetics | Embryo, Mammalian - pathology | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Ganglia, Spinal - embryology | MAP Kinase Kinase Kinases - genetics | Mice, Transgenic | MAP Kinase Kinase Kinases - metabolism | Mice, Knockout | Central Nervous System - cytology | Embryo, Mammalian - embryology | Axons - pathology | Ganglia, Spinal - pathology | Nerve Growth Factor - deficiency | Mice | Protein Binding - physiology | Neurons - pathology | Phosphorylation | Spinal Cord - metabolism | JNK Mitogen-Activated Protein Kinases - metabolism | Protein Transport - physiology | Extracellular Signal-Regulated MAP Kinases - metabolism | MAP Kinase Kinase Kinases - deficiency | Spinal Cord - pathology | Neurons - drug effects | Proto-Oncogene Proteins c-jun - genetics | Cells, Cultured | Axons - metabolism | Nerve Growth Factor - pharmacology | Mice, Inbred Strains | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Spinal Cord - embryology | Animals | Proto-Oncogene Proteins c-jun - metabolism | Adaptor Proteins, Signal Transducing - genetics | Apoptosis - physiology | Adaptor Proteins, Signal Transducing - metabolism | Physiological aspects | Neurons | Apoptosis | Signal transduction | Kinases | Cells | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 05/2010, Volume 30, Issue 21, pp. 7377 - 7391
The continuous release of neurotransmitter could be seen to place a persistent burden on presynaptic proteins, one that could compromise nerve terminal... 
NERVOUS-SYSTEM | GLUTAMATE RECEPTORS | SYNAPTOTAGMIN-I | PYRAMIDAL CELLS | SYNAPTIC-TRANSMISSION | CA2+ CHANNELS | RAT HIPPOCAMPUS | HIPPOCAMPAL-NEURONS | NEUROSCIENCES | CALCIUM-CHANNEL | CSP-ALPHA | Age Factors | Microscopy, Electron, Transmission - methods | gamma-Aminobutyric Acid - metabolism | Gene Expression Regulation, Developmental - genetics | Nerve Degeneration - genetics | Neurons - cytology | Synapses - genetics | Presynaptic Terminals - ultrastructure | Excitatory Postsynaptic Potentials - drug effects | Nerve Degeneration - metabolism | Membrane Proteins - deficiency | Synapses - metabolism | Inhibitory Postsynaptic Potentials - genetics | Excitatory Amino Acid Agents - pharmacology | Excitatory Postsynaptic Potentials - genetics | Gene Expression Regulation, Developmental - physiology | Animals, Newborn | Cells, Cultured | Inhibitory Postsynaptic Potentials - physiology | Rats | Synapses - ultrastructure | Bicuculline - pharmacology | HSP40 Heat-Shock Proteins - deficiency | Hippocampus - cytology | Mutation - genetics | Microscopy, Confocal - methods | Mice, Knockout | Nerve Tissue Proteins - metabolism | Astrocytes - physiology | GABA Agents - pharmacology | Patch-Clamp Techniques | Animals | Presynaptic Terminals - metabolism | Glutamic Acid - metabolism | Mice | Inhibitory Postsynaptic Potentials - drug effects | Index Medicus
Journal Article
Neuron, ISSN 0896-6273, 2005, Volume 45, Issue 6, pp. 847 - 859
Transgenic (Tg) mice overexpressing human wild-type α-synuclein in oligodendrocytes under the control of the 2,′ 3′-cyclic nucleotide 3′-phosphodiesterase... 
NEUROFILAMENT PHOSPHORYLATION | OLIVOPONTOCEREBELLAR ATROPHY | HUMAN BRAIN | PROTEIN | PERIPHERAL NERVOUS-SYSTEM | ALZHEIMERS-DISEASE | CYTOPLASMIC INCLUSIONS | NEUROSCIENCES | LEWY BODIES | NEURODEGENERATIVE DISEASES | PARKINSONS-DISEASE | Neurons - pathology | Oligodendroglia - metabolism | Central Nervous System - metabolism | Presynaptic Terminals - pathology | Neuroglia - pathology | Humans | Central Nervous System - pathology | Phagocytosis - genetics | Presynaptic Terminals - ultrastructure | Promoter Regions, Genetic - genetics | Oligodendroglia - ultrastructure | Myelin Sheath - metabolism | Axons - ultrastructure | Multiple System Atrophy - metabolism | Inclusion Bodies - metabolism | Disease Models, Animal | Wallerian Degeneration - genetics | Microscopy, Electron, Transmission | Myelin Sheath - pathology | Wallerian Degeneration - metabolism | Wallerian Degeneration - physiopathology | Axons - metabolism | Mice, Transgenic | Phosphoric Diester Hydrolases - genetics | Multiple System Atrophy - genetics | Synucleins | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Oligodendroglia - pathology | Inclusion Bodies - genetics | 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase | Animals | Axons - pathology | Inclusion Bodies - pathology | Presynaptic Terminals - metabolism | Mice | Myelin Sheath - ultrastructure | Central Nervous System - physiopathology | Multiple System Atrophy - physiopathology | alpha-Synuclein | Index Medicus
Journal Article
British Journal of Pharmacology, ISSN 0007-1188, 1997, Volume 121, Issue 5, pp. 889 - 900
Journal Article
Journal Article
Experimental Eye Research, ISSN 0014-4835, 03/2014, Volume 120, pp. 175 - 185
Cannabinoids have been demonstrated to exert neuroprotective effects on different types of neuronal insults. Here we have addressed the therapeutic potential... 
P23H | confocal microscopy | neurodegeneration | retinitis pigmentosa | apoptosis | immunohistochemistry | electroretinography | Electroretinography | Immunohistochemistry | Neurodegeneration | Retinitis pigmentosa | Confocal microscopy | Apoptosis | NEUROTROPHIC FACTOR | ENDOCANNABINOID SYSTEM | RAT MODEL | DOMINANT RETINITIS-PIGMENTOSA | CELL-DEATH | ACID AMIDE HYDROLASE | PRESSURE-INDUCED ISCHEMIA | GANGLION-CELLS | OPHTHALMOLOGY | TRANSGENIC RAT | DELAYS PHOTORECEPTOR DEGENERATION | Neuroprotective Agents - therapeutic use | Retina - drug effects | Retinal Bipolar Cells - pathology | Retina - metabolism | Presynaptic Terminals - pathology | Cannabinoid Receptor Agonists - therapeutic use | Dronabinol - analogs & derivatives | Retinitis Pigmentosa - physiopathology | Disease Models, Animal | Biomarkers - metabolism | Cell Survival - drug effects | Retinal Bipolar Cells - metabolism | Presynaptic Terminals - drug effects | Rats, Transgenic | Night Vision | Retina - physiopathology | Retinitis Pigmentosa - drug therapy | Rats | Retinitis Pigmentosa - metabolism | Retinal Bipolar Cells - drug effects | Microscopy, Confocal | Animals | Eye Proteins - metabolism | Presynaptic Terminals - metabolism | Photic Stimulation | Dronabinol - therapeutic use | Physiological aspects | Retinal degeneration | Genetic engineering | Analysis | Index Medicus
Journal Article