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BBA - Molecular and Cell Biology of Lipids, ISSN 1388-1981, 06/2016, Volume 1861, Issue 6, pp. 491 - 500
Journal Article
Molecular Pharmacology, ISSN 0026-895X, 2010, Volume 78, Issue 3, pp. 466 - 477
Parkinson's disease (PD) is the second most common neurodegenerative disease characterized by a progressive loss of dopamine (DA) neurons in the substantia... 
RESPONSES | IN-VITRO | MICROGLIAL ACTIVATION | PHOSPHORYLATION | GENE-EXPRESSION | NITRIC-OXIDE | PHARMACOLOGY & PHARMACY | NECROSIS-FACTOR-ALPHA | NADPH OXIDASE ACTIVITY | PARKINSONS-DISEASE | DEGENERATION | Microglia - metabolism | Mesencephalon - cytology | Reactive Oxygen Species - metabolism | Embryo, Mammalian | Rats, Inbred F344 | NADPH Oxidases - metabolism | Lipopolysaccharides - antagonists & inhibitors | Anti-Inflammatory Agents - metabolism | Nerve Degeneration - metabolism | Neuroprotective Agents - metabolism | Microglia - physiology | Neuroprotective Agents - pharmacology | Stilbenes | Dopamine - physiology | Anti-Inflammatory Agents - therapeutic use | Polyphenols | Neurons - metabolism | Dopamine - metabolism | Phenols - pharmacology | Anti-Inflammatory Agents - pharmacology | NADPH Oxidases - antagonists & inhibitors | Rats | Reactive Oxygen Species - therapeutic use | Lipopolysaccharides - pharmacology | Mitogen-Activated Protein Kinases - pharmacology | Neurotoxicity Syndromes - metabolism | Mice | NADPH Oxidases - physiology | Neuroprotective Agents - therapeutic use | Mesencephalon - metabolism | Reactive Oxygen Species - pharmacology | Lipopolysaccharides - metabolism | Parkinson Disease - drug therapy | Substantia Nigra - metabolism | Flavonoids - therapeutic use | Neuroglia - drug effects | Nerve Degeneration - prevention & control | Neurons - physiology | Female | Flavonoids - pharmacology | Parkinson Disease - metabolism | Neurons - drug effects | Microglia - drug effects | Mice, Inbred C57BL | Dopamine - pharmacology | Phenols - metabolism | Pregnancy | Animals | Flavonoids - metabolism | Phenols - therapeutic use | Neuroglia - metabolism | Mitogen-Activated Protein Kinases - metabolism | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2012, Volume 109, Issue 47, pp. 19071 - 19078
Neurons within each layer in the mammalian cortex have Stereotypic projections. Four genes—Fezf2, Ctip2, Tbr1, and Satb2—regulate these projection identities.... 
Axons | Brain | Mesencephalon | Neurons | Thalamus | Genetic loci | Gene expression regulation | Pyramidal tracts | Repression | Identity | Cerebral cortex | Cell fate | Axon guidance | Transcription factor | transcription factor | CALLOSAL | cell fate | MULTIDISCIPLINARY SCIENCES | AUTISM SPECTRUM DISORDER | TBR1 | GUIDANCE | SPECIFICATION | DEVELOPING CEREBRAL-CORTEX | cerebral cortex | NEURON IDENTITY | CORTICOSPINAL TRACT | NETRIN-1 | DIFFERENTIATION | axon guidance | Axons - enzymology | Thalamus - metabolism | Alkaline Phosphatase - metabolism | Genetic Loci - genetics | Receptor, EphA4 - metabolism | Gene Regulatory Networks | Cerebral Cortex - metabolism | DNA-Binding Proteins - metabolism | Neocortex - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Gene Expression Regulation, Developmental | Isoenzymes - metabolism | Cell Adhesion Molecules, Neuronal - metabolism | Neurons - metabolism | Netrin Receptors | Repressor Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Neocortex - growth & development | Receptors, Cell Surface - metabolism | Repressor Proteins - genetics | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Mutation - genetics | GPI-Linked Proteins - metabolism | Nerve Tissue Proteins - metabolism | Animals | Protein Binding | Mice | Physiological aspects | Genetic aspects | Gene mutations | Neocortex | Mutation | Gene expression | Medical disorders | Genes | Index Medicus | Biological Sciences
Journal Article
SCIENCE, ISSN 0036-8075, 09/2017, Volume 357, Issue 6357, pp. 1255 - 1255
Mitochondrial and lysosomal dysfunction have been implicated in substantia nigra dopaminergic neurodegeneration in Parkinson's disease (PD), but how these... 
GLUCOCEREBROSIDASE | PACEMAKING | DJ-1 | ALPHA-SYNUCLEIN | SUBSTANTIA-NIGRA | MULTIDISCIPLINARY SCIENCES | Mitochondria - enzymology | Mesencephalon - metabolism | Humans | Protein Deglycase DJ-1 - genetics | Substantia Nigra - metabolism | Melanins - metabolism | Glucosylceramidase - deficiency | Lysosomes - metabolism | Dopaminergic Neurons - metabolism | Tacrolimus - pharmacology | Parkinson Disease - metabolism | Dopamine - metabolism | Disease Models, Animal | Substantia Nigra - enzymology | Cell Line | Calcineurin Inhibitors - pharmacology | Oxidation-Reduction | Mesencephalon - enzymology | Mitochondria - metabolism | Antioxidants - pharmacology | Mitochondria - drug effects | Parkinson Disease - genetics | Mice, Knockout | Animals | Parkinson Disease - enzymology | Mice | Oxidative Stress - drug effects | alpha-Synuclein - metabolism | Oxidation-reduction reaction | Development and progression | Mitochondria | Dopamine | Parkinson's disease | Health aspects | Brain | Energy metabolism | Animal models | Target recognition | Mesencephalon | Pathogenesis | Substantia nigra | Parkinsons disease | Lysosomes | Synuclein | Accumulation | Pathways | Enzymatic activity | Neurodegeneration | Rodents | Oxidation | Degeneration | Species | Movement disorders | Dopamine receptors | Neurodegenerative diseases | Neurons | Medical treatment | Metabolism | Patients | Glucosylceramidase | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 09/2008, Volume 28, Issue 38, pp. 9525 - 9535
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 7/2018, Volume 55, Issue 7, pp. 5847 - 5867
In addition to the classical hormonal (tissue-to-tissue) renin-angiotensin system (RAS), there are a paracrine (cell-to-cell) and an intracrine... 
Neurology | Neuroprotection | Neurosciences | Biomedicine | Neurobiology | Aging | Nuclear receptors | Renin-angiotensin system | Parkinson’s disease | Cell Biology | Dopaminergic | SYSTEM | NADPH OXIDASE | OXIDATIVE STRESS | Parkinson's disease | TYPE-2 RECEPTOR | NEUROSCIENCES | DOPAMINE NEURONS | II TYPE-1 | EXPRESSION | BRAIN | MAS | PARKINSONS-DISEASE | Microglia - metabolism | Mesencephalon - cytology | Reactive Oxygen Species - metabolism | Oxidative Stress | Receptors, G-Protein-Coupled - metabolism | Male | Substantia Nigra - metabolism | Case-Control Studies | Cell Nucleus - metabolism | Dopaminergic Neurons - metabolism | Gene Deletion | Peptidyl-Dipeptidase A - metabolism | Angiotensin II | Proto-Oncogene Proteins - metabolism | Peptide Fragments - metabolism | Paracrine Communication | Signal Transduction | Reactive Nitrogen Species - metabolism | Cells, Cultured | Rodentia | Mitochondria - metabolism | Angiotensin I - metabolism | Haplorhini | Animals | Receptor, Angiotensin, Type 2 - metabolism | Models, Biological | Receptor, Angiotensin, Type 1 - metabolism | Aging - metabolism | Astrocytes - metabolism | Medical research | Nervous system diseases | Neurons | Cell death | Angiotensin | Medicine, Experimental | Superoxide | Neurophysiology | Brain | Neurodegenerative diseases | Substantia nigra | Paracrine signalling | Glial cells | Neuronal-glial interactions | Mitochondria | Renin | Neurodegeneration | Rodents | Intracellular | Pluripotency | Movement disorders | Dopamine receptors | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2017, Volume 12, Issue 4, pp. e0174470 - e0174470
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 04/2012, Volume 21, Issue 8, pp. 1725 - 1743
Mutations in the ATP13A2 gene (PARK9, OMIM 610513) cause autosomal recessive, juvenile-onset Kufor-Rakeb syndrome and early-onset parkinsonism. ATP13A2 is an... 
CELLS | DEMENTIA | PROTEIN | CHAPERONE-MEDIATED AUTOPHAGY | P-TYPE ATPASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETICS & HEREDITY | PYRAMIDAL DEGENERATION | KUFOR-RAKEB SYNDROME | ALPHA-SYNUCLEIN | MUTATIONS | PARKINSONS-DISEASE | Lewy Bodies - ultrastructure | Pyramidal Cells - metabolism | Neurites - physiology | Proton-Translocating ATPases - immunology | Substantia Nigra - pathology | Calcium - metabolism | Humans | Substantia Nigra - metabolism | Adenosine Triphosphatases - immunology | Autophagy | Mitochondria - ultrastructure | Brain - metabolism | Proton-Translocating ATPases - metabolism | Neurons - ultrastructure | RNA Interference | Neurites - ultrastructure | Dopaminergic Neurons - metabolism | Cytoplasmic Vesicles - metabolism | Neurons - physiology | Dopaminergic Neurons - physiology | Membrane Proteins - metabolism | Neurons - metabolism | Parkinson Disease - metabolism | Parkinson Disease - pathology | Cells, Cultured | Adenosine Triphosphatases - metabolism | Rats | Membrane Proteins - immunology | Animals | Brain - pathology | Mice | Hydrogen-Ion Concentration | Brain | Cadmium | Neuroprotection | Basal ganglia | Calcium (intracellular) | Dopamine | Mesencephalon | Neurodegenerative diseases | Axonogenesis | Neurons | Substantia nigra | Adenosinetriphosphatase | Cortex | pH effects | Lewy bodies | Mitochondria | Pyramidal cells | Kinetics | Movement disorders | Index Medicus
Journal Article
European Journal of Neuroscience, ISSN 0953-816X, 04/2017, Volume 45, Issue 7, pp. 922 - 931
Although certain drugs of abuse are known to disrupt brain glucose metabolism ( BG luM), the effects of opiates on BG luM are not well characterized. Moreover,... 
brain imaging | brain energy metabolism | opiate addition | drug self‐administration | drug self-administration | 2-DEOXYGLUCOSE | SMALL ANIMAL PET | NALOXONE | NEUROSCIENCES | ADDICTION | DEPENDENCE | POSITRON-EMISSION-TOMOGRAPHY | NUCLEUS | RECEPTORS | WITHDRAWAL | BRAIN | Anesthetics, Inhalation - pharmacology | Fluorodeoxyglucose F18 - pharmacokinetics | Radiopharmaceuticals - pharmacokinetics | Anesthetics, Inhalation - administration & dosage | Isoflurane - pharmacology | Morphine - pharmacology | Substance Withdrawal Syndrome - etiology | Anesthesia, Intravenous - adverse effects | Analgesics, Opioid - pharmacology | Rats | Isoflurane - adverse effects | Male | Anesthetics, Inhalation - adverse effects | Corpus Striatum - metabolism | Rats, Sprague-Dawley | Positron Emission Tomography Computed Tomography | Analgesics, Opioid - adverse effects | Animals | Analgesics, Opioid - administration & dosage | Corpus Striatum - drug effects | Corpus Striatum - diagnostic imaging | Morphine - administration & dosage | Morphine - adverse effects | Glucose metabolism | Brain research | PET imaging | Physiological aspects | Anesthesia | Morphine | Glucose | Dextrose | Cerebellum | Brain | Cortex (olfactory) | Drug abuse | Basal ganglia | Intravenous administration | Mesencephalon | Emission analysis | Stimulation | Opiates | Hypothalamus | Infusion | Computed tomography | Rodents | Neostriatum | Thalamus | Defecation | Jugular vein | Self-administration | Narcotics | Therapeutic applications | Positron emission | Injection | Metabolism | Isoflurane | Ganglia | Emissions control | Positron emission tomography | Hippocampus | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2011, Volume 6, Issue 12, pp. e28574 - e28574
In rats and mice, ascending and descending axons from neurons producing melanin-concentrating hormone (MCH) reach the cerebral cortex and spinal cord. However,... 
EXPRESSION PATTERNS | ROBO-SLIT | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | SEMAPHORIN 3F | CENTRAL-NERVOUS-SYSTEM | VENTRAL MIDBRAIN | MELANIN-CONCENTRATING HORMONE | AXONAL GROWTH | MICE LACKING | SONIC-HEDGEHOG | Mesencephalon - cytology | Mesencephalon - metabolism | Netrin-1 | Hedgehog Proteins - metabolism | Neurons - cytology | Nerve Growth Factors - metabolism | Melanins - metabolism | Embryo, Mammalian - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Time Factors | Gene Expression Regulation, Developmental | Pituitary Hormones - metabolism | Cell Differentiation | Neurons - metabolism | Bromodeoxyuridine - metabolism | Green Fluorescent Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Telencephalon - metabolism | Telencephalon - cytology | Axons - metabolism | Rats | Nerve Tissue Proteins - metabolism | Phenotype | Animals | Hypothalamus - metabolism | Hypothalamus - cytology | Hypothalamic Hormones - metabolism | Models, Biological | Mice | Receptors, Immunologic - metabolism | Brain | Neurons | Genes | Spinal cord | Cerebral cortex | Transcription | Mesencephalon | Forebrain | Neuropeptides | Hypothalamus | Hybridization | Neurogenesis | Proteins | Neural tube | Neuroblasts | Rodents | Dopamine receptors | Medial forebrain bundle | Dopamine | Cortex | Telencephalon | Gene expression | Nkx2.2 protein | Embryos | Axons | Amphetamine | Melanin-concentrating hormone | Hedgehog protein | Adenoviruses | Stem cells | Cocaine | Diencephalon | Melanin | Index Medicus | Green Fluorescent Proteins | Embryo, Mammalian | Neurons and Cognition | Melanins | Bromodeoxyuridine | Hedgehog Proteins | Life Sciences | Pituitary Hormones | Intercellular Signaling Peptides and Proteins | Nerve Tissue Proteins | Nerve Growth Factors | Hypothalamic Hormones | Receptors, Immunologic | Tumor Suppressor Proteins
Journal Article
Science, ISSN 0036-8075, 9/2011, Volume 333, Issue 6051, pp. 1903 - 1907
Journal Article