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Nature, ISSN 0028-0836, 07/2012, Volume 487, Issue 7408, pp. 443 - 448
Journal Article
Nature Neuroscience, ISSN 1097-6256, 11/2012, Volume 15, Issue 11, pp. 1488 - 1497
FUS/TLS (fused in sarcoma/translocated in liposarcoma) and TDP-43 are integrally involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.... 
NEURODEGENERATIVE DISEASE | GENE | AMYOTROPHIC-LATERAL-SCLEROSIS | FAMILY PROTEINS | FUS PATHOLOGY | MUTATIONS | FRONTOTEMPORAL LOBAR DEGENERATION | BINDING | NEUROSCIENCES | BRAIN | NASCENT TRANSCRIPTION | RNA, Small Interfering - genetics | Protein Binding - genetics | Oligonucleotide Array Sequence Analysis | Humans | tau Proteins - metabolism | Gene Expression Profiling | RNA, Messenger - metabolism | Kv Channel-Interacting Proteins - metabolism | Brain - metabolism | Frontotemporal Dementia - metabolism | RNA Splicing - genetics | Frontotemporal Dementia - genetics | RNA-Binding Protein FUS - deficiency | Amyotrophic Lateral Sclerosis - genetics | Cell Cycle Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | RNA-Binding Protein FUS - genetics | Mice, Knockout | Motor Neurons - metabolism | Amyotrophic Lateral Sclerosis - pathology | Shal Potassium Channels - metabolism | Brain - pathology | Mice | Neurofilament Proteins - metabolism | RNA, Small Interfering - metabolism | Immunoprecipitation | Spinal Cord - metabolism | DNA-Binding Proteins - deficiency | DNA-Binding Proteins - metabolism | tau Proteins - genetics | Cell Cycle Proteins - genetics | Female | RNA Precursors - metabolism | Excitatory Amino Acid Transporter 2 - genetics | Membrane Proteins - metabolism | Frontotemporal Dementia - pathology | Gene Expression Regulation - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | RNA Precursors - genetics | Protein Structure, Tertiary - genetics | RNA-Binding Protein FUS - metabolism | DNA-Binding Proteins - genetics | Excitatory Amino Acid Transporter 2 - metabolism | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Histone-Lysine N-Methyltransferase - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Neural Cell Adhesion Molecules - metabolism | Neural Stem Cells - metabolism | Cell Line, Transformed | Amyotrophic lateral sclerosis | Development and progression | Genetic aspects | Messenger RNA | Health aspects | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 03/2010, Volume 30, Issue 9, pp. 3326 - 3338
Journal Article
Neuron, ISSN 0896-6273, 2005, Volume 47, Issue 6, pp. 817 - 831
The molecular mechanisms controlling the differentiation of neural progenitors into distinct subtypes of neurons during neocortical development are unknown.... 
AREA IDENTITY | NEOCORTICAL NEURONS | CELL FATE SPECIFICATION | CEREBRAL CORTICAL DEVELOPMENT | LAYER NEURONS | CENTRAL-NERVOUS-SYSTEM | SUBCORTICAL TARGETS | ZINC-FINGER GENE | SUBVENTRICULAR ZONE | NEUROSCIENCES | ZEBRAFISH FOREBRAIN | Membrane Glycoproteins - metabolism | Embryo, Mammalian | Homeodomain Proteins - metabolism | Nerve Tissue Proteins - deficiency | S100 Proteins - genetics | POU Domain Factors - genetics | Forkhead Transcription Factors - metabolism | In Situ Hybridization - methods | Repressor Proteins - metabolism | Gene Expression Regulation, Developmental - physiology | POU Domain Factors - metabolism | Animals, Newborn | DNA-Binding Proteins - physiology | Motor Neurons - physiology | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cell Cycle Proteins - metabolism | S100 Proteins - metabolism | In Situ Nick-End Labeling - methods | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Immunohistochemistry - methods | Annexin A2 - genetics | Cell Death - physiology | Green Fluorescent Proteins - biosynthesis | Mice | Annexin A2 - metabolism | Age Factors | Phosphopyruvate Hydratase - metabolism | Cell Movement - physiology | DNA-Binding Proteins - deficiency | DNA-Binding Proteins - metabolism | Amino Acids - metabolism | Motor Neurons - cytology | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Membrane Proteins - metabolism | Bromodeoxyuridine - metabolism | Cell Differentiation - physiology | Pyramidal Tracts - physiology | Nerve Tissue Proteins - physiology | Neocortex - growth & development | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Dopamine and cAMP-Regulated Phosphoprotein 32 - metabolism | Nerve Tissue Proteins - genetics | Homeodomain Proteins - genetics | Membrane Glycoproteins - genetics | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Cell Count - methods | Neocortex - cytology | Receptors, Antigen, T-Cell, alpha-beta - metabolism | Neurosciences | Neurons | Developmental biology | Stem cells | Studies | Brain | Ultrasonic imaging | Transcription factors | Hybridization | Neurogenesis | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 07/2012, Volume 32, Issue 28, pp. 9677 - 9689
Passive immunization against beta-amyloid (A beta) has become an increasingly desirable strategy as a therapeutic treatment for Alzheimer's disease (AD).... 
APP TRANSGENIC MICE | NATURAL OLIGOMERS | HUMAN IGG1 | ALZHEIMERS-DISEASE | PROTEIN-KINASE | LONG-TERM POTENTIATION | SYNAPTIC PLASTICITY | NEUROSCIENCES | PASSIVE-IMMUNIZATION | SECRETED OLIGOMERS | P38 MAP KINASE | Microglia - metabolism | Humans | Middle Aged | Male | Green Fluorescent Proteins - genetics | Neuroprotective Agents - metabolism | Alzheimer Disease - pathology | Neuroprotective Agents - pharmacology | Time Factors | Protein Binding - drug effects | Amyloid beta-Peptides - metabolism | Statistics, Nonparametric | Aged, 80 and over | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Alzheimer Disease - immunology | Receptors, Chemokine - genetics | Plaque, Amyloid - immunology | Disease Models, Animal | Animals, Newborn | Rats | Mice, Transgenic | Mutation - genetics | Rats, Sprague-Dawley | Microscopy, Confocal | Plaque, Amyloid - metabolism | Mice | CX3C Chemokine Receptor 1 | Alzheimer Disease - blood | Immunoglobulin G - metabolism | Tumor Necrosis Factor-alpha - metabolism | Dose-Response Relationship, Immunologic | Cerebral Cortex - cytology | Dose-Response Relationship, Drug | Immunoglobulin G - pharmacology | Female | Neurons - drug effects | Peptide Fragments - metabolism | Double-Blind Method | Enzyme-Linked Immunosorbent Assay | Microglia - drug effects | Plaque, Amyloid - pathology | Gene Expression Regulation - genetics | Gene Expression Regulation - immunology | Alzheimer Disease - therapy | Cells, Cultured | Presenilin-1 - genetics | Hippocampus - cytology | Gene Expression Regulation - drug effects | Amyloid beta-Protein Precursor - genetics | Animals | Amyloid beta-Peptides - immunology | Aged | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 12/2009, Volume 284, Issue 52, pp. 36213 - 36222
Journal Article
Nature Communications, ISSN 2041-1723, 01/2016, Volume 7, Issue 1, pp. 10242 - 10242
Metabolic syndrome (MetS) and Type 2 diabetes mellitus (T2DM) increase risk for Alzheimer's disease (AD). The molecular mechanism for this association remains... 
GLUTAMATE NEUROTOXICITY | METABOLIC SYNDROME | INSULIN-DEGRADING ENZYME | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | NITRIC-OXIDE | A-BETA | COGNITIVE IMPAIRMENT | SYNAPTIC PLASTICITY | NEURODEGENERATIVE DISEASES | MITOCHONDRIAL FISSION | Dynamins - metabolism | Microtubule-Associated Proteins - metabolism | Humans | Cerebral Cortex - pathology | Immunoblotting | Male | Metabolic Syndrome - metabolism | Reactive Nitrogen Species | Diabetes Mellitus, Type 2 - metabolism | Cerebral Cortex - cytology | Case-Control Studies | Cerebral Cortex - metabolism | Alzheimer Disease - pathology | Brain - metabolism | Nitroso Compounds - metabolism | Synapses - metabolism | Mitochondrial Proteins - metabolism | Dendritic Spines | Amyloid beta-Peptides - metabolism | Aged, 80 and over | Adult | Female | Neurons - metabolism | Disease Models, Animal | Insulysin - metabolism | Brain - cytology | Memantine - pharmacology | Oxygen Consumption | Rats | Mice, Transgenic | Excitatory Amino Acid Antagonists - pharmacology | Hippocampus - pathology | Hippocampus - cytology | Hyperglycemia - metabolism | Hippocampus - metabolism | Insulin - metabolism | Animals | GTP Phosphohydrolases - metabolism | Alzheimer Disease - metabolism | Long-Term Potentiation | Brain - pathology | Glucose - metabolism | Aged | Mice | Nitric Oxide - metabolism | Induced Pluripotent Stem Cells | Index Medicus
Journal Article
Biomaterials, ISSN 0142-9612, 2011, Volume 32, Issue 23, pp. 5438 - 5458
Abstract Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. We sought to elucidate possible effects of... 
Advanced Basic Science | Dentistry | Oxidative stress | Mitochondria | Caspase-dependent apoptosis | Endoplasmic reticulum | Alginate oligosaccharide | PC12 cells | SIGNALING PATHWAYS | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | CASCADES | P53 | DISEASES | BAX | CYTOCHROME-C RELEASE | PROTEINS | BINDING | MEMBRANE PERMEABILIZATION | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Calcium - metabolism | Glutathione - metabolism | Amyloid beta-Peptides - pharmacology | Oxidative Stress - physiology | Caspase 3 - metabolism | Endoplasmic Reticulum - metabolism | NF-kappa B - metabolism | Neurons - cytology | Peptide Fragments - pharmacology | Extracellular Signal-Regulated MAP Kinases - metabolism | PC12 Cells | Oligosaccharides - pharmacology | Proto-Oncogene Proteins c-bcl-2 - metabolism | Apoptosis Inducing Factor - pharmacology | Cell Nucleus - metabolism | Endoplasmic Reticulum - drug effects | Oxidation-Reduction - drug effects | Neurons - metabolism | Phosphorylation - drug effects | Glucuronic Acid - chemistry | Neurons - drug effects | Polysaccharide-Lyases - chemistry | Apoptosis Inducing Factor - metabolism | Cell Survival - drug effects | Cytochromes c - metabolism | Hydrogen Peroxide - pharmacology | Tumor Suppressor Protein p53 - metabolism | bcl-2-Associated X Protein - metabolism | Rats | Mitochondria - metabolism | Caspase 12 - metabolism | Hexuronic Acids - chemistry | Mitochondria - drug effects | HSP70 Heat-Shock Proteins - metabolism | Cell Shape - drug effects | Poly(ADP-ribose) Polymerases - metabolism | Animals | Models, Biological | Alginates - chemistry | NF-E2-Related Factor 2 - metabolism | HSP90 Heat-Shock Proteins - metabolism | Apoptosis - physiology | Oxidative Stress - drug effects | Cell Nucleus - drug effects | Neurosciences | Nervous system diseases | Biological products | Hydrogen peroxide | Heat shock proteins | Nerve growth factor | Superoxide | Mitochondrial DNA | Biochemistry | Antioxidants | Tumor proteins | Protein kinases | Alzheimer's disease | Apoptosis | Stresses | Surgical implants | Biomedical materials | Cell death | Cascades | Blocking | Activation | Kinases | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2011, Volume 6, Issue 9, pp. e25178 - e25178
Imbalance of the excitatory neurotransmitter glutamate and of the inhibitory neurotransmitter GABA is one of several causes of seizures. ATP has also been... 
HIPPOCAMPAL SLICES | ADENOSINE KINASE | P2X RECEPTOR | HEMICHANNELS | BIOLOGY | ASTROCYTE PROGENITORS | CENTRAL-NERVOUS-SYSTEM | RAT HIPPOCAMPUS | CHANNELS | CELL-CELL COMMUNICATION | ATP RELEASE | Potassium - metabolism | Seizures - prevention & control | Connexins - physiology | Epilepsy - metabolism | Neurons - cytology | Seizures - metabolism | Seizures - chemically induced | Brain - metabolism | Adenosine Triphosphate - metabolism | Behavior, Animal - drug effects | Neurons - metabolism | Astrocytes - cytology | Epilepsy - prevention & control | Brain - cytology | Nerve Tissue Proteins - physiology | Kainic Acid - pharmacology | Mice, Inbred C57BL | Cells, Cultured | Mice, Transgenic | Hippocampus - cytology | Blotting, Western | Hippocampus - metabolism | Animals | Epilepsy - chemically induced | Fluorescent Antibody Technique | Mice | Status Epilepticus - metabolism | Astrocytes - metabolism | Brain | Neurons | Epilepsy | GABA | Genetic engineering | Seizures (Medicine) | Glutamate | Neurosciences | Hyperactivity | Nervous system | Membrane channels | Channels | γ-Aminobutyric acid | Membrane conductance | Metabolites | Rodents | Cooperation | Physiology | Seizures | Seizing | Adenosine | Astrocytes | Transgenic mice | Pharmacology | Metabolism | Embryos | Resistance | Medicine | Signaling | Conductance | ATP | Kainic acid | Hippocampus | Index Medicus
Journal Article
Neuron, ISSN 0896-6273, 08/2012, Volume 75, Issue 4, pp. 618 - 632
Mitochondrial abnormalities have been documented in Alzheimer’s disease and related neurodegenerative disorders, but the causal relationship between... 
ALZHEIMERS-DISEASE BRAIN | DOMINANT OPTIC ATROPHY | MITOCHONDRIAL-FUNCTION | MOUSE MODEL | LIGHT-CHAIN | FRONTOTEMPORAL DEMENTIA | AXONAL-TRANSPORT | NEUROSCIENCES | DYNAMIN-RELATED PROTEIN | PHOSPHORYLATION SITES | TRANSGENIC MICE | Neurons - pathology | Microtubule-Associated Proteins - genetics | Tauopathies - genetics | Cytoskeletal Proteins - genetics | Gelsolin - metabolism | Microtubule-Associated Proteins - metabolism | Humans | Actins - metabolism | Tauopathies - pathology | Cytoplasm - metabolism | MicroRNAs - metabolism | Green Fluorescent Proteins - genetics | Mitochondrial Proteins - genetics | Drosophila Proteins - metabolism | GTP-Binding Proteins - genetics | Nerve Degeneration - metabolism | Neurons - ultrastructure | tau Proteins - genetics | Cell Death - genetics | Mitochondria - genetics | Mitochondrial Proteins - metabolism | ATP Synthetase Complexes - metabolism | Cell Cycle Proteins - genetics | Tauopathies - complications | Cytoskeletal Proteins - metabolism | Myosins - metabolism | Cytoplasm - genetics | RNA Interference - physiology | Disease Models, Animal | In Situ Nick-End Labeling | Green Fluorescent Proteins - metabolism | Animals, Genetically Modified | Gene Expression Regulation - genetics | Drosophila | Cell Cycle Proteins - metabolism | Mitochondria - metabolism | Mitochondria - pathology | Mutation - genetics | Animals | GTP Phosphohydrolases - metabolism | Analysis of Variance | GTP Phosphohydrolases - genetics | Gelsolin - genetics | Mice | Drosophila Proteins - genetics | Nerve Degeneration - etiology | Voltage-Dependent Anion Channels - metabolism | GTP-Binding Proteins - metabolism | Nervous system diseases | Actin | Neurons | Utrophin | Myosin | Mitochondrial DNA | Alzheimer's disease | Proteins | Phosphorylation | Mitochondria | Neurotoxicity | Insects | Microscopy | Neurodegeneration | Pathogenesis | Morphology | Mutation | Defects | Index Medicus | Neurodegenerative diseases | Tau protein | Cell death | Elongation
Journal Article