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PloS one, ISSN 1932-6203, 2017, Volume 12, Issue 7, p. e0177962
Adult neural crest stem-derived cells (NCSC) are of extraordinary high plasticity and promising candidates for use in regenerative medicine. Several locations... 
PROGENITOR CELLS | MESENCHYMAL STROMAL CELLS | STEM-CELLS | TRUNK | MULTIDISCIPLINARY SCIENCES | PERIODONTAL-LIGAMENT | ONTOGENY | GENERATION | SKIN-DERIVED PRECURSORS | DIFFERENTIATION | MELANOCYTES | RNA-Binding Proteins - genetics | Humans | Adipose Tissue - cytology | Melanocytes - metabolism | Neurons - cytology | Receptors, Nerve Growth Factor - metabolism | Neural Stem Cells - cytology | Schwann Cells - cytology | Neural Crest - metabolism | Adipose Tissue - metabolism | Mesenchymal Stromal Cells - cytology | Snail Family Transcription Factors - genetics | Melanocytes - cytology | Nestin - genetics | Adult | Female | Cell Differentiation | Neurons - metabolism | Dermis - cytology | Nuclear Proteins - genetics | Biomarkers - metabolism | SOX9 Transcription Factor - metabolism | Gene Expression | Neural Crest - cytology | Dermis - metabolism | Snail Family Transcription Factors - metabolism | Microinjections | Bone Marrow Cells - cytology | Neural Crest - growth & development | Mesenchymal Stromal Cells - metabolism | Nuclear Proteins - metabolism | Schwann Cells - metabolism | Transcription Factor Brn-3A - metabolism | Chick Embryo | Nerve Tissue Proteins - genetics | Receptors, Nerve Growth Factor - genetics | Nerve Tissue Proteins - metabolism | Nestin - metabolism | Animals | Transcription Factor Brn-3A - genetics | Twist-Related Protein 1 - genetics | Twist-Related Protein 1 - metabolism | Neural Stem Cells - metabolism | SOX9 Transcription Factor - genetics | Bone Marrow Cells - metabolism | Mesenchymal Stem Cell Transplantation | RNA-Binding Proteins - metabolism | Adipose tissues | Comparative analysis | Skin | Neurosciences | Nestin | Adipose tissue | Leukocyte migration | Laboratories | Sox9 protein | Dermis | Melanocytes | Nervous system | Human tissues | Regeneration (physiology) | Cell adhesion & migration | Msi1 protein | Plasticity (neural) | Ethics | Immunology | Pathways | Surgery | Bone marrow | Hair | Hematology | Neurons | Tissue engineering | Schwann cells | Brn-3 protein | Gene expression | Embryos | Neural crest | Medicine | Regeneration | Human performance | Stromal cells | Stem cells | Cell migration | Dental pulp
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 03/2010, Volume 30, Issue 9, pp. 3326 - 3338
Journal Article
Nature neuroscience, ISSN 1546-1726, 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
Journal Article
Nature (London), ISSN 1476-4687, 2012, Volume 487, Issue 7408, pp. 443 - 448
Journal Article
Cell reports (Cambridge), ISSN 2211-1247, 2016, Volume 16, Issue 10, pp. 2576 - 2592
The mechanisms underlying Zika virus (ZIKV)-related microcephaly and other neurodevelopment defects remain poorly understood. Here, we describe the derivation... 
NEURAL PROGENITORS | LONG-TERM | HUMAN BRAIN | ADAPTER | CENTRAL-NERVOUS-SYSTEM | INFECTION | MICE | BINDING KINASE 1 | ORGANOIDS | INNATE IMMUNITY | CELL BIOLOGY | Neocortex - pathology | Neurons - pathology | Transcription, Genetic - drug effects | Brain - embryology | Neuroglia - ultrastructure | Neuroglia - pathology | Humans | Brain - virology | Centrosome - drug effects | Gene Expression Profiling | Microcephaly - virology | Neural Stem Cells - ultrastructure | Zika Virus Infection - virology | Neural Stem Cells - immunology | Neuroepithelial Cells - immunology | Neuroprotective Agents - pharmacology | Spinal Cord - pathology | Microcephaly - pathology | Neuroepithelial Cells - virology | Nucleosides - pharmacology | Fetus - virology | Cell Death - drug effects | Phosphorylation - drug effects | Neurons - drug effects | Protein-Serine-Threonine Kinases - metabolism | Zika Virus - pathogenicity | Proto-Oncogene Proteins - metabolism | Zika Virus - ultrastructure | Neurons - virology | Virus Replication - drug effects | Neuroepithelial Cells - ultrastructure | Immunity, Innate - drug effects | Zika Virus Infection - pathology | Neural Stem Cells - virology | Zika Virus - physiology | Zika Virus - drug effects | Mitochondria - metabolism | Mitochondria - drug effects | Receptor Protein-Tyrosine Kinases - metabolism | Neural Stem Cells - enzymology | Centrosome - metabolism | Mitosis - drug effects | Brain - pathology | Protein Kinase Inhibitors - pharmacology | Neuroglia - virology | Neuroepithelial Cells - drug effects | Neurons/pathology | Zika Virus/pathogenicity | Mitochondria/metabolism | Virus Replication/drug effects | Microcephaly/pathology | Neurons/drug effects | Protein-Serine-Threonine Kinases/metabolism | Neural Stem Cells/immunology | Neuroglia/ultrastructure | Neuroepithelial Cells/drug effects | Neuroepithelial Cells/virology | Life Sciences | Brain/pathology | Zika Virus/drug effects | Brain/embryology | Mitochondria/drug effects | Fetus/virology | Neocortex/pathology | Neuroglia/pathology | Cell Death/drug effects | Mitosis/drug effects | Transcription, Genetic/drug effects | Nucleosides/pharmacology | Neural Stem Cells/enzymology | Neural Stem Cells/ultrastructure | Neuroepithelial Cells/ultrastructure | Receptor Protein-Tyrosine Kinases/metabolism | Microcephaly/virology | Proto-Oncogene Proteins/metabolism | Neuroprotective Agents/pharmacology | Zika Virus/ultrastructure | Neuroepithelial Cells/immunology | Brain/virology | Immunity, Innate/drug effects | Spinal Cord/pathology | Zika Virus/physiology | Neuroglia/virology | Microbiology and Parasitology | Zika Virus Infection/pathology | Neurons/virology | Zika Virus Infection/virology | Neural Stem Cells/virology | Centrosome/drug effects | Protein Kinase Inhibitors/pharmacology | Centrosome/metabolism | Phosphorylation/drug effects
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
Journal Article
Nature Communications, ISSN 2041-1723, 01/2016, Volume 7, Issue 1, p. 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
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 11, p. e79977
... to the transition into reproductive senescence. The deficit in brain metabolism was sustained thereafter... 
MECHANISM | ASTROCYTE | MULTIDISCIPLINARY SCIENCES | LACTATE | DISEASE | HIPPOCAMPAL | ESTRADIOL | COGNITIVE IMPAIRMENT | ENERGY-METABOLISM | EXPRESSION | OLIGODENDROCYTES | Adaptation, Physiological | Ketone Oxidoreductases - metabolism | Neurons - pathology | Humans | Ketone Bodies - metabolism | Astrocytes - pathology | Glucose Transporter Type 1 - metabolism | Alzheimer Disease - pathology | Biological Transport, Active | Monocarboxylic Acid Transporters - metabolism | Aging - genetics | Female | Neurons - metabolism | Hexokinase - genetics | Disease Models, Animal | Gene Expression | Lactic Acid - metabolism | Mice, Transgenic | Hippocampus - pathology | Mitochondria - metabolism | Ketone Oxidoreductases - genetics | Aging - pathology | Blood-Brain Barrier - metabolism | Hippocampus - metabolism | Animals | Energy Metabolism | Glucose Transporter Type 1 - genetics | Alzheimer Disease - metabolism | Glucose - metabolism | Mice | Monocarboxylic Acid Transporters - genetics | Alzheimer Disease - genetics | Hexokinase - metabolism | Aging - metabolism | Astrocytes - metabolism | Lactates | Glucose metabolism | Enzymes | Brain | Neurons | Glucose | Alzheimer's disease | Dextrose | Neurosciences | Senescence | Adaptive systems | Dehydrogenases | Pyruvic acid | Ketone bodies | Fuels | Mitochondria | Bioenergetics | Blood-brain barrier | Rodents | Aging | Pharmaceutical sciences | Age | Glucose transporter | Phenotypes | Medical imaging | Neurodegenerative diseases | Ketones | Astrocytes | Pharmacology | Metabolism | Glucose transport | Fatty acids | Hexokinase | Utilization | Pharmacy | Glycolysis | Lactic acid | Laboratory animals | Alzheimers disease | Axonal transport | Transporter | Hippocampus | Animal cognition
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 | LOCALIZATION | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | STABILIZATION | CHAPERONE | APOPTOSOME | CA2 | BAX | CYTOCHROME-C RELEASE | PROTEINS | 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
Journal Article