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Neuron (Cambridge, Mass.), ISSN 0896-6273, 02/2013, Volume 77, Issue 3, pp. 472 - 484
Major outputs of the neocortex are conveyed by corticothalamic axons (CTAs), which form reciprocal connections with thalamocortical axons, and... 
MUTANT MICE | CORTICAL AXONS | THALAMOCORTICAL AXONS | GROWTH | SEMAPHORIN 3E | CENTRAL-NERVOUS-SYSTEM | GUIDANCE | CHICK HINDLIMB | CAJAL-RETZIUS CELLS | NEUROSCIENCES | CEREBRAL-CORTEX | Thyroid Nuclear Factor 1 | Age Factors | Embryo, Mammalian | Leukocyte L1 Antigen Complex - metabolism | Gene Expression Regulation, Developmental - genetics | Axons - physiology | Cerebral Cortex - cytology | Neural Pathways - physiology | DNA-Binding Proteins - metabolism | POU Domain Factors - genetics | tau Proteins - genetics | Thalamus - physiology | Contactin 2 - metabolism | Repressor Proteins - metabolism | Glycoproteins - genetics | Tumor Suppressor Proteins - metabolism | Wnt3A Protein - genetics | Membrane Proteins - genetics | Mice, Inbred C57BL | Mice, Transgenic | Nuclear Proteins - metabolism | Transcription Factors - genetics | Nerve Tissue Proteins - genetics | Homeodomain Proteins - genetics | Membrane Glycoproteins - genetics | Nerve Tissue Proteins - metabolism | S100 Calcium Binding Protein G - metabolism | Transcription Factors - metabolism | Animals | Calbindin 2 | Thalamus - cytology | Cerebral Cortex - physiology | Luminescent Proteins - genetics | Mice | Body Patterning - genetics | Luminescent Proteins - metabolism | Developmental biology | Neurons | Studies | Laboratories | Experiments | Repressor Proteins | Cerebral Cortex | Cellular Biology | Neural Pathways | tau Proteins | Life Sciences | Contactin 2 | Gene Expression Regulation, Developmental | Body Patterning | Thalamus | Membrane Glycoproteins | Luminescent Proteins | DNA-Binding Proteins | POU Domain Factors | Calcium-Binding Protein, Vitamin D-Dependent | Glycoproteins | Nerve Tissue Proteins | Nuclear Proteins | Membrane Proteins | Axons | Homeodomain Proteins | Leukocyte L1 Antigen Complex | Transcription Factors | Wnt3A Protein | Tumor Suppressor Proteins | reciprocal connections | handshake | waiting period | PlexinD1 | axon guidance | Sema3E | thalamocortical | corticothalamic
Journal Article
The FEBS journal, ISSN 1742-464X, 10/2017, Volume 284, Issue 19, pp. 3218 - 3229
Bridging integrator 1 (bin1) gene is a genetic determinant of Alzheimer's disease (AD... 
SH3 domain | nuclear magnetic resonance spectroscopy | protein–protein interaction | Tau | BIN1 | Alzheimer's disease | ALZHEIMERS-DISEASE | NMR-SPECTROSCOPY | BIOCHEMISTRY & MOLECULAR BIOLOGY | PATHOLOGY | MODEL | IDENTIFIES VARIANTS | AMPHIPHYSIN | MEMBRANE CURVATURE | protein-protein interaction | BINDING | EXPRESSION | GENOME-WIDE ASSOCIATION | Adaptor Proteins, Signal Transducing - chemistry | Humans | Peptides - genetics | tau Proteins - metabolism | tau Proteins - chemistry | Peptides - metabolism | Protein Isoforms - metabolism | tau Proteins - genetics | Protein Isoforms - chemistry | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Cloning, Molecular | Escherichia coli - metabolism | Nuclear Magnetic Resonance, Biomolecular | Neurons - metabolism | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Binding Sites | Recombinant Proteins - metabolism | Protein Conformation, alpha-Helical | Gene Expression | Tumor Suppressor Proteins - metabolism | Neurons - chemistry | Peptides - chemistry | Models, Molecular | Recombinant Proteins - chemistry | Nuclear Proteins - metabolism | Recombinant Proteins - genetics | Nuclear Proteins - chemistry | Amino Acid Motifs | Sequence Homology, Amino Acid | Sequence Alignment | Protein Conformation, beta-Strand | Escherichia coli - genetics | Adaptor Proteins, Signal Transducing - genetics | Protein Binding | Kinetics | Adaptor Proteins, Signal Transducing - metabolism | Protein Isoforms - genetics | Nuclear magnetic resonance spectroscopy | Neurons | Protein-protein interactions | Spectroscopy | Clathrin | Nuclear magnetic resonance--NMR | Peptides | Neurodegenerative diseases | Pathogenesis | Complexity | Proteins | Magnetic resonance spectroscopy | Tau protein | Spectrum analysis | Isoforms | Alzheimers disease | Binding sites | tau Proteins/metabolism | Nuclear Proteins/chemistry | Protein Isoforms/chemistry | Protein Isoforms/genetics | Adaptor Proteins, Signal Transducing/genetics | Recombinant Proteins/metabolism | Peptides/metabolism | Life Sciences | Recombinant Proteins/chemistry | Adaptor Proteins, Signal Transducing/chemistry | Nuclear Proteins/metabolism | Tumor Suppressor Proteins/chemistry | Nuclear Proteins/genetics | Tumor Suppressor Proteins/metabolism | Protein Isoforms/metabolism | Peptides/chemistry | Recombinant Proteins/genetics | Biochemistry, Molecular Biology | Escherichia coli/genetics | Escherichia coli/metabolism | Adaptor Proteins, Signal Transducing/metabolism | Neurons/chemistry | Tumor Suppressor Proteins/genetics | tau Proteins/genetics | Neurons/metabolism | Peptides/genetics | tau Proteins/chemistry
Journal Article
Nature neuroscience, ISSN 1546-1726, 2012, Volume 15, Issue 11, pp. 1488 - 1497
... and that encode proteins that are essential... 
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
PLoS genetics, ISSN 1553-7404, 2014, Volume 10, Issue 10, p. e1004758
Journal Article
PLoS genetics, ISSN 1553-7404, 2017, Volume 13, Issue 7, pp. e1006849 - e1006849
The unfolded protein response (UPR) in the endoplasmic reticulum (ER) and the cytoplasmic heat stress response are two major stress response systems necessary for maintaining proteostasis for cellular health... 
UNFOLDED-PROTEIN RESPONSE | ALZHEIMERS-DISEASE | ER STRESS | HEAT-SHOCK RESPONSE | MOUSE MODEL | GENETICS & HEREDITY | PAIRED HELICAL FILAMENTS | ENDOPLASMIC-RETICULUM STRESS | ALPHA-SYNUCLEIN | HUNTINGTONS-DISEASE | NEURODEGENERATIVE DISEASES | Neurons - pathology | Transcription Factor CHOP - genetics | Phosphorylation | Tauopathies - genetics | Humans | Tauopathies - pathology | tau Proteins - metabolism | Endoplasmic Reticulum Stress - genetics | Alzheimer Disease - pathology | Heat Shock Transcription Factors | Heat-Shock Proteins - genetics | tau Proteins - genetics | Proteolysis | Neurons - metabolism | Autophagy - genetics | Transcription Factor CHOP - biosynthesis | Protein Aggregation, Pathological - genetics | Unfolded Protein Response - genetics | Gene Expression Regulation | Rats | Transcription Factors - biosynthesis | Hippocampus - pathology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Heat-Shock Response - genetics | Mice, Knockout | Hippocampus - metabolism | Tauopathies - metabolism | Animals | Alzheimer Disease - metabolism | Mice | Alzheimer Disease - genetics | DNA-Binding Proteins - biosynthesis | Genetic aspects | Neural circuitry | Protein folding | Health aspects | Tau proteins | Huntingtons disease | Brain | Neurosciences | Animal models | Toxicity | Pathogenesis | Crosstalk | Cognitive ability | Neurobiology | Homeostasis | Homology | Agglomeration | Activation | Biochemistry | CCAAT/enhancer-binding protein | Kinases | Heat shock factors | Degradation | Proteins | Neurodegeneration | Heat stress | Stress response | HSF1 protein | Alzheimer's disease | Inducers | Departments | Neurodegenerative diseases | Hsp70 protein | Pharmacology | Pathology | Tau protein | Aberration | Alzheimers disease | Endoplasmic reticulum | Phagocytosis | Apoptosis | Heat shock | Dementia | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2016, Volume 113, Issue 50, pp. E8187 - E8196
...) tau prions, were used to infect HEK293T cells expressing 3R tau fused to yellow fluorescent protein (YFP... 
Pick's disease | Tauopathies | Argyrophilic grain disease | Progressive supranuclear palsy | Corticobasal degeneration | MOUSE-BRAIN | NEUROFIBRILLARY TANGLES | corticobasal degeneration | BRAIN-INJURY | MULTIDISCIPLINARY SCIENCES | FRONTOTEMPORAL DEMENTIA | SHARE ANTIGENIC DETERMINANTS | PICKS-DISEASE | ABNORMAL PHOSPHORYLATION | argyrophilic grain disease | MICROTUBULE-ASSOCIATED PROTEIN | PAIRED HELICAL FILAMENTS | tauopathies | progressive supranuclear palsy | TRANSGENIC MICE | Up-Regulation | Chronic Traumatic Encephalopathy - metabolism | Humans | Bacterial Proteins - chemistry | tau Proteins - metabolism | Pick Disease of the Brain - genetics | Recombinant Fusion Proteins - metabolism | tau Proteins - chemistry | Protein Isoforms - metabolism | tau Proteins - genetics | Chronic Traumatic Encephalopathy - genetics | HEK293 Cells | Luminescent Proteins - chemistry | Pick Disease of the Brain - metabolism | Supranuclear Palsy, Progressive - genetics | Cell Line | Bacterial Proteins - genetics | Recombinant Fusion Proteins - chemistry | Alzheimer Disease - metabolism | Recombinant Fusion Proteins - genetics | Supranuclear Palsy, Progressive - metabolism | Bacterial Proteins - metabolism | Luminescent Proteins - genetics | Mutation | Alzheimer Disease - genetics | Luminescent Proteins - metabolism | Protein Isoforms - genetics | Physiological aspects | Alzheimer's disease | Health aspects | Prions | Encephalopathy | Biological Sciences | PNAS Plus | Pick’s disease
Journal Article
Neuron (Cambridge, Mass.), ISSN 0896-6273, 09/2013, Volume 79, Issue 6, pp. 1136 - 1151
Neurogenesis underlies plastic changes in defined neuronal circuits in the postnatal and adult brain. Here we identify connective tissue growth factor (CTGF)... 
NEURAL STEM-CELLS | SYNCHRONIZATION | EXTERNAL TUFTED CELLS | ADULT-BORN NEURONS | DISCRIMINATION | FACTOR CTGF | ROSTRAL MIGRATORY STREAM | GENE-EXPRESSION | NEUROGENESIS | RECEPTOR | NEUROSCIENCES | Interneurons - physiology | RNA, Small Interfering - genetics | Receptors, Odorant - metabolism | Receptors, Transforming Growth Factor beta - genetics | Smell - genetics | Humans | Cell Survival - genetics | Male | MicroRNAs - metabolism | Odorants | Transfection | tau Proteins - genetics | Female | Lysine - metabolism | Bromodeoxyuridine - metabolism | Organ Culture Techniques | Olfactory Bulb - cytology | Animals, Newborn | Lysine - analogs & derivatives | Gene Expression Regulation - genetics | Synaptic Potentials - genetics | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Mice, Transgenic | Memory, Long-Term - physiology | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Animals | Analysis of Variance | Sensory Thresholds - physiology | Discrimination (Psychology) - physiology | Receptors, Odorant - genetics | Olfactory Bulb - physiology | Luminescent Proteins - genetics | Connective Tissue Growth Factor - genetics | Mice | MicroRNAs - genetics | Cell Line, Transformed | Connective Tissue Growth Factor - metabolism | Luminescent Proteins - metabolism | RNA, Small Interfering - metabolism | Nervous system diseases | Research | Transforming growth factors | Neurons | Oncology, Experimental | Cancer | Software | Gene expression | Experiments | Rodents | Interneurons | Receptors, Odorant | Protein-Serine-Threonine Kinases | Neurons and Cognition | Bromodeoxyuridine | tau Proteins | Life Sciences | Odors | Discrimination (Psychology) | Luminescent Proteins | Synaptic Potentials | Memory, Long-Term | Sensory Thresholds | Cell Survival | Gene Expression Regulation | Nerve Tissue Proteins | Olfactory Bulb | Smell | Lysine | MicroRNAs | Receptors, Transforming Growth Factor beta | RNA, Small Interfering | Connective Tissue Growth Factor
Journal Article
Neuron (Cambridge, Mass.), ISSN 0896-6273, 2012, Volume 75, Issue 4, pp. 618 - 632
.... We have previously demonstrated that stabilization of actin by tau is critical for neurotoxicity of the protein... 
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 | Neurodegenerative diseases | Tau protein | Cell death | Elongation
Journal Article