Annals of Neurology, ISSN 0364-5134, 08/2010, Volume 68, Issue 2, pp. 220 - 230
Objective Recent evidence suggests that high molecular weight soluble oligomeric Aβ (oAβ) assemblies (also known as Aβ‐derived diffusible ligands, or ADDLs)...
NATURAL OLIGOMERS | MEMORY | MOUSE MODEL | DISEASE | A-BETA | HEREDITARY CEREBRAL-HEMORRHAGE | DEFICITS | NEUROSCIENCES | PEPTIDE | CLINICAL NEUROLOGY | IMPAIR SYNAPTIC PLASTICITY | TRANSGENIC MICE | Alzheimer Disease - etiology | Peptide Fragments - toxicity | Amyloid beta-Protein Precursor - chemistry | Humans | Protein Processing, Post-Translational - genetics | Male | Alzheimer Disease - pathology | Amyloid beta-Peptides - genetics | Behavior, Animal - drug effects | Female | Peptide Fragments - genetics | Brain Chemistry - genetics | Disease Models, Animal | Maze Learning - physiology | Amyloid beta-Peptides - toxicity | Mice, Inbred C57BL | Behavior, Animal - physiology | Mice, Transgenic | Maze Learning - drug effects | Amyloid beta-Protein Precursor - toxicity | Peptide Fragments - chemistry | Amyloid beta-Protein Precursor - genetics | Animals | Mice | Amyloid beta-Peptides - chemistry | Alzheimer Disease - genetics | Spatial Recognition | Amyloid Precursor Protein | Amyloid | Alzheimer’s Disease | Days-to-Criterion
NATURAL OLIGOMERS | MEMORY | MOUSE MODEL | DISEASE | A-BETA | HEREDITARY CEREBRAL-HEMORRHAGE | DEFICITS | NEUROSCIENCES | PEPTIDE | CLINICAL NEUROLOGY | IMPAIR SYNAPTIC PLASTICITY | TRANSGENIC MICE | Alzheimer Disease - etiology | Peptide Fragments - toxicity | Amyloid beta-Protein Precursor - chemistry | Humans | Protein Processing, Post-Translational - genetics | Male | Alzheimer Disease - pathology | Amyloid beta-Peptides - genetics | Behavior, Animal - drug effects | Female | Peptide Fragments - genetics | Brain Chemistry - genetics | Disease Models, Animal | Maze Learning - physiology | Amyloid beta-Peptides - toxicity | Mice, Inbred C57BL | Behavior, Animal - physiology | Mice, Transgenic | Maze Learning - drug effects | Amyloid beta-Protein Precursor - toxicity | Peptide Fragments - chemistry | Amyloid beta-Protein Precursor - genetics | Animals | Mice | Amyloid beta-Peptides - chemistry | Alzheimer Disease - genetics | Spatial Recognition | Amyloid Precursor Protein | Amyloid | Alzheimer’s Disease | Days-to-Criterion
Journal Article
Progress in Neurobiology, ISSN 0301-0082, 2008, Volume 85, Issue 4, pp. 393 - 406
Since the discovery of the amyloid precursor protein (APP) in 1987, extensive research has been conducted analyzing the APP-derived β-amyloid (Aβ) which is...
Amyloid precursor protein (APP) intracellular domain (AICD) | Transcription | Alzheimer's disease | Cytoskeletal dynamics | FE65 | Apoptosis | intracellular domain (AICD) | cytoskeletal dynamics | RECEPTOR-RELATED PROTEIN | transcription | MESSENGER-RNA ISOFORMS | apoptosis | KINESIN LIGHT-CHAIN | amyloid precursor protein (APP) | NEUROSCIENCES | C-TERMINAL FRAGMENT | GLYCOGEN-SYNTHASE KINASE-3-BETA | APP FAMILY-MEMBERS | FE65 ADAPTER PROTEIN | JNK-INTERACTING PROTEIN-1 | PHOSPHOTYROSINE-BINDING DOMAIN | GAMMA-SECRETASE ACTIVITY | Alzheimer Disease - physiopathology | Apoptosis - drug effects | Humans | Gene Expression Regulation - physiology | Amyloid beta-Protein Precursor - toxicity | Gene Expression Regulation - drug effects | Animals | Models, Biological | Alzheimer Disease - metabolism | Amyloid beta-Protein Precursor - metabolism | Cytoskeleton - physiology | Apoptosis - physiology | Alzheimer Disease - genetics | Genetic research | Gene expression | Analysis | Amyloid beta-protein | Index Medicus
Amyloid precursor protein (APP) intracellular domain (AICD) | Transcription | Alzheimer's disease | Cytoskeletal dynamics | FE65 | Apoptosis | intracellular domain (AICD) | cytoskeletal dynamics | RECEPTOR-RELATED PROTEIN | transcription | MESSENGER-RNA ISOFORMS | apoptosis | KINESIN LIGHT-CHAIN | amyloid precursor protein (APP) | NEUROSCIENCES | C-TERMINAL FRAGMENT | GLYCOGEN-SYNTHASE KINASE-3-BETA | APP FAMILY-MEMBERS | FE65 ADAPTER PROTEIN | JNK-INTERACTING PROTEIN-1 | PHOSPHOTYROSINE-BINDING DOMAIN | GAMMA-SECRETASE ACTIVITY | Alzheimer Disease - physiopathology | Apoptosis - drug effects | Humans | Gene Expression Regulation - physiology | Amyloid beta-Protein Precursor - toxicity | Gene Expression Regulation - drug effects | Animals | Models, Biological | Alzheimer Disease - metabolism | Amyloid beta-Protein Precursor - metabolism | Cytoskeleton - physiology | Apoptosis - physiology | Alzheimer Disease - genetics | Genetic research | Gene expression | Analysis | Amyloid beta-protein | Index Medicus
Journal Article
PLoS Pathogens, ISSN 1553-7366, 05/2015, Volume 11, Issue 5, p. e1004896
Clostridium perfringens epsilon-toxin (ETX) is a potent pore-forming toxin responsible for a central nervous system (CNS) disease in ruminant animals with...
NERVOUS-SYSTEM | MDCK CELLS | MICROBIOLOGY | PLASMA-MEMBRANE | INTESTINAL INFECTIONS | DARBY CANINE KIDNEY | VIROLOGY | PORE-FORMING TOXIN | APICAL SORTING MACHINERY | RAFT-ASSOCIATED PROTEIN | HUMAN T-LYMPHOCYTES | PARASITOLOGY | INFLUENZA-VIRUS HEMAGGLUTININ | Injections, Intravenous | Cricetulus | Myelin and Lymphocyte-Associated Proteolipid Proteins - metabolism | Humans | Bacterial Toxins - toxicity | Recombinant Fusion Proteins - metabolism | Tissue Distribution | Protein Precursors - toxicity | Bacterial Toxins - genetics | Clostridium perfringens - metabolism | Protein Interaction Domains and Motifs | Cell Death - drug effects | Binding Sites | Clostridium perfringens - pathogenicity | Recombinant Fusion Proteins - administration & dosage | CHO Cells | Recombinant Proteins - metabolism | Protein Precursors - genetics | Protein Precursors - administration & dosage | Mice, Inbred C57BL | Rats | Recombinant Proteins - chemistry | Recombinant Fusion Proteins - toxicity | Recombinant Fusion Proteins - chemistry | Recombinant Proteins - administration & dosage | Mice, Knockout | Protein Precursors - metabolism | Toxicokinetics | Bacterial Toxins - metabolism | Animals | Myelin and Lymphocyte-Associated Proteolipid Proteins - chemistry | Recombinant Proteins - toxicity | Ligands | Mutagenesis, Insertional | Myelin and Lymphocyte-Associated Proteolipid Proteins - genetics
NERVOUS-SYSTEM | MDCK CELLS | MICROBIOLOGY | PLASMA-MEMBRANE | INTESTINAL INFECTIONS | DARBY CANINE KIDNEY | VIROLOGY | PORE-FORMING TOXIN | APICAL SORTING MACHINERY | RAFT-ASSOCIATED PROTEIN | HUMAN T-LYMPHOCYTES | PARASITOLOGY | INFLUENZA-VIRUS HEMAGGLUTININ | Injections, Intravenous | Cricetulus | Myelin and Lymphocyte-Associated Proteolipid Proteins - metabolism | Humans | Bacterial Toxins - toxicity | Recombinant Fusion Proteins - metabolism | Tissue Distribution | Protein Precursors - toxicity | Bacterial Toxins - genetics | Clostridium perfringens - metabolism | Protein Interaction Domains and Motifs | Cell Death - drug effects | Binding Sites | Clostridium perfringens - pathogenicity | Recombinant Fusion Proteins - administration & dosage | CHO Cells | Recombinant Proteins - metabolism | Protein Precursors - genetics | Protein Precursors - administration & dosage | Mice, Inbred C57BL | Rats | Recombinant Proteins - chemistry | Recombinant Fusion Proteins - toxicity | Recombinant Fusion Proteins - chemistry | Recombinant Proteins - administration & dosage | Mice, Knockout | Protein Precursors - metabolism | Toxicokinetics | Bacterial Toxins - metabolism | Animals | Myelin and Lymphocyte-Associated Proteolipid Proteins - chemistry | Recombinant Proteins - toxicity | Ligands | Mutagenesis, Insertional | Myelin and Lymphocyte-Associated Proteolipid Proteins - genetics
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 05/2011, Volume 31, Issue 20, pp. 7563 - 7567
Chronic itch accompanying many dermatological, neurological, and systemic diseases is unresponsive to antihistamines. Our knowledge of endogenous chemicals...
PATHWAYS | MAGNITUDE | FLARE | INJECTIONS | SUBSTANCE-P | RECEPTORS | NEUROSCIENCES | PROTEASE | FAMILY | Enkephalins - toxicity | Sensation - physiology | Peptide Fragments - toxicity | Humans | Middle Aged | Histamine Release - physiology | Male | Pain - chemically induced | Pruritus - physiopathology | Young Adult | Sensation - drug effects | Animals | Cattle | Pain - physiopathology | Protein Precursors - toxicity | Adult | Female | Pruritus - chemically induced | Histamine Release - drug effects | Brief Communications
PATHWAYS | MAGNITUDE | FLARE | INJECTIONS | SUBSTANCE-P | RECEPTORS | NEUROSCIENCES | PROTEASE | FAMILY | Enkephalins - toxicity | Sensation - physiology | Peptide Fragments - toxicity | Humans | Middle Aged | Histamine Release - physiology | Male | Pain - chemically induced | Pruritus - physiopathology | Young Adult | Sensation - drug effects | Animals | Cattle | Pain - physiopathology | Protein Precursors - toxicity | Adult | Female | Pruritus - chemically induced | Histamine Release - drug effects | Brief Communications
Journal Article
Advances in Experimental Medicine and Biology, ISSN 0065-2598, 2015, Volume 855, pp. 67 - 94
Aggregation of amyloid-beta (A beta) peptide is the major event underlying neuronal damage in Alzheimer's disease (AD). Specific lipids and their homeostasis...
Protofibrils and fibrils | Cellular membranes and lipid rafts | Alzheimer’s disease | Apolipoprotein E | Peptide oligomers | Amyloid-β peptide | Gangliosides | Amyloid precursor protein | Cholesterol | Peptide oligomers, protofibrils and fibrils | MEDICINE, RESEARCH & EXPERIMENTAL | GM1 GANGLIOSIDE | ALZHEIMERS-DISEASE | CONFORMATIONAL TRANSITION | APOLIPOPROTEIN-E ISOFORMS | LOW-DENSITY-LIPOPROTEIN | TRANSMEMBRANE DOMAIN | PRECURSOR-PROTEIN APP | MEMBRANE INTERACTIONS | Amyloid-beta peptide | BIOLOGY | ION CHANNELS | Alzheimer's disease | GAMMA-SECRETASE | Amino Acid Sequence | Lipids - chemistry | Amyloid beta-Protein Precursor - chemistry | Humans | Alzheimer Disease - metabolism | Amyloid beta-Protein Precursor - metabolism | Molecular Sequence Data | Apolipoproteins E - metabolism | Lipids - toxicity | Amyloid beta-Protein Precursor - toxicity
Protofibrils and fibrils | Cellular membranes and lipid rafts | Alzheimer’s disease | Apolipoprotein E | Peptide oligomers | Amyloid-β peptide | Gangliosides | Amyloid precursor protein | Cholesterol | Peptide oligomers, protofibrils and fibrils | MEDICINE, RESEARCH & EXPERIMENTAL | GM1 GANGLIOSIDE | ALZHEIMERS-DISEASE | CONFORMATIONAL TRANSITION | APOLIPOPROTEIN-E ISOFORMS | LOW-DENSITY-LIPOPROTEIN | TRANSMEMBRANE DOMAIN | PRECURSOR-PROTEIN APP | MEMBRANE INTERACTIONS | Amyloid-beta peptide | BIOLOGY | ION CHANNELS | Alzheimer's disease | GAMMA-SECRETASE | Amino Acid Sequence | Lipids - chemistry | Amyloid beta-Protein Precursor - chemistry | Humans | Alzheimer Disease - metabolism | Amyloid beta-Protein Precursor - metabolism | Molecular Sequence Data | Apolipoproteins E - metabolism | Lipids - toxicity | Amyloid beta-Protein Precursor - toxicity
Journal Article
Scientific Reports, ISSN 2045-2322, 10/2015, Volume 5, Issue 1, pp. 15107 - 15107
Transgenic crops that produce Bacillus thuringiensis (Bt) proteins for pest control are grown extensively, but insect adaptation can reduce their...
SUGARCANE BORER | HELICOVERPA-ZEA BODDIE | CRY1AC TOXIN | OSTRINIA-NUBILALIS | EUROPEAN CORN-BORER | PEST RESISTANCE | MULTIDISCIPLINARY SCIENCES | SUSCEPTIBLE STRAINS | BACILLUS-THURINGIENSIS TOXINS | FIELD-EVOLVED RESISTANCE | COTTON BOLLWORM | Intestines - drug effects | Bacillus thuringiensis - chemistry | Protein Precursors - chemistry | Hemolysin Proteins - genetics | Lepidoptera - physiology | Bacterial Proteins - chemistry | Intestines - metabolism | Hemolysin Proteins - chemistry | Lepidoptera - metabolism | Bacterial Proteins - toxicity | Bacillus thuringiensis - pathogenicity | Larva - drug effects | Endotoxins - chemistry | Plants, Genetically Modified | Protein Precursors - toxicity | Hemolysin Proteins - toxicity | Lepidoptera - drug effects | Intestines - physiology | Transgenes | Bacillus thuringiensis - physiology | Insect Proteins - metabolism | Protein Structure, Tertiary | Gene Expression | Protein Precursors - genetics | Crops, Agricultural - parasitology | Protein Structure, Secondary | Endotoxins - genetics | Larva - metabolism | Bacterial Proteins - genetics | Models, Molecular | Insect Proteins - antagonists & inhibitors | Animals | Insect Proteins - chemistry | Protein Binding | Crops, Agricultural - genetics | Larva - physiology | Endotoxins - toxicity | Proteins | Insects | Toxicity | Crops | Cry1Ac toxin | Pest control | Pests | Protoxins | Index Medicus
SUGARCANE BORER | HELICOVERPA-ZEA BODDIE | CRY1AC TOXIN | OSTRINIA-NUBILALIS | EUROPEAN CORN-BORER | PEST RESISTANCE | MULTIDISCIPLINARY SCIENCES | SUSCEPTIBLE STRAINS | BACILLUS-THURINGIENSIS TOXINS | FIELD-EVOLVED RESISTANCE | COTTON BOLLWORM | Intestines - drug effects | Bacillus thuringiensis - chemistry | Protein Precursors - chemistry | Hemolysin Proteins - genetics | Lepidoptera - physiology | Bacterial Proteins - chemistry | Intestines - metabolism | Hemolysin Proteins - chemistry | Lepidoptera - metabolism | Bacterial Proteins - toxicity | Bacillus thuringiensis - pathogenicity | Larva - drug effects | Endotoxins - chemistry | Plants, Genetically Modified | Protein Precursors - toxicity | Hemolysin Proteins - toxicity | Lepidoptera - drug effects | Intestines - physiology | Transgenes | Bacillus thuringiensis - physiology | Insect Proteins - metabolism | Protein Structure, Tertiary | Gene Expression | Protein Precursors - genetics | Crops, Agricultural - parasitology | Protein Structure, Secondary | Endotoxins - genetics | Larva - metabolism | Bacterial Proteins - genetics | Models, Molecular | Insect Proteins - antagonists & inhibitors | Animals | Insect Proteins - chemistry | Protein Binding | Crops, Agricultural - genetics | Larva - physiology | Endotoxins - toxicity | Proteins | Insects | Toxicity | Crops | Cry1Ac toxin | Pest control | Pests | Protoxins | Index Medicus
Journal Article
Annals of Neurology, ISSN 0364-5134, 12/2003, Volume 54, Issue 6, pp. 781 - 789
The amyloid‐β protein precursor, a type 1 transmembrane protein, gives rise to the amyloid β‐protein, a neurotoxic peptide postulated to be involved in the...
NEURONAL APOPTOSIS | CYTOPLASMIC DOMAIN | ALZHEIMERS-DISEASE | TERMINAL FRAGMENTS | ANTIBODY | CASPASE CLEAVAGE | NEUROTOXICITY | SUFFICIENT | NEUROSCIENCES | OLIGOMERS | CLINICAL NEUROLOGY | DEGENERATION | Amyloid beta-Peptides - toxicity | Humans | Brain - enzymology | Amyloid beta-Protein Precursor - toxicity | Amyloid beta-Protein Precursor - genetics | Animals | Caspases - metabolism | Cell Death - genetics | Amyloid beta-Peptides - genetics | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Brain - pathology | Cell Line, Tumor | Mice
NEURONAL APOPTOSIS | CYTOPLASMIC DOMAIN | ALZHEIMERS-DISEASE | TERMINAL FRAGMENTS | ANTIBODY | CASPASE CLEAVAGE | NEUROTOXICITY | SUFFICIENT | NEUROSCIENCES | OLIGOMERS | CLINICAL NEUROLOGY | DEGENERATION | Amyloid beta-Peptides - toxicity | Humans | Brain - enzymology | Amyloid beta-Protein Precursor - toxicity | Amyloid beta-Protein Precursor - genetics | Animals | Caspases - metabolism | Cell Death - genetics | Amyloid beta-Peptides - genetics | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Brain - pathology | Cell Line, Tumor | Mice
Journal Article
Biological Psychiatry, ISSN 0006-3223, 12/2006, Volume 60, Issue 12, pp. 1314 - 1323
Background: In aging mice, activity maintains hippocampal plasticity and adult hippocampal neurogenesis at a level corresponding to a younger age. Here we...
mouse | neurotrophin | enriched environment | stem cell | water maze | Adult neurogenesis | adult neurogenesis | APP23 TRANSGENIC MICE | TERM ENVIRONMENTAL ENRICHMENT | PSYCHIATRY | NEUROTROPHIC FACTOR | FACTOR MESSENGER-RNA | VOLUNTARY EXERCISE | ADULT HIPPOCAMPAL NEUROGENESIS | SUBVENTRICULAR ZONE | NEUROSCIENCES | DENTATE GYRUS | CARDIOVASCULAR FITNESS | GROWTH-FACTOR-I | Brain-Derived Neurotrophic Factor - genetics | Motor Activity - physiology | Vascular Endothelial Growth Factor A - biosynthesis | Nerve Growth Factor - biosynthesis | Cell Count | Neurotrophin 3 - genetics | Vascular Endothelial Growth Factor A - genetics | Cerebral Cortex - metabolism | Alzheimer Disease - pathology | RNA, Messenger - biosynthesis | Cognition - physiology | Female | Brain-Derived Neurotrophic Factor - biosynthesis | Alzheimer Disease - chemically induced | Alzheimer Disease - psychology | Insulin-Like Growth Factor I - biosynthesis | Maze Learning - physiology | RNA, Messenger - genetics | Fibroblast Growth Factor 2 - biosynthesis | Mice, Transgenic | Nerve Growth Factor - genetics | Reverse Transcriptase Polymerase Chain Reaction | Amyloid beta-Protein Precursor - toxicity | Disease Progression | Hippocampus - metabolism | Neurotrophin 3 - biosynthesis | Animals | Brain - pathology | Environment | Mice | Proteins | Physical fitness | Alzheimer's disease | Analysis
mouse | neurotrophin | enriched environment | stem cell | water maze | Adult neurogenesis | adult neurogenesis | APP23 TRANSGENIC MICE | TERM ENVIRONMENTAL ENRICHMENT | PSYCHIATRY | NEUROTROPHIC FACTOR | FACTOR MESSENGER-RNA | VOLUNTARY EXERCISE | ADULT HIPPOCAMPAL NEUROGENESIS | SUBVENTRICULAR ZONE | NEUROSCIENCES | DENTATE GYRUS | CARDIOVASCULAR FITNESS | GROWTH-FACTOR-I | Brain-Derived Neurotrophic Factor - genetics | Motor Activity - physiology | Vascular Endothelial Growth Factor A - biosynthesis | Nerve Growth Factor - biosynthesis | Cell Count | Neurotrophin 3 - genetics | Vascular Endothelial Growth Factor A - genetics | Cerebral Cortex - metabolism | Alzheimer Disease - pathology | RNA, Messenger - biosynthesis | Cognition - physiology | Female | Brain-Derived Neurotrophic Factor - biosynthesis | Alzheimer Disease - chemically induced | Alzheimer Disease - psychology | Insulin-Like Growth Factor I - biosynthesis | Maze Learning - physiology | RNA, Messenger - genetics | Fibroblast Growth Factor 2 - biosynthesis | Mice, Transgenic | Nerve Growth Factor - genetics | Reverse Transcriptase Polymerase Chain Reaction | Amyloid beta-Protein Precursor - toxicity | Disease Progression | Hippocampus - metabolism | Neurotrophin 3 - biosynthesis | Animals | Brain - pathology | Environment | Mice | Proteins | Physical fitness | Alzheimer's disease | Analysis
Journal Article
American Journal of Pathology, ISSN 0002-9440, 2007, Volume 171, Issue 6, pp. 2012 - 2020
Alzheimer's disease presents morphologically with senile plaques, primarily made of extracellular amyloid-beta (A beta) deposits, and neurofibrillary lesions,...
NEUROFIBRILLARY TANGLES | PROTEIN | FIBRILS | ALZHEIMERS-DISEASE | MOUSE MODEL | A-BETA | EXOGENOUS INDUCTION | LEADS | NEURODEGENERATION | PATHOLOGY | Tauopathies - genetics | Amyloid beta-Peptides - toxicity | Cell Extracts - administration & dosage | Cell Extracts - toxicity | Tauopathies - pathology | Mice, Transgenic | Amyloid beta-Protein Precursor - toxicity | Alzheimer Disease - pathology | Tauopathies - metabolism | Animals | tau Proteins - genetics | Alzheimer Disease - metabolism | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Female | Amyloid beta-Protein Precursor - administration & dosage | Brain Chemistry | Mice | Amyloid beta-Peptides - administration & dosage | Alzheimer Disease - genetics
NEUROFIBRILLARY TANGLES | PROTEIN | FIBRILS | ALZHEIMERS-DISEASE | MOUSE MODEL | A-BETA | EXOGENOUS INDUCTION | LEADS | NEURODEGENERATION | PATHOLOGY | Tauopathies - genetics | Amyloid beta-Peptides - toxicity | Cell Extracts - administration & dosage | Cell Extracts - toxicity | Tauopathies - pathology | Mice, Transgenic | Amyloid beta-Protein Precursor - toxicity | Alzheimer Disease - pathology | Tauopathies - metabolism | Animals | tau Proteins - genetics | Alzheimer Disease - metabolism | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Female | Amyloid beta-Protein Precursor - administration & dosage | Brain Chemistry | Mice | Amyloid beta-Peptides - administration & dosage | Alzheimer Disease - genetics
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2011, Volume 286, Issue 5, pp. 3209 - 3218
In protein conformational disorders ranging from Alzheimer to Parkinson disease, proteins of unrelated sequence misfold into a similar array of aggregated...
FIBRIL FORMATION | METHYLENE-BLUE | IN-VITRO | PROTEIN OLIGOMERS | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | A-BETA | TANNIC-ACID | SHEET STRUCTURES | ALPHA-SYNUCLEIN | AGGREGATION | Cell Survival - drug effects | Molecular Weight | Amyloid beta-Protein Precursor - chemistry | Cells, Cultured | Solubility | Rats | Structure-Activity Relationship | Amyloid - chemistry | Amyloid beta-Protein Precursor - toxicity | Adrenal Medulla - cytology | Animals | Protein Conformation | Amyloid beta-Protein Precursor - antagonists & inhibitors | Index Medicus | Protein Structure and Folding | Protein Misfolding | Protein Self-assembly | Protein Aggregation | Amyloid | Peptide Conformation | Protein Folding
FIBRIL FORMATION | METHYLENE-BLUE | IN-VITRO | PROTEIN OLIGOMERS | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | A-BETA | TANNIC-ACID | SHEET STRUCTURES | ALPHA-SYNUCLEIN | AGGREGATION | Cell Survival - drug effects | Molecular Weight | Amyloid beta-Protein Precursor - chemistry | Cells, Cultured | Solubility | Rats | Structure-Activity Relationship | Amyloid - chemistry | Amyloid beta-Protein Precursor - toxicity | Adrenal Medulla - cytology | Animals | Protein Conformation | Amyloid beta-Protein Precursor - antagonists & inhibitors | Index Medicus | Protein Structure and Folding | Protein Misfolding | Protein Self-assembly | Protein Aggregation | Amyloid | Peptide Conformation | Protein Folding
Journal Article
Nature Communications, ISSN 2041-1723, 2012, Volume 3, Issue 1, pp. 1312 - 1312
The conserved kinases PAR-1/MARK are critically involved in processes such as asymmetric cell division, cell polarity and neuronal differentiation. Their...
DENDRITIC SPINES | DESTRUCTION | POLARITY | PHOSPHORYLATION | SYNAPSES | ALZHEIMERS-DISEASE | AMYLOID-BETA | MULTIDISCIPLINARY SCIENCES | F-BOX | NEUROMUSCULAR-JUNCTION | PROTEIN-KINASES | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Retina - metabolism | Retina - growth & development | Humans | Caenorhabditis elegans Proteins - metabolism | tau Proteins - metabolism | Male | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Drosophila melanogaster - metabolism | Ubiquitination | Synapses - metabolism | tau Proteins - genetics | Proteolysis | Retina - enzymology | Amyloid beta-Protein Precursor - metabolism | HEK293 Cells | Cell Cycle Proteins - genetics | Female | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Ubiquitin-Protein Ligases - metabolism | Synapses - enzymology | Amyloid beta-Protein Precursor - toxicity | Animals | Alzheimer Disease - metabolism | Drosophila melanogaster - enzymology | Drosophila melanogaster - growth & development | Drosophila Proteins - genetics | Alzheimer Disease - genetics | Ubiquitin-Protein Ligases - genetics | Caenorhabditis elegans Proteins - genetics | Index Medicus
DENDRITIC SPINES | DESTRUCTION | POLARITY | PHOSPHORYLATION | SYNAPSES | ALZHEIMERS-DISEASE | AMYLOID-BETA | MULTIDISCIPLINARY SCIENCES | F-BOX | NEUROMUSCULAR-JUNCTION | PROTEIN-KINASES | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Retina - metabolism | Retina - growth & development | Humans | Caenorhabditis elegans Proteins - metabolism | tau Proteins - metabolism | Male | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Drosophila melanogaster - metabolism | Ubiquitination | Synapses - metabolism | tau Proteins - genetics | Proteolysis | Retina - enzymology | Amyloid beta-Protein Precursor - metabolism | HEK293 Cells | Cell Cycle Proteins - genetics | Female | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Ubiquitin-Protein Ligases - metabolism | Synapses - enzymology | Amyloid beta-Protein Precursor - toxicity | Animals | Alzheimer Disease - metabolism | Drosophila melanogaster - enzymology | Drosophila melanogaster - growth & development | Drosophila Proteins - genetics | Alzheimer Disease - genetics | Ubiquitin-Protein Ligases - genetics | Caenorhabditis elegans Proteins - genetics | Index Medicus
Journal Article
Neuroscience, ISSN 0306-4522, 2010, Volume 169, Issue 1, pp. 516 - 531
Abstract A central issue in the pathogenesis of tauopathy is the question of how tau protein dysfunction leads to neurodegeneration. We have previously...
Neurology | APP | Tau | axonal degeneration | spheroids | head injury | immunization | Immunization | Head injury | Axonal degeneration | Spheroids | HEAD-INJURY | FRONTOTEMPORAL DEMENTIA | AMYLOID PRECURSOR PROTEIN | NEUROSCIENCES | TRAUMATIC BRAIN-INJURY | STEREOLOGICAL ESTIMATION | A-BETA-PEPTIDE | CENTRAL-NERVOUS-SYSTEM | PROGRESSIVE SUPRANUCLEAR PALSY | TRANSGENIC MICE | CORTICOBASAL DEGENERATION | Humans | Ataxia - etiology | Brain Injuries - metabolism | Amyloid beta-Protein Precursor - immunology | Alzheimer Disease - pathology | Neuropil - ultrastructure | tau Proteins - genetics | Neurites - ultrastructure | tau Proteins - physiology | Disease Models, Animal | Mice, Inbred C57BL | Mice, Transgenic | Recombinant Fusion Proteins - toxicity | Brain Injuries - genetics | Microscopy, Electron | Amyloid beta-Protein Precursor - toxicity | Nerve Degeneration - pathology | Mice, Knockout | tau Proteins - deficiency | Amyloid beta-Protein Precursor - genetics | Animals | Axons - pathology | Alzheimer Disease - metabolism | Recombinant Fusion Proteins - genetics | Mice | Plaque, Amyloid - ultrastructure | Alzheimer Disease - genetics | Brain Injuries - pathology
Neurology | APP | Tau | axonal degeneration | spheroids | head injury | immunization | Immunization | Head injury | Axonal degeneration | Spheroids | HEAD-INJURY | FRONTOTEMPORAL DEMENTIA | AMYLOID PRECURSOR PROTEIN | NEUROSCIENCES | TRAUMATIC BRAIN-INJURY | STEREOLOGICAL ESTIMATION | A-BETA-PEPTIDE | CENTRAL-NERVOUS-SYSTEM | PROGRESSIVE SUPRANUCLEAR PALSY | TRANSGENIC MICE | CORTICOBASAL DEGENERATION | Humans | Ataxia - etiology | Brain Injuries - metabolism | Amyloid beta-Protein Precursor - immunology | Alzheimer Disease - pathology | Neuropil - ultrastructure | tau Proteins - genetics | Neurites - ultrastructure | tau Proteins - physiology | Disease Models, Animal | Mice, Inbred C57BL | Mice, Transgenic | Recombinant Fusion Proteins - toxicity | Brain Injuries - genetics | Microscopy, Electron | Amyloid beta-Protein Precursor - toxicity | Nerve Degeneration - pathology | Mice, Knockout | tau Proteins - deficiency | Amyloid beta-Protein Precursor - genetics | Animals | Axons - pathology | Alzheimer Disease - metabolism | Recombinant Fusion Proteins - genetics | Mice | Plaque, Amyloid - ultrastructure | Alzheimer Disease - genetics | Brain Injuries - pathology
Journal Article