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Acta Neuropathologica, ISSN 0001-6322, 9/2011, Volume 122, Issue 3, pp. 293 - 311
Cerebrovascular lesions related to congophilic amyloid angiopathy (CAA) often accompany deposition of β-amyloid (Aβ) in Alzheimer’s disease (AD), leading to... 
Pathology | Neurosciences | Congophilic amyloid angiopathy | Medicine & Public Health | Alzheimer’s disease | Astrocytes | Cerebral glucose metabolism | Alzheimer's disease | MICROVASCULAR PATHOLOGY | ALZHEIMERS-DISEASE | NEUROVASCULAR MECHANISMS | GLUCOSE-UTILIZATION | PATHOLOGY | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | CLINICAL NEUROLOGY | MOUSE MODEL | ENDOTHELIAL-CELLS | A-BETA | SMOOTH-MUSCLE-CELLS | RAT-BRAIN | Microdialysis - methods | Humans | Astrocytes - pathology | Dystroglycans - metabolism | Glucose Transporter Type 1 - metabolism | Muscle, Smooth - ultrastructure | Glial Fibrillary Acidic Protein - metabolism | Microscopy, Electron, Scanning - methods | Amyloid beta-Peptides - genetics | Amyloid beta-Peptides - metabolism | Cell Culture Techniques | Disease Models, Animal | Endothelium - pathology | Mice, Transgenic | Cerebral Arteries - ultrastructure | Basement Membrane - metabolism | Disease Progression | Symporters - metabolism | Astrocytes - ultrastructure | Blood-Brain Barrier - pathology | Cerebral Arteries - metabolism | Brain - pathology | Glucose - metabolism | Plaque, Amyloid - metabolism | Mice | Astrocytes - metabolism | Blood-Brain Barrier - physiopathology | Basement Membrane - pathology | Cerebral Amyloid Angiopathy - complications | Monocarboxylic Acid Transporters - metabolism | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Hemorrhage - etiology | Amyloid beta-Protein Precursor - metabolism | Lactase - metabolism | Cerebral Amyloid Angiopathy - genetics | Astrocytes - drug effects | Plaque, Amyloid - pathology | Gene Expression Regulation - genetics | Hemorrhage - metabolism | Muscle, Smooth - metabolism | Cerebrovascular Disorders - etiology | Cerebral Amyloid Angiopathy - pathology | Animals | Endothelium - metabolism | Glucose Transporter Type 1 - genetics | Symporters - genetics | Cerebral Arteries - pathology | Laminin - metabolism | Monocarboxylic Acid Transporters - genetics | Cerebrovascular Disorders - pathology | Hemorrhage - pathology | Muscle, Smooth - pathology | Index Medicus | Glucose transporter | Leakage | Brain | Neurodegenerative diseases | Cognitive ability | Transgenic mice | Blood vessels | Data processing | Smooth muscle | beta -Amyloid | Glucose transport | Metabolism | Amyloid precursor protein | Blood-brain barrier | Cerebral blood flow | Lactic acid | Mutation | Original Paper
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
BBA - Molecular and Cell Biology of Lipids, ISSN 1388-1981, 06/2016, Volume 1861, Issue 6, pp. 491 - 500
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
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
Neuron, ISSN 0896-6273, 04/2013, Volume 78, Issue 1, pp. 57 - 64
Valosin-containing protein (VCP) is a highly expressed member of the type II AAA+ ATPase family. mutations are the cause of inclusion body myopathy, Paget’s... 
LIPID-PEROXIDATION | SPINAL-CORD PATHOLOGY | MOUSE MODEL | ALS | AMYOTROPHIC-LATERAL-SCLEROSIS | DYSFUNCTION | BONE | NEUROSCIENCES | PAGET-DISEASE | TRANSGENIC MICE | REVEALS | RNA, Small Interfering - genetics | Humans | Middle Aged | Male | Frontotemporal Dementia - metabolism | Neurons - ultrastructure | Muscular Dystrophies, Limb-Girdle - genetics | Adenosine Triphosphate - metabolism | Membrane Potential, Mitochondrial - genetics | Muscular Dystrophies, Limb-Girdle - pathology | NAD - metabolism | Fibroblasts - metabolism | Animals, Newborn | Frontotemporal Dementia - genetics | Magnesium - metabolism | Mitochondria - pathology | Fibroblasts - pathology | Mutation - genetics | Myositis, Inclusion Body - genetics | Osteitis Deformans - pathology | Muscular Dystrophies, Limb-Girdle - metabolism | Analysis of Variance | Luminescent Proteins - genetics | Adenosine Triphosphatases - genetics | Mice | Lipid Peroxidation - genetics | RNA, Small Interfering - metabolism | Valosin Containing Protein | Osteitis Deformans - metabolism | Family Health | Cerebral Cortex - cytology | Case-Control Studies | Osteitis Deformans - genetics | Transfection | Mitochondria - genetics | Cell Cycle Proteins - genetics | Myositis, Inclusion Body - pathology | Adult | Female | Neuroblastoma - pathology | Frontotemporal Dementia - pathology | Adenosine Triphosphatases - deficiency | Mice, Inbred C57BL | Cells, Cultured | Cell Cycle Proteins - deficiency | Mitochondria - metabolism | Animals | Oxygen Consumption - genetics | Myositis, Inclusion Body - metabolism | Aged | Nervous system diseases | Neurosciences | Genes | Amyotrophic lateral sclerosis | Genetic aspects | Adenosine triphosphatase | Dementia | Proteins | Medical research | Phosphorylation | Biomedical research | Disease | Rodents | Respiration | Experiments | Patients | Index Medicus | Report
Journal Article
Neuron, 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 | Index Medicus | 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
Neuron, ISSN 0896-6273, 03/2012, Volume 73, Issue 6, pp. 1116 - 1126
The precise connectivity of inputs and outputs is critical for cerebral cortex function; however, the cellular mechanisms that establish these connections are... 
SYNAPTIC SPECIFICITY | ADULT BRAIN | SIGNALING PATHWAY | IN-VIVO | BOC | GROWTH | MECHANISMS | AXON-GUIDANCE | MEMBRANE-PROTEINS | NEUROSCIENCES | CEREBRAL-CORTEX | Silver Staining - methods | RNA, Small Interfering - genetics | Furans - metabolism | Electric Stimulation | gamma-Aminobutyric Acid - metabolism | Channelrhodopsins | Hedgehog Proteins - metabolism | Dendritic Spines - metabolism | Functional Laterality - genetics | Nerve Net - cytology | Synaptophysin - genetics | Neurons - ultrastructure | Neurons - metabolism | Repressor Proteins - metabolism | Gene Expression Regulation, Developmental - physiology | Synaptophysin - metabolism | Animals, Newborn | Fluorobenzenes - metabolism | Tumor Suppressor Proteins - metabolism | Matrix Attachment Region Binding Proteins - metabolism | Dendritic Spines - physiology | Mice, Transgenic | Synapses - ultrastructure | Electroporation - methods | Mutation - genetics | Corpus Callosum - cytology | Patch-Clamp Techniques | Immunoglobulin G - genetics | Cerebral Cortex - growth & development | Luminescent Proteins - genetics | Corpus Callosum - growth & development | Mice | Immunoglobulin G - metabolism | RNA, Small Interfering - metabolism | Receptors, Cell Surface - genetics | Membrane Potentials - genetics | Age Factors | Gene Expression Regulation, Developmental - genetics | Phosphopyruvate Hydratase - metabolism | Cerebral Cortex - cytology | DNA-Binding Proteins - metabolism | Synapses - metabolism | Hedgehog Proteins - genetics | Pyramidal Tracts - physiology | Stilbamidines - metabolism | Receptors, Cell Surface - metabolism | Nuclear Proteins - metabolism | Transcription Factors - metabolism | Animals | Nerve Net - metabolism | In Vitro Techniques | Luminescent Proteins - metabolism | Stem cell research | Neurosciences | Nervous system diseases | Neurons | Stem cells | Collateralized debt obligations | Physiological aspects | Cells | Proteins | Transcription factors | Software | Sucrose | Synaptogenesis | Circuits | Hedgehog protein | Neural networks | Pyramidal cells | Cortex | Synapses | Index Medicus
Journal Article
Immunity, ISSN 1074-7613, 09/2017, Volume 47, Issue 3, pp. 566 - 581.e9
Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic function during neurodegenerative disorders. We identified a... 
Alzheimer’s disease | multiple sclerosis | transcriptional regulation | neurodegeneration | TREM2 | APOE | amyotrophic lateral sclerosis | microglia | Alzheimer's disease | GENE-EXPRESSION SIGNATURE | ACTIVATION | MULTIPLE-SCLEROSIS | ALZHEIMERS-DISEASE | MOUSE MODEL | MACROPHAGE | MICE | IMMUNOLOGY | DEFICIENCY | APOLIPOPROTEIN-E | CELL-DEATH | Microglia - metabolism | Apolipoproteins E - deficiency | Membrane Glycoproteins - metabolism | Humans | Cerebral Cortex - pathology | Transcriptome | Apoptosis - genetics | Monocytes - metabolism | Gene Expression Profiling | Monocytes - immunology | Phagocytosis - genetics | Neurodegenerative Diseases - immunology | Apolipoproteins E - metabolism | Cerebral Cortex - metabolism | Alzheimer Disease - pathology | Microglia - immunology | Superoxide Dismutase-1 - metabolism | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Female | Neurons - metabolism | Disease Models, Animal | Gene Targeting | Plaque, Amyloid - pathology | Signal Transduction | Gene Expression Regulation | Phagocytosis - immunology | Immune Tolerance | Mice, Transgenic | Neurodegenerative Diseases - genetics | Neurodegenerative Diseases - metabolism | Mice, Knockout | Encephalomyelitis, Autoimmune, Experimental | Phenotype | Animals | Apoptosis - immunology | Apolipoproteins E - genetics | Alzheimer Disease - metabolism | Superoxide Dismutase-1 - genetics | Plaque, Amyloid - metabolism | Mice | Alzheimer Disease - genetics | Transforming Growth Factor beta - metabolism | Receptors, Immunologic - metabolism | Cluster Analysis | Nervous system diseases | Multiple sclerosis | Neurons | Analysis | Amyotrophic lateral sclerosis | Genetic aspects | Genetic transcription | Apolipoproteins | Brain | Animal models | Disease | Transcription | Genes | Homeostasis | Sclerosis | Proteins | Restoration | Neurodegeneration | Apolipoprotein E | Rodents | Plaques | Myeloid cells | Neurodegenerative diseases | Microglia | Neurological diseases | Molecular modelling | β-Amyloid | Phagocytosis | Apoptosis | Index Medicus
Journal Article