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Immunity (Cambridge, Mass.), ISSN 1074-7613, 2017, Volume 47, Issue 3, pp. 566 - 581.e9
...), multiple sclerosis (MS), and Alzheimer’s disease (AD) and in microglia surrounding neuritic β-amyloid (Aβ... 
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 | Myeloid cells | Disease | Transcription | Neurodegenerative diseases | Genes | Homeostasis | Microglia | Neurological diseases | Proteins | Molecular modelling | Restoration | Neurodegeneration | Apolipoprotein E | Rodents | β-Amyloid | Plaques | Phagocytosis | Apoptosis
Journal Article
Seminars in immunopathology, ISSN 1863-2300, 2011, Volume 34, Issue 1, pp. 43 - 62
The interaction of coagulation factors with the perivascular environment affects the development of disease in ways that extend beyond their traditional roles in the acute hemostatic cascade... 
Autoimmunity | Complement receptor 3 | Multiple sclerosis | Stroke | Alzheimer’s disease | Internal Medicine | Macrophages | Blood brain barrier | Inflammatory disease | Microglia | Biomedicine | Immunology | Rheumatoid arthritis | CD11b/CD18 | Atherosclerosis | Plasminogen | Anticoagulant therapy | Alzheimer's disease | ALZHEIMERS-DISEASE | IMMUNOLOGY | PATHOLOGY | GAMMA-C-DOMAIN | BINDING-SITE | CENTRAL-NERVOUS-SYSTEM | MULTIPLE-SCLEROSIS LESIONS | CRYSTAL-STRUCTURE | BLOOD-BRAIN-BARRIER | INTEGRIN ALPHA(M)BETA | PROTEASE-ACTIVATED RECEPTORS | PERIPHERAL ARTERIAL-DISEASE | Colitis - genetics | Humans | Brain Injuries - metabolism | Arthritis, Rheumatoid - metabolism | Bacterial Infections - genetics | Inflammation - metabolism | Blood Coagulation - immunology | Muscular Dystrophy, Duchenne - immunology | Alzheimer Disease - immunology | Fibrinogen - immunology | Thromboplastin - immunology | Pulmonary Fibrosis - immunology | Vascular Diseases - genetics | Brain Injuries - genetics | Thrombin - genetics | Kidney Diseases - immunology | Arthritis, Rheumatoid - genetics | Neoplasms - immunology | Colitis - metabolism | Muscular Dystrophy, Duchenne - genetics | Bacterial Infections - metabolism | Neoplasms - metabolism | Pulmonary Fibrosis - genetics | Spinal Cord Injuries - genetics | Kidney Diseases - genetics | Stroke - genetics | Brain Injuries - immunology | Neoplasms - genetics | Bacterial Infections - immunology | Pulmonary Fibrosis - metabolism | Colitis - immunology | Thrombin - immunology | Stroke - immunology | Kidney Diseases - metabolism | Multiple Sclerosis - metabolism | Vascular Diseases - immunology | Spinal Cord Injuries - metabolism | Multiple Sclerosis - genetics | Inflammation - immunology | Fibrinogen - genetics | Stroke - metabolism | Animals | Thromboplastin - genetics | Alzheimer Disease - metabolism | Fibrinogen - metabolism | Inflammation - genetics | Multiple Sclerosis - immunology | Blood Coagulation - genetics | Spinal Cord Injuries - immunology | Muscular Dystrophy, Duchenne - metabolism | Thrombin - metabolism | Thromboplastin - metabolism | Alzheimer Disease - genetics | Arthritis, Rheumatoid - immunology | Vascular Diseases - metabolism | Nervous system diseases | Bacterial infections | Oncology, Experimental | Thrombin | Inflammation | Anticoagulants (Medicine) | Research | Rheumatoid factor | Fibrin | Fibrinogen | Genetic research | Colitis | Cancer | Traumatic brain injury | Coagulation | Tissue factor | hemostasis | Spinal cord injury | Inflammatory diseases | Kidney | Signal transduction | Duchenne's muscular dystrophy | Neurodegenerative diseases | Therapeutic applications | Thrombosis | Coagulation factors | Infection | Molecular modelling | Fibrosis | Brain injury
Journal Article
Experimental & molecular medicine, ISSN 2092-6413, 2015, Volume 47, Issue 3, pp. e147 - e147
Mammalian cells remove misfolded proteins using various proteolytic systems, including the ubiquitin (Ub)-proteasome system (UPS), chaperone mediated autophagy... 
MEDICINE, RESEARCH & EXPERIMENTAL | UBIQUITIN-PROTEASOME SYSTEM | CHAPERONE-MEDIATED AUTOPHAGY | ALPHA-SYNUCLEIN AGGREGATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | QUALITY CONTROL DEGRADATION | CENTRAL-NERVOUS-SYSTEM | AMYOTROPHIC-LATERAL-SCLEROSIS | SOD1 TRANSGENIC MICE | ENDOPLASMIC-RETICULUM STRESS | END RULE PATHWAY | PARKINSONS-DISEASE | Proteostasis Deficiencies - metabolism | Humans | Ubiquitin - metabolism | tau Proteins - metabolism | Parkinson Disease - drug therapy | Molecular Targeted Therapy | Neurodegenerative Diseases - drug therapy | Amyotrophic Lateral Sclerosis - drug therapy | Autophagy - drug effects | DNA-Binding Proteins - metabolism | PrPSc Proteins - metabolism | Lysosomes - metabolism | Proteolysis | Amyloid beta-Peptides - metabolism | Parkinson Disease - metabolism | Huntington Disease - drug therapy | Superoxide Dismutase - metabolism | Prion Diseases - drug therapy | Alzheimer Disease - drug therapy | Neurodegenerative Diseases - metabolism | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Huntingtin Protein | Animals | Alzheimer Disease - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Huntington Disease - genetics | Mutation | Proteasome Endopeptidase Complex - metabolism | alpha-Synuclein - metabolism | Prion Diseases - metabolism | Review
Journal Article
Journal of the neurological sciences, ISSN 0022-510X, 2012, Volume 323, Issue 1-2, pp. 1 - 8
...), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS). Several studies have demonstrated that altered kynurenine metabolism plays an important role in the pathogenesis of this group of diseases... 
Neurology | Aging | Alzheimer's disease (AD) | Amyotrophic lateral sclerosis (ALS) | Huntington's disease (HD) | Parkinson's disease (PD) | Kynurenine pathway | TRYPTOPHAN-METABOLISM | ACID | ALZHEIMERS-DISEASE | INDOLEAMINE 2,3-DIOXYGENASE | DISORDERS | NEUROSCIENCES | CLINICAL NEUROLOGY | QUINOLINATE LEVELS | CELL-DEATH | 3-MONOOXYGENASE | BRAIN | PARKINSONS-DISEASE | Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism | Neuroprotective Agents - therapeutic use | Microglia - metabolism | Kynurenine - therapeutic use | Humans | Neurodegenerative Diseases - prevention & control | Parkinson Disease - drug therapy | Kynurenic Acid - metabolism | Molecular Targeted Therapy | Neurodegenerative Diseases - drug therapy | Quinolinic Acid - antagonists & inhibitors | Tryptophan - metabolism | Amyotrophic Lateral Sclerosis - drug therapy | Inflammation - metabolism | Neuroprotective Agents - pharmacology | Alzheimer Disease - prevention & control | Neurons - metabolism | Parkinson Disease - metabolism | Kynurenine - metabolism | Huntington Disease - drug therapy | Receptors, G-Protein-Coupled - drug effects | Receptors, G-Protein-Coupled - physiology | Receptors, N-Methyl-D-Aspartate - drug effects | Kynurenine - pharmacology | Enzyme Inhibitors - pharmacology | Alzheimer Disease - drug therapy | Neurodegenerative Diseases - metabolism | Enzyme Inhibitors - therapeutic use | Huntington Disease - metabolism | Kynurenine - analogs & derivatives | Receptors, N-Methyl-D-Aspartate - physiology | Parkinson Disease - prevention & control | Animals | Quinolinic Acid - metabolism | Alzheimer Disease - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Neurotoxins - metabolism | Kynurenic Acid - antagonists & inhibitors | Aging - metabolism | Enzymes | Nervous system diseases | Enzyme inhibitors | Parkinson's disease | Metabolites | Huntington's chorea | Analysis | Physiological aspects | Tryptophan | Amyotrophic lateral sclerosis | Health aspects | Alzheimer's disease | Index Medicus
Journal Article
Cell (Cambridge), ISSN 0092-8674, 2017, Volume 170, Issue 4, pp. 649 - 663.e13
Journal Article
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... 
Pathology | Neurosciences | Congophilic amyloid angiopathy | Medicine & Public Health | Alzheimer’s disease | Astrocytes | Cerebral glucose metabolism | Alzheimer's disease | MICROVASCULAR PATHOLOGY | ALZHEIMERS-DISEASE | NEUROVASCULAR MECHANISMS | PATHOLOGY | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | CLINICAL NEUROLOGY | GLUCOSE | MOUSE MODEL | LACTATE | A-BETA | SMOOTH-MUSCLE-CELLS | ANGIOPATHY | 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 | 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
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2002, Volume 296, Issue 5575, pp. 1991 - 1995
...Neurodegenerative disorders as diverse as Alzheimer's disease, Parkinson's disease, priori diseases, Huntington's disease, frontotemporal dementia, and motor... 
Nervous system diseases | Reviews | Neurodegenerative diseases | Disease models | Huntington disease | Parkinson disease | Prion diseases | Amyotrophic lateral sclerosis | Nervous system heredodegenerative disorders | Alzheimers disease | Genetic mutation | Parkinson Disease - therapy | Neurons - pathology | Prion Diseases - genetics | Humans | Peptides - genetics | Tauopathies - pathology | Alzheimer Disease - pathology | Peptides - metabolism | Tauopathies - therapy | Neurons - metabolism | Parkinson Disease - metabolism | Inclusion Bodies - metabolism | Prion Diseases - therapy | Parkinson Disease - pathology | Neurodegenerative Diseases - pathology | Amyotrophic Lateral Sclerosis - therapy | Amyotrophic Lateral Sclerosis - genetics | Alzheimer Disease - therapy | Neurodegenerative Diseases - genetics | Neurodegenerative Diseases - therapy | Prion Diseases - pathology | Neurodegenerative Diseases - metabolism | Parkinson Disease - genetics | Protein Folding | Trinucleotide Repeat Expansion | Proteins - genetics | Amyotrophic Lateral Sclerosis - pathology | Tauopathies - metabolism | Animals | Proteins - metabolism | Alzheimer Disease - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Mutation | Proteins - chemistry | Alzheimer Disease - genetics | Prion Diseases - metabolism | Parkinson's disease | Nervous system | Degeneration | Research | Alzheimer's disease | Proteins | Neurological disorders
Journal Article