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Journal of Neuroscience, ISSN 0270-6474, 03/2010, Volume 30, Issue 9, pp. 3326 - 3338
Journal Article
Acta Neuropathologica, ISSN 0001-6322, 9/2011, Volume 122, Issue 3, pp. 293 - 311
...ORIGINAL PAPER Vascular b-amyloid and early astrocyte alterations impair cerebrovascular function and cerebral metabolism in transgenic arcAb mice Mario... 
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
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
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
Immunity (Cambridge, Mass.), ISSN 1074-7613, 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 | 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
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
Nature (London), ISSN 1476-4687, 2012, Volume 482, Issue 7384, pp. 216 - 220
Our understanding of Alzheimer's disease pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model... 
AMYLOID BETA-PROTEIN | APP | MICROTUBULE-BINDING | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | DOWN-SYNDROME | MOUSE MODEL | TAU | DYSFUNCTION | FIBROBLASTS | SENILE PLAQUES | Neurons - pathology | Coculture Techniques | Humans | Middle Aged | Amyloid beta-Peptides - secretion | tau Proteins - metabolism | Male | Phosphoproteins - metabolism | Endosomes - metabolism | Synapsins - metabolism | Alzheimer Disease - pathology | Cellular Reprogramming | Protease Inhibitors - pharmacology | Amyloid beta-Protein Precursor - secretion | Proteolysis | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Aged, 80 and over | Female | Neurons - metabolism | Phosphorylation - drug effects | Neurons - drug effects | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | Astrocytes - cytology | Biomarkers - metabolism | Induced Pluripotent Stem Cells - pathology | Peptide Fragments - metabolism | Cells, Cultured | Peptide Fragments - secretion | Glycogen Synthase Kinase 3 - metabolism | Amyloid Precursor Protein Secretases - metabolism | Amyloid beta-Protein Precursor - genetics | Models, Biological | Alzheimer Disease - metabolism | Fibroblasts - cytology | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Enzyme Activation | Messenger RNA | Synthesis | Glycogen | Stem cells | Physiological aspects | Research | Alzheimer's disease | Proteins | Phosphorylation | Neurons | Efficiency | Genomes | Mutation | Alzheimers disease
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
Journal of Neuroscience, ISSN 0270-6474, 09/2012, Volume 32, Issue 39, pp. 13454 - 13469
Abnormal deposition and intercellular propagation of alpha-synuclein plays a central role in the pathogenesis of disorders such as Parkinson's Disease (PD) and... 
IMMUNIZATION | PROTEIN | PLASMA | BIOMARKER | ALZHEIMERS-DISEASE | MOUSE MODEL | PATHOLOGY | FC-GAMMA-RIIA | NEUROSCIENCES | NEURODEGENERATIVE DISEASES | PARKINSONS-DISEASE | Synaptic Transmission - physiology | Antibodies - metabolism | Lewy Body Disease - immunology | Humans | alpha-Synuclein - immunology | Extracellular Space - drug effects | Nerve Degeneration - genetics | Cell Communication - physiology | Culture Media, Conditioned - pharmacology | Phosphopyruvate Hydratase - metabolism | Amyloid - ultrastructure | Antigens, CD - metabolism | Neuroglia - drug effects | Brain - metabolism | Lewy Body Disease - genetics | Extracellular Space - metabolism | Amyloid - metabolism | Microfilament Proteins - metabolism | alpha-Synuclein - genetics | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Cell Line | Microscopy, Electron, Transmission | Cytokines - metabolism | Mice, Transgenic | Nerve Degeneration - immunology | Cathepsin D - metabolism | Extracellular Space - immunology | Antibodies - pharmacology | Caveolin 1 - metabolism | Lewy Body Disease - metabolism | Platelet-Derived Growth Factor - metabolism | Animals | Analysis of Variance | Brain - pathology | Immunization, Passive | Neuroglia - metabolism | Mice | Chromatography, Gel | alpha-Synuclein - metabolism | Nerve Degeneration - drug therapy | Astrocytes - metabolism
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 6, pp. e0130624 - e0130624
Neuroinflammation is the local reaction of the brain to infection, trauma, toxic molecules or protein aggregates. The brain resident macrophages, microglia,... 
INTERLEUKIN-1 | ACTIVATION | MOLECULAR PLATFORM | INHIBITION | DISTINCT PATHWAYS | NEUROINFLAMMATION | MULTIDISCIPLINARY SCIENCES | IL-1-BETA | MECHANISMS | RECEPTORS | NALP3 INFLAMMASOME | Microglia - metabolism | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Peptide Fragments - toxicity | Caspase 1 - metabolism | Interleukin-1alpha - metabolism | alpha-Synuclein - pharmacology | Interleukin-1beta - metabolism | Interleukin-1beta - secretion | Microglia - cytology | Brain - cytology | Interleukin-1beta - analysis | Enzyme-Linked Immunosorbent Assay | Microglia - drug effects | Amyloid beta-Peptides - toxicity | Mice, Inbred C57BL | Cells, Cultured | Mice, Knockout | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Caspase 1 - genetics | Caspase 1 - deficiency | Receptors, Purinergic P2X7 - metabolism | Mice | Interleukin-18 - metabolism | Astrocytes - metabolism | Cytokines | Health aspects | Nervous system diseases | Brain | Cell culture | Traumatic brain injury | Peptides | Aluminum sulfate | Homeostasis | Nervous system | Activation | Macrophages | Synuclein | Proteins | Rodents | Amyloid | Life sciences | Communication | Immune system | Neurodegenerative diseases | Astrocytes | Inflammation | Trauma | Molecular chains | Microglia | Interleukin 18 | Mode of action | Neurological diseases | Nigericin |