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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
The Journal of Cell Biology, ISSN 0021-9525, 8/2007, Volume 178, Issue 5, pp. 829 - 841
The tumor necrosis factor type 1 death receptor (TNFR1) contributes to apoptosis. TNFR1, a subgroup of the TNFR superfamily, contains a cytoplasmic death... 
Pathology | Neurons | Transgenic animals | Entorhinal cortex | Memory | Antibodies | Amyloids | Alzheimers disease | Hippocampus | Microglia | TNF RECEPTOR | SECRETASE EXPRESSION | KAPPA-B ACTIVATION | COGNITIVE DECLINE | CEREBRAL-HEMORRHAGE | IN-VIVO | PRECURSOR PROTEIN | TRANSGENIC MOUSE MODEL | NEURONAL LOSS | NEOCORTICAL NEUROFIBRILLARY TANGLES | CELL BIOLOGY | Tumor Necrosis Factor-alpha - metabolism | Amyloid Precursor Protein Secretases - genetics | Memory Disorders - physiopathology | Microglia - metabolism | Memory Disorders - genetics | Humans | Memory Disorders - metabolism | NF-kappa B - metabolism | Neurons - cytology | Aspartic Acid Endopeptidases - genetics | Receptors, Tumor Necrosis Factor, Type I - metabolism | Alzheimer Disease - pathology | Amyloid beta-Peptides - genetics | Gene Deletion | Amyloid beta-Peptides - metabolism | Neprilysin - genetics | Neurons - metabolism | Cerebral Amyloid Angiopathy - genetics | Disease Models, Animal | Microglia - cytology | Insulysin - metabolism | Promoter Regions, Genetic | Alzheimer Disease - physiopathology | Cerebral Amyloid Angiopathy - physiopathology | Gene Expression Regulation | Behavior, Animal - physiology | Mice, Transgenic | Neprilysin - metabolism | Receptors, Tumor Necrosis Factor, Type I - genetics | Mice, Knockout | Learning - physiology | Amyloid Precursor Protein Secretases - metabolism | Cerebral Amyloid Angiopathy - pathology | Animals | Aspartic Acid Endopeptidases - metabolism | Alzheimer Disease - metabolism | Insulysin - genetics | Mice | Alzheimer Disease - genetics
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 12/2016, Volume 53, Issue 10, pp. 6730 - 6744
Our earlier studies showed that insulin receptor (IR) dysfunction along with neuroinflammation and amyloidogenesis played a major role in streptozotocin... 
Neurology | Neurotrophic factor | Neurosciences | Biomedicine | Memantine | Insulin receptor signaling | Astrocytes | Neurobiology | Amyloidogenic protein expression | Streptozotocin | Cell Biology | AMYLOID BETA-PROTEIN | NMDA RECEPTOR | ALZHEIMERS-DISEASE | NEUROSCIENCES | COGNITIVE DECLINE | PEPTIDE LEVELS | IN-VIVO | RAT-BRAIN | EXPRESSION | CELL-LINE | TRANSGENIC MICE | Inflammation - pathology | Streptozocin | Astrocytes - pathology | Nitrites - metabolism | NF-kappa B - metabolism | Nerve Growth Factors - metabolism | Insulin Receptor Substrate Proteins - metabolism | RNA, Messenger - metabolism | Inflammation - metabolism | Amyloid - metabolism | Nervous System - pathology | Amyloid beta-Protein Precursor - metabolism | Phosphorylation - drug effects | Biomarkers - metabolism | Astrocytes - drug effects | Insulysin - metabolism | Memantine - pharmacology | RNA, Messenger - genetics | Rats | Down-Regulation - drug effects | Glycogen Synthase Kinase 3 - metabolism | Glycogen Synthase Kinase 3 beta - metabolism | Animals | Signal Transduction - drug effects | Nerve Growth Factors - genetics | Cyclooxygenase 2 - metabolism | Fluorescent Antibody Technique | Cell Line, Tumor | Receptor, Insulin - metabolism | Oxidative Stress - drug effects | Astrocytes - metabolism | Nitric Oxide Synthase Type II - metabolism | COX-2 inhibitors | Methyl aspartate | Amyloid beta-protein | Amyloidosis | Intermediate filament proteins | Nervous system agents | Alzheimer's disease | Insulin | Studies | Proteins
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 05/2013, Volume 288, Issue 18, pp. 12920 - 12931
Journal Article
Neurodegenerative Diseases, ISSN 1660-2854, 09/2012, Volume 11, Issue 1, pp. 33 - 41
Background: Alzheimer’s disease (AD) is characterized by progressive neuronal loss and cognitive decline. Epidemiological studies suggest that the risk of AD... 
Original Paper | Neuroinflammation | β-Secretase-1 | Alzheimer's disease | Insulin-degrading enzyme | Spatial memory | APP | NEPRILYSIN | PROTEIN | ALZHEIMERS-DISEASE | PATHOLOGY | NEUROSCIENCES | PEPTIDE | CLINICAL NEUROLOGY | AMYLOID-BETA | GENDER | TRANSGENIC MOUSE MODEL | beta-Secretase-1 | BRAIN | Amyloid Precursor Protein Secretases - genetics | Glial Fibrillary Acidic Protein - genetics | Microglia - metabolism | Humans | Male | Aspartic Acid Endopeptidases - genetics | Interleukin-1beta - genetics | Glial Fibrillary Acidic Protein - metabolism | RNA, Messenger - metabolism | Antigens, CD - genetics | Antigens, CD - metabolism | Learning Disorders - pathology | CD11b Antigen - genetics | Interleukin-1beta - metabolism | Amyloid beta-Peptides - metabolism | Female | Neprilysin - genetics | Insulysin - metabolism | Enzyme-Linked Immunosorbent Assay | Maze Learning - physiology | Gene Expression Regulation - genetics | Presenilin-1 - genetics | Mice, Transgenic | Neprilysin - metabolism | Reaction Time - genetics | Sex Characteristics | Antigens, Differentiation, Myelomonocytic - genetics | Amyloid Precursor Protein Secretases - metabolism | Amyloid beta-Protein Precursor - genetics | Animals | Analysis of Variance | Antigens, Differentiation, Myelomonocytic - metabolism | Aspartic Acid Endopeptidases - metabolism | Insulysin - genetics | Learning Disorders - genetics | Mice | CD11b Antigen - metabolism
Journal Article
Journal Article
Endocrinology, ISSN 0013-7227, 07/2011, Volume 152, Issue 7, pp. 2704 - 2715
In most cases, the molecular mechanism underlying the pathogenesis of sporadic Alzheimer's disease (AD) is unknown. Elevated basal cortisol levels in AD... 
SECRETASE | IN-VITRO | PROTEIN | ALZHEIMERS-DISEASE | MOUSE MODEL | ENDOCRINOLOGY & METABOLISM | RECEPTOR | RAT-BRAIN | ENZYMATIC-ACTIVITY | STRESS | TRANSGENIC MICE | Amyloid Precursor Protein Secretases - genetics | Receptors, Glucocorticoid - antagonists & inhibitors | Corticosterone - pharmacology | Male | Receptors, Glucocorticoid - metabolism | Aspartic Acid Endopeptidases - genetics | Hippocampus - drug effects | RNA, Messenger - metabolism | Cerebral Cortex - cytology | Cerebral Cortex - metabolism | Matrix Metalloproteinase 9 - metabolism | Dexamethasone - pharmacology | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Cerebral Cortex - drug effects | Astrocytes - cytology | Astrocytes - drug effects | Insulysin - metabolism | Nerve Tissue Proteins - antagonists & inhibitors | Aspartic Acid Endopeptidases - antagonists & inhibitors | Mice, Inbred C57BL | Cells, Cultured | Random Allocation | Hippocampus - cytology | Nerve Tissue Proteins - genetics | Gene Expression Regulation - drug effects | Nerve Tissue Proteins - metabolism | Hippocampus - metabolism | Amyloid Precursor Protein Secretases - metabolism | Amyloid beta-Protein Precursor - genetics | Animals | Aspartic Acid Endopeptidases - metabolism | Receptors, Glucocorticoid - genetics | Glucocorticoids - pharmacology | Mice | RNA, Small Interfering | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Astrocytes - metabolism
Journal Article
Journal Article
The FASEB journal : official publication of the Federation of American Societies for Experimental Biology, ISSN 0892-6638, 2004, Volume 18, Issue 7, pp. 902 - 904
Journal Article