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Brain Research, ISSN 0006-8993, 2007, Volume 1148, Issue 1, pp. 243 - 248
Abstract A number of studies reported that oxidative and nitrosative damage may be important in the pathogenesis of Alzheimer's disease (AD). However, whether... 
Neurology | Inferior parietal lobule | Mild cognitive impairment | Nitrosative stress | Alzheimer's disease | Protein nitration | Hippocampus | NEURODEGENERATIVE DISORDERS | hippocampus | PEROXYNITRITE | protein nitration | PROTEOMIC IDENTIFICATION | NEUROTOXICITY | NEUROSCIENCES | DAMAGE | nitrosative stress | CREATINE-KINASE BB | TYROSINE | inferior parietal lobule | OXIDATIVELY MODIFIED PROTEINS | mild cognitive impairment | NITROTYROSINE | STRESS | Amnesia - diagnosis | Immunohistochemistry | Predictive Value of Tests | Prognosis | Humans | Oxidative Stress - physiology | Cognition Disorders - metabolism | Male | Parietal Lobe - metabolism | Parietal Lobe - physiopathology | Tyrosine - analogs & derivatives | Brain - metabolism | Up-Regulation - physiology | Aged, 80 and over | Female | Amnesia - metabolism | Biomarkers - metabolism | Alzheimer Disease - physiopathology | Cognition Disorders - physiopathology | Brain - physiopathology | Biomarkers - analysis | Tyrosine - analysis | Disease Progression | Nerve Tissue Proteins - metabolism | Cognition Disorders - diagnosis | Hippocampus - metabolism | Nitrates - metabolism | Tyrosine - metabolism | Amnesia - physiopathology | Alzheimer Disease - metabolism | Alzheimer Disease - genetics | Early Diagnosis | Hippocampus - physiopathology | Development and progression | Analysis
Journal Article
Journal of Neurotrauma, ISSN 0897-7151, 09/2011, Volume 28, Issue 9, pp. 177 - 1717
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2014, Volume 9, Issue 11, p. e111899
Amyloid beta (Abeta) 1-42 oligomers accumulate in brains of patients with Mild Cognitive Impairment (MCI) and disrupt synaptic plasticity processes that... 
ACTIVATION | PROTEIN | LIGANDS | SOLUBLE A-BETA | MULTIDISCIPLINARY SCIENCES | DISEASE | MEMBRANE COMPONENT 1 | SYNAPTIC PLASTICITY | MOLECULAR-BASIS | BRAIN | CELL-DEATH | Protein Structure, Tertiary | Synapses - drug effects | Membrane Proteins - genetics | Humans | Alzheimer Disease - drug therapy | Rats | Receptors, Progesterone - genetics | Cognition - drug effects | Cognition Disorders - drug therapy | Rats, Sprague-Dawley | Receptors, Progesterone - metabolism | Brain - metabolism | Autoradiography | Peptide Fragments - chemistry | Animals | Synapses - metabolism | Alzheimer Disease - metabolism | Protein Binding | Cell Membrane - metabolism | Membrane Proteins - metabolism | Mice | Neurons - metabolism | Amyloid beta-Peptides - chemistry | RNA, Small Interfering - metabolism | Proteins | Oligomers | Hormones, Sex | Chemical properties | Health aspects | Alzheimer's disease | Potentiation | Brain | Neurosciences | Animal models | Toxicity | Spine | Memory | Cognitive ability | Antibodies | Receptors | Rodents | Biocompatibility | Amnesia | Binding | Neurodegenerative diseases | Neurons | Long-term potentiation | Pathological effects | siRNA | Patients | Embryos | Displacement | Membrane proteins | Neurology | Plasticity (synaptic) | Membrane trafficking | Progesterone | Laboratory animals | Alzheimers disease | Synapses | Cancer | Apoptosis | Animal cognition
Journal Article
Glia, ISSN 0894-1491, 09/2017, Volume 65, Issue 9, pp. 1471 - 1490
Lipocalin‐2 (LCN2) has diverse functions in multiple pathophysiological conditions; however, its pathogenic role in vascular dementia (VaD) is unknown. Here,... 
global cerebral ischemia | neuroinflammation | chronic cerebral hypoperfusion | microglia | ARTERY OCCLUSION | ALZHEIMERS-DISEASE | BINSWANGERS-DISEASE | FOREBRAIN ISCHEMIA | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | WHITE-MATTER INJURY | IMPAIRMENT | NEURONAL DEATH | MICE | Microglia - metabolism | Humans | Astrocytes - pathology | Microvessels - metabolism | Microvessels - pathology | Male | Vascular Endothelial Growth Factor A - metabolism | Dementia, Vascular - metabolism | Cognition - physiology | Microglia - pathology | Dementia, Vascular - pathology | Lipocalin-2 - genetics | Lipocalin-2 - administration & dosage | Disease Models, Animal | Recombinant Proteins - metabolism | Hippocampus - blood supply | Cognitive Dysfunction - metabolism | Mice, Inbred C57BL | Cells, Cultured | Hippocampus - pathology | Biomarkers - blood | Cognitive Dysfunction - pathology | Recombinant Proteins - administration & dosage | Mice, Knockout | Hippocampus - metabolism | Animals | Lipocalin-2 - metabolism | Astrocytes - metabolism | Vascular dementia | Binswanger's disease | Neurons | Analysis | Brain damage | Models | Permeability | Occlusion | Animal models | Cognitive ability | Membrane permeability | Impairment | Activation | Carotid arteries | Neuronal-glial interactions | Neurotoxicity | Hypoxia-inducible factor 1a | Ischemia | Blood-brain barrier | Cerebral blood flow | Rodents | Dementia disorders | Amnesia | Carotid artery | Recombinant | Astrocytes | Lipocalin | Mortality | Inflammation | Substantia alba | Patients | Microglia | Gliosis | Death | Mice | Plasma levels | Hippocampus | Brain injury | Dementia | Index Medicus
Journal Article
by Han, F and Zhuang, TT and Chen, JJ and Zhu, XL and Cai, YF and Lu, YP
PLOS ONE, ISSN 1932-6203, 09/2017, Volume 12, Issue 9, p. e0185102
Alzheimer's disease (AD) is a typical hippocampal amnesia and the most common senile dementia. Many studies suggest that cognitive impairments are more closely... 
AMYLOID CASCADE HYPOTHESIS | D-GALACTOSE | E/AMYLOID-BETA INTERACTION | MULTIDISCIPLINARY SCIENCES | A-BETA | COGNITIVE IMPAIRMENT | LONG-TERM POTENTIATION | SYNAPTIC PLASTICITY | WILD-TYPE TAU | COFILIN PHOSPHORYLATION | TRANSGENIC MICE | Dendrites - pathology | Phosphorylation | Atrophy - pathology | tau Proteins - metabolism | Male | cdc42 GTP-Binding Protein - metabolism | Hippocampus - drug effects | Alzheimer Disease - pathology | Neuroprotective Agents - pharmacology | Acetophenones - pharmacology | Amyloid beta-Peptides - metabolism | Atrophy - drug therapy | Drug Evaluation, Preclinical | Alzheimer Disease - psychology | Disease Models, Animal | Dendrites - drug effects | Dendrites - metabolism | Peptide Fragments - metabolism | Alzheimer Disease - drug therapy | Hippocampus - pathology | Random Allocation | Maze Learning - drug effects | Rats, Sprague-Dawley | Hippocampus - metabolism | Animals | Cofilin 1 - metabolism | Alzheimer Disease - metabolism | Galactose | Atrophy - metabolism | rac1 GTP-Binding Protein - metabolism | Care and treatment | Usage | Genetic aspects | Research | Alzheimer's disease | Sodium compounds | Cdc42 protein | Oxidative stress | Motility | Pathogenesis | Cognitive ability | Kinases | Learning behavior | Cell adhesion & migration | Dendritic spines | Chinese medicine | Rodents | Cell cycle | Dementia disorders | Dendrites | Life sciences | Behavior | Amnesia | Pretreatment | D-Galactose | Open-field behavior | Emotional behavior | Damage assessment | Neurodegenerative diseases | Neurons | Traditional Chinese medicine | Rats | Inhibition (psychology) | Rac1 protein | Pharmacology | Gene expression | Chemical compounds | Studies | Sodium | Correlation analysis | β-Amyloid | Regulation | Alzheimers disease | Hippocampus | Dementia | Animal cognition
Journal Article