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Neuron (Cambridge, Mass.), ISSN 0896-6273, 08/2012, Volume 75, Issue 4, pp. 618 - 632
Mitochondrial abnormalities have been documented in Alzheimer’s disease and related neurodegenerative disorders, but the causal relationship between... 
Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Neurons - pathology | Microtubule-Associated Proteins - genetics | Tauopathies - genetics | Cytoskeletal Proteins - genetics | Gelsolin - metabolism | Microtubule-Associated Proteins - metabolism | Humans | Actins - metabolism | Tauopathies - pathology | Cytoplasm - metabolism | MicroRNAs - metabolism | Green Fluorescent Proteins - genetics | Mitochondrial Proteins - genetics | Drosophila Proteins - metabolism | GTP-Binding Proteins - genetics | Nerve Degeneration - metabolism | Neurons - ultrastructure | tau Proteins - genetics | Cell Death - genetics | Mitochondria - genetics | Mitochondrial Proteins - metabolism | ATP Synthetase Complexes - metabolism | Cell Cycle Proteins - genetics | Tauopathies - complications | Cytoskeletal Proteins - metabolism | Myosins - metabolism | Cytoplasm - genetics | RNA Interference - physiology | Disease Models, Animal | In Situ Nick-End Labeling | Green Fluorescent Proteins - metabolism | Animals, Genetically Modified | Gene Expression Regulation - genetics | Drosophila | Cell Cycle Proteins - metabolism | Mitochondria - metabolism | Mitochondria - pathology | Mutation - genetics | Animals | GTP Phosphohydrolases - metabolism | Analysis of Variance | GTP Phosphohydrolases - genetics | Gelsolin - genetics | Mice | Drosophila Proteins - genetics | Nerve Degeneration - etiology | Voltage-Dependent Anion Channels - metabolism | GTP-Binding Proteins - metabolism | Nervous system diseases | Actin | Neurons | Utrophin | Myosin | Mitochondrial DNA | Alzheimer's disease | Proteins | Phosphorylation | Mitochondria | Neurotoxicity | Insects | Microscopy | Neurodegeneration | Pathogenesis | Morphology | Mutation | Defects | Index Medicus | Neurodegenerative diseases | Tau protein | Cell death | Elongation
Journal Article
Journal Article
Autophagy, ISSN 1554-8635, 11/2014, Volume 8, Issue 4, pp. 609 - 622
Journal Article
Neuron (Cambridge, Mass.), ISSN 0896-6273, 02/2012, Volume 73, Issue 4, pp. 685 - 697
Journal Article
Nature (London), ISSN 1476-4687, 09/2017, Volume 549, Issue 7673, pp. 523 - 527
APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. ApoE4 increases brain amyloid-beta pathology relative to other ApoE isoforms(1).... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Microglia - metabolism | Neurons - pathology | Phosphorylation | Apolipoprotein E4 - genetics | Tauopathies - genetics | Coculture Techniques | Humans | Tauopathies - pathology | tau Proteins - metabolism | Phosphoproteins - metabolism | Inflammation - metabolism | Microglia - immunology | tau Proteins - genetics | Apolipoprotein E4 - deficiency | Phosphoproteins - analysis | Apolipoprotein E4 - toxicity | Neurons - metabolism | Neurons - drug effects | Disease Models, Animal | Cell Survival - drug effects | Apolipoprotein E4 - metabolism | Genotype | Mice, Transgenic | Phosphoproteins - genetics | Immunity, Innate | Disease Progression | Gene Knock-In Techniques | Mice, Knockout | Tauopathies - metabolism | Animals | Alleles | Inflammation - genetics | Mice | Nervous system | Development and progression | Degeneration | Models | Apolipoproteins | Health aspects | Tau proteins | Brain | Pathogenesis | Genomes | Autophagy | Neuronal-glial interactions | Risk factors | Atrophy | Neurodegeneration | Apolipoprotein E | Rodents | Aging | Alzheimer's disease | Genotypes | Apolipoprotein E4 | Neurodegenerative diseases | Neurons | Health risks | Transgenic mice | Inflammation | Gene expression | Microglia | Pathology | Tau protein | Tumor necrosis factor | β-Amyloid | Alzheimers disease | Viability | Tumors | Dementia | Index Medicus
Journal Article
Journal Article