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PLoS Genetics, ISSN 1553-7390, 10/2014, Volume 10, Issue 10, pp. e1004758 - e1004758
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 07/2018, Volume 115, Issue 28, pp. E6640 - E6649
Endosomes have emerged as a central hub and pathogenic driver of Alzheimer's disease (AD). The earliest brain cytopathology in neurodegeneration, occurring... 
Histone deacetylase | Amyloid beta | Na | ApoE4 | exchanger | H | Trichostatin A | Na+/H+ exchanger | CHRISTIANSON SYNDROME | HUMAN BRAIN | trichostatin A | MULTIDISCIPLINARY SCIENCES | SPORADIC ALZHEIMERS-DISEASE | histone deacetylase | SYNAPTIC PLASTICITY | amyloid beta | APOLIPOPROTEIN-E | LYSOSOMAL DYSFUNCTION | DOWN-SYNDROME | A-BETA | GENE-EXPRESSION | PRECURSOR PROTEIN | Protons | Brain | Membranes | Transcription | Gene regulation | Trafficking | Cognitive ability | Acidification | pH effects | Neuronal-glial interactions | Risk factors | Proteins | Apolipoprotein E | Neurodegeneration | Compartments | Down-regulation | Alzheimer's disease | Plaques | Translocation | Pathogens | Apolipoprotein E4 | Therapeutic applications | Astrocytes | Na+/H+-exchanging ATPase | Risk analysis | Apolipoproteins | Nuclear transport | Alleles | Epigenetics | Cytopathology | Receptor density | Mutation | Alzheimers disease | Endosomes | Microcephaly - genetics | Epigenesis, Genetic | Humans | Astrocytes - pathology | Epilepsy - metabolism | Endosomes - metabolism | Alzheimer Disease - pathology | Intellectual Disability - metabolism | Amyloid beta-Peptides - genetics | Amyloid beta-Peptides - metabolism | Ataxia - drug therapy | Genetic Diseases, X-Linked - genetics | Ataxia - genetics | Ataxia - metabolism | Microcephaly - drug therapy | Ataxia - pathology | Ocular Motility Disorders - pathology | Tumor Suppressor Proteins - metabolism | Apolipoprotein E4 - metabolism | Endosomes - genetics | Histone Deacetylases - genetics | Ocular Motility Disorders - metabolism | Intellectual Disability - pathology | Alzheimer Disease - drug therapy | Receptors, LDL - metabolism | Mice, Knockout | Genetic Diseases, X-Linked - pathology | Epilepsy - drug therapy | Histone Deacetylase Inhibitors - pharmacology | Mice | Astrocytes - metabolism | Hydrogen-Ion Concentration | Apolipoprotein E4 - genetics | Ocular Motility Disorders - genetics | Intellectual Disability - genetics | Sodium-Hydrogen Exchangers - metabolism | Genetic Diseases, X-Linked - drug therapy | Microcephaly - pathology | Tumor Suppressor Proteins - genetics | Epilepsy - genetics | Sodium-Hydrogen Exchangers - genetics | Receptors, LDL - genetics | Microcephaly - metabolism | Histone Deacetylases - metabolism | Endosomes - pathology | Genetic Diseases, X-Linked - metabolism | Intellectual Disability - drug therapy | Ocular Motility Disorders - drug therapy | Animals | Alzheimer Disease - metabolism | Alzheimer Disease - genetics | Epilepsy - pathology | Physiological aspects | Epigenetic inheritance | Glycoproteins | Genetic aspects | Observations | Index Medicus
Journal Article
Nature Neuroscience, ISSN 1097-6256, 05/2012, Volume 15, Issue 5, pp. 713 - 721
The Huntington's disease gene product, huntingtin, is indispensable for neural tube formation, but its role is obscure. We studied neurulation in htt-null... 
TARGETED DISRUPTION | ZEBRAFISH | LACKING HUNTINGTIN | EMBRYONIC STEM-CELLS | MUTANT HUNTINGTIN | ADAM10 | MICE | DISEASE GENE HOMOLOG | WILD-TYPE HUNTINGTIN | NEUROSCIENCES | N-CADHERIN CLEAVAGE | Brain | Green Fluorescent Proteins | Embryo, Mammalian | 3-(formylhydroxyamino)-2-(3-phenyl-1-propyl)butanoic acid (2,2-dimethyl-1-methylcarbamoyl-1-propyl)amide | Dlgh1 protein, mouse | Hedgehog Proteins | pax2a protein, zebrafish | Cerebral Ventricles | Amyloid Precursor Protein Secretases | Body Patterning | Cell Differentiation | Adam10 protein, mouse | Zebrafish | Nerve Tissue Proteins | Cell Adhesion | Tissue Inhibitor of Metalloproteinase-1 | Hydroxamic Acids | Nuclear Proteins | Biological Evolution | Membrane Proteins | Analysis of Variance | Neuroepithelial Cells | Cdh2 protein, mouse | CTF-1 transcription factor | Embryo, Nonmammalian | Cadherins | Mice | RNA, Small Interfering | Shha protein, zebrafish | Embryonic Stem Cells | Mutation | Drosophila melanogaster | Wnt1 Protein | Nestin | Immunoprecipitation | Nes protein, mouse | Huntington protein, mouse | Transfection | Gene Expression Regulation, Developmental | PAX2 Transcription Factor | Animals, Genetically Modified | Neurons | Cells, Cultured | Zebrafish Proteins | ADAM Proteins | NFI Transcription Factors | Morpholines | Guanylate Kinase | Animals | Dictyostelium | enhanced green fluorescent protein | Dipeptides | Intermediate Filament Proteins | Apoptosis | Phenotypes | Huntingtin | Embryo cells | Danio rerio | Nervous system | Gene products | Huntington's disease | Disease control | Adhesion | Freshwater | Dictyostelium discoideum | Reversion | Inhibitors | Neural tube | Cell adhesion | Stem cells | Chromium | Evolution | Freshwater fish | Metalloproteinase | Rosette formation | Body Patterning - drug effects | Guanylate Kinases - genetics | Amyloid Precursor Protein Secretases - genetics | RNA, Small Interfering - genetics | Wnt1 Protein - genetics | Brain - embryology | PAX2 Transcription Factor - metabolism | Cadherins - metabolism | Apoptosis - drug effects | Hedgehog Proteins - metabolism | Apoptosis - genetics | Green Fluorescent Proteins - genetics | Brain - metabolism | NFI Transcription Factors - metabolism | Cadherins - genetics | Tissue Inhibitor of Metalloproteinase-1 - pharmacology | Discs Large Homolog 1 Protein | Membrane Proteins - genetics | Gene Expression Regulation, Developmental - drug effects | PAX2 Transcription Factor - genetics | Cell Adhesion - drug effects | Mutation - genetics | Brain - drug effects | Huntingtin Protein | ADAM Proteins - metabolism | Amyloid Precursor Protein Secretases - metabolism | Membrane Proteins - antagonists & inhibitors | Cell Adhesion - physiology | Guanylate Kinases - metabolism | Neuroepithelial Cells - physiology | Zebrafish Proteins - genetics | ADAM Proteins - genetics | Cerebral Ventricles - cytology | Neuroepithelial Cells - drug effects | Embryonic Stem Cells - metabolism | Gene Expression Regulation, Developmental - genetics | Wnt1 Protein - metabolism | Zebrafish - embryology | Cell Differentiation - genetics | Hedgehog Proteins - genetics | Intermediate Filament Proteins - genetics | Neurons - physiology | Membrane Proteins - metabolism | Cerebral Ventricles - embryology | Neurons - drug effects | Nuclear Proteins - genetics | Hydroxamic Acids - pharmacology | Green Fluorescent Proteins - metabolism | Brain - cytology | ADAM Proteins - antagonists & inhibitors | Zebrafish Proteins - metabolism | Dipeptides - pharmacology | ADAM10 Protein | Morpholines - pharmacology | Nuclear Proteins - metabolism | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Embryonic Stem Cells - drug effects | Cell Differentiation - drug effects | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Body Patterning - genetics | Huntington's chorea | Physiological aspects | Genetic aspects | Research | Embryonic stem cells | Risk factors | Index Medicus
Journal Article
Neuron, ISSN 0896-6273, 12/2009, Volume 64, Issue 6, pp. 828 - 840
The N-terminal 17 amino acids of huntingtin (NT17) can be phosphorylated on serines 13 and 16; however, the significance of these modifications in Huntington's... 
humdisease | molneuro | NEURONAL INTRANUCLEAR INCLUSIONS | NUCLEAR | PHOSPHORYLATION | EXPANSION | NEURODEGENERATION | TOXICITY | PATHOLOGY | TRANSGENIC MOUSE MODEL | NEUROSCIENCES | AGGREGATION | TRINUCLEOTIDE REPEAT | Proteins | Huntingtons disease | Phosphorylation | Neurodegeneration | Pathogenesis | Neuropathology | Rodents | Mutation | Fibrillogenesis | Alanine | Huntingtin | Serine | Transgenic mice | Amino acids | Amyloid | Huntington's disease | Bacterial artificial chromosomes | Molecular Weight | Humans | Nerve Degeneration - physiopathology | Nerve Degeneration - genetics | Alanine - chemistry | Amino Acid Sequence - genetics | Nerve Degeneration - metabolism | Aspartic Acid - genetics | Nerve Tissue Proteins - chemistry | Alanine - genetics | Amyloid - metabolism | Nuclear Proteins - genetics | Huntington Disease - physiopathology | Disease Models, Animal | Amyloid - genetics | Genetic Predisposition to Disease - genetics | Gene Expression Regulation - genetics | Serine - genetics | Alanine - metabolism | Mice, Transgenic | Protein Structure, Tertiary - genetics | Mutation - genetics | Nuclear Proteins - chemistry | Serine - chemistry | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | Serine - metabolism | Huntingtin Protein | Phenotype | Animals | Huntington Disease - genetics | Trinucleotide Repeat Expansion - genetics | Amino Acid Substitution - genetics | Aspartic Acid - metabolism | Mice | Aspartic Acid - chemistry | Medical colleges | Nervous system diseases | Neurosciences | Huntington's chorea | Neurons | Physiological aspects | Aspartate | Index Medicus
Journal Article
Molecular Psychiatry, ISSN 1359-4184, 11/2013, Volume 18, Issue 11, pp. 1225 - 1234
Genome-wide association studies (GWAS) have identified a region upstream the BIN1 gene as the most important genetic susceptibility locus in Alzheimer's... 
Brain | Tau | BIN1 | Alzheimer | Drosophila | COMMON VARIANTS | PHOSPHORYLATION | PSYCHIATRY | BIOCHEMISTRY & MOLECULAR BIOLOGY | MODEL | brain | ENDOCYTOSIS | NEUROSCIENCES | IDENTIFIES VARIANTS | DISEASE | AMPHIPHYSIN-II | GENOME-WIDE ASSOCIATION | MAPT protein, human | Endophenotypes | Humans | tau Proteins | Case-Control Studies | Plaque, Amyloid | Synaptosomes | Carrier Proteins | BIN1 protein, human | bicoid interacting protein 1, Drosophila | Drosophila Proteins | Gene Expression | Genetic Predisposition to Disease | Cells, Cultured | Alzheimer Disease | Nuclear Proteins | Adaptor Proteins, Signal Transducing | Animals | Mice | Polymorphism, Single Nucleotide | Transcription Factors | Nerve Degeneration | Drosophila melanogaster | Tumor Suppressor Proteins | Index Medicus | Neurotoxicity | Neurodegenerative diseases | Tau protein | Transcription | Apolipoprotein E | Susceptibility | Insertion | beta -Amyloid | Alzheimer's disease | Neuroblastoma cells | Gene Expression - genetics | Transcription Factors - deficiency | Nerve Degeneration - genetics | tau Proteins - metabolism | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Alzheimer Disease - pathology | Brain - metabolism | Drosophila melanogaster - metabolism | Synaptosomes - pathology | Nuclear Proteins - biosynthesis | Tumor Suppressor Proteins - genetics | Nuclear Proteins - genetics | tau Proteins - antagonists & inhibitors | Genetic Predisposition to Disease - genetics | Plaque, Amyloid - pathology | Transcription Factors - genetics | Nerve Degeneration - pathology | Transcription Factors - metabolism | Carrier Proteins - genetics | Carrier Proteins - metabolism | Adaptor Proteins, Signal Transducing - genetics | Alzheimer Disease - metabolism | Drosophila Proteins - deficiency | Brain - pathology | Polymorphism, Single Nucleotide - genetics | Adaptor Proteins, Signal Transducing - biosynthesis | Drosophila Proteins - genetics | Alzheimer Disease - genetics | Tumor Suppressor Proteins - biosynthesis | Physiological aspects | Complications and side effects | Genetic aspects | Risk factors | Amyloid beta-protein
Journal Article
by Cruchaga, Carlos and Karch, Celeste M and Jin, Sheng Chih and Benitez, Bruno A and Cai, Yefei and Guerreiro, Rita and Harari, Oscar and Norton, Joanne and Budde, John and Bertelsen, Sarah and Jeng, Amanda T and Cooper, Breanna and Skorupa, Tara and Carrell, David and Levitch, Denise and Hsu, Simon and Choi, Jiyoon and Ryten, Mina and Hardy, John and Trabzuni, Daniah and Weale, Michael E and Ramasamy, Adaikalavan and Smith, Colin and Sassi, Celeste and Bras, Jose and Gibbs, J. Raphael and Hernandez, Dena G and Lupton, Michelle K and Powell, John and Forabosco, Paola and Ridge, Perry G and Corcoran, Christopher D and Tschanz, Joann T and Norton, Maria C and Munger, Ronald G and Schmutz, Cameron and Leary, Maegan and Demirci, F. Yesim and Bamne, Mikhil N and Wang, Xingbin and Lopez, Oscar L and Ganguli, Mary and Medway, Christopher and Turton, James and Lord, Jenny and Braae, Anne and Barber, Imelda and Brown, Kristelle and Passmore, Peter and Craig, David and Johnston, Janet and McGuinness, Bernadette and Todd, Stephen and Heun, Reinhard and Kölsch, Heike and Kehoe, Patrick G and Hooper, Nigel M and Vardy, Emma R.L.C and Mann, David M and Pickering-Brown, Stuart and Kalsheker, Noor and Lowe, James and Morgan, Kevin and David Smith, A and Wilcock, Gordon and Warden, Donald and Holmes, Clive and Pastor, Pau and Lorenzo-Betancor, Oswaldo and Brkanac, Zoran and Scott, Erick and Topol, Eric and Rogaeva, Ekaterina and Singleton, Andrew B and Kamboh, M. Ilyas and St George-Hyslop, Peter and Cairns, Nigel and Morris, John C and Kauwe, John S. K and Goate, Alison M and Alzheimers Res UK ARUK Consortium and UKBEC and Alzheimer's Research UK (ARUK) Consortium
Nature, ISSN 0028-0836, 2014, Volume 505, Issue 7484, pp. 550 - 554
Genome-wide association studies (GWAS) have identified several risk variants for late-onset Alzheimer's disease (LOAD)(1,2). These common variants have... 
NETWORK ANALYSIS | DIAGNOSIS | DEMENTIA | MULTIDISCIPLINARY SCIENCES | MUTATION | NEURONS | PROTEOLYSIS | EXPRESSION | ASSOCIATION | AGE | INSIGHTS | APP protein, human | Brain | Peptide Fragments | Pathogenesis | Humans | African Americans | Male | Genomes | Case-Control Studies | Exome | Genetic Variation | Genotype & phenotype | Proteolysis | Amyloid beta-Peptides | Population | Female | Age | Deoxyribonucleic acid--DNA | amyloid beta-protein (1-40) | Genetic Predisposition to Disease | amyloid beta-protein (1-42) | Europe | Gene expression | Alzheimer Disease | Phospholipase D | phospholipase D3, human | Aged, 80 & over | Age of Onset | Aged | Protein Processing, Post-Translational | Alzheimers disease | Amyloid beta-Protein Precursor | Genetic Predisposition to Disease - genetics | Peptide Fragments - metabolism | Phospholipase D - deficiency | Protein Processing, Post-Translational - genetics | African Americans - genetics | Phospholipase D - metabolism | Europe - ethnology | Brain - metabolism | Exome - genetics | Alzheimer Disease - metabolism | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Aged, 80 and over | Genetic Variation - genetics | Phospholipase D - genetics | Alzheimer Disease - genetics | Medical research | Genetic susceptibility | Genetic variation | Physiological aspects | Medicine, Experimental | Genetic aspects | Research | Phospholipases | Alzheimer's disease | Identification and classification | Risk factors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7388, pp. 222 - 226
Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer's disease(1). The causes... 
REMOTE MEMORIES | LONG-TERM-MEMORY | CDK5 | CHROMATIN | PHOSPHORYLATION | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | CLINICAL-IMPLICATIONS | SYNAPTIC PLASTICITY | EXPRESSION | TRANSGENIC MICE | Histone deacetylase | Brain | Animal models | Transcription | Neurodegenerative diseases | Memory | Central nervous system | Cognitive ability | epigenetics | Learning | Gene silencing | Neurotoxicity | Plasticity (synaptic) | Acetylation | Alzheimer's disease | HDAC2 protein, human | Peptide Fragments | Phosphorylation | Epigenesis, Genetic | Humans | Hydrogen Peroxide | Kinases | Gene Knockdown Techniques | Hdac2 protein, mouse | Neurodegeneration | Amyloid beta-Peptides | Histones | Genetics | Disease Models, Animal | Neurodegenerative Diseases | Promoter Regions, Genetic | amyloid beta-protein (1-42) | Cyclin-dependent kinases | Gene Expression Regulation | Histone Deacetylase 2 | Receptors, Glucocorticoid | RNA polymerase | Alzheimer Disease | Memory Disorders | Animals | Neuronal Plasticity | Epigenetics | Mice | RNA Polymerase II | Hippocampus | Memory Disorders - physiopathology | Alzheimer Disease - complications | Memory Disorders - genetics | Peptide Fragments - toxicity | Neuronal Plasticity - drug effects | Receptors, Glucocorticoid - metabolism | Hippocampus - drug effects | RNA Polymerase II - metabolism | Memory Disorders - complications | Promoter Regions, Genetic - drug effects | Promoter Regions, Genetic - genetics | Brain - metabolism | Neuronal Plasticity - genetics | Epigenesis, Genetic - drug effects | Phosphorylation - drug effects | Hydrogen Peroxide - toxicity | Histone Deacetylase 2 - genetics | Alzheimer Disease - physiopathology | Amyloid beta-Peptides - toxicity | Brain - physiopathology | Neurodegenerative Diseases - genetics | Neurodegenerative Diseases - complications | Brain - drug effects | Gene Expression Regulation - drug effects | Hippocampus - metabolism | Acetylation - drug effects | Neurodegenerative Diseases - physiopathology | Histone Deacetylase 2 - deficiency | Histone Deacetylase 2 - metabolism | Histones - metabolism | Alzheimer Disease - genetics | Epigenetic inheritance | Complications and side effects | Causes of | Nervous system | Genetic aspects | Degeneration | Cognition disorders | Health aspects | Index Medicus
Journal Article