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European Heart Journal, ISSN 0195-668X, 08/2014, Volume 35, Issue 29, pp. 1917 - 1924
Epidemiological research over the last 50 years has discovered a plethora of biomarkers (including molecules, traits or other diseases) that associate with... 
Coronary artery disease | Mendelian randomization | C-REACTIVE PROTEIN | FUTURE MYOCARDIAL-INFARCTION | CARDIAC & CARDIOVASCULAR SYSTEMS | ESTER TRANSFER PROTEIN | CARDIOVASCULAR EVENTS | SUBTILISIN/KEXIN TYPE 9 | ISCHEMIC-HEART-DISEASE | PHOSPHOLIPASE A | DENSITY-LIPOPROTEIN CHOLESTEROL | LAPLACE-TIMI 57 | GENOME-WIDE ASSOCIATION | Triglycerides - physiology | Cholesterol Ester Transfer Proteins - physiology | Humans | Obesity - genetics | Cholesterol, HDL - physiology | C-Reactive Protein - metabolism | Cholesterol Ester Transfer Proteins - genetics | Mendelian Randomization Analysis | Diabetes Complications - genetics | Genetic Pleiotropy - genetics | Hypertension - genetics | Phospholipases A2 - physiology | Telomere - genetics | Fibrinogen - physiology | Obesity - complications | Receptors, Interleukin-6 - genetics | Risk Factors | Linkage Disequilibrium - genetics | Lipoprotein(a) - physiology | C-Reactive Protein - genetics | Cholesterol, LDL - physiology | Cholesterol, HDL - genetics | Randomized Controlled Trials as Topic | Cholesterol, LDL - genetics | Serum Amyloid P-Component - genetics | Genetic Markers - genetics | Coronary Artery Disease - genetics | Hypertension - complications | Polymorphism, Single Nucleotide - genetics | Triglycerides - genetics | Lipoprotein(a) - genetics | Phospholipases A2 - genetics
Journal Article
by Kunkle, Brian W and Grenier-Boley, Benjamin and Sims, Rebecca and Bis, Joshua C and Damotte, Vincent and Naj, Adam C and Boland, Anne and Vronskaya, Maria and van der Lee, Sven J and Amlie-Wolf, Alexandre and Bellenguez, Céline and Frizatti, Aura and Chouraki, Vincent and Martin, Eden R and Sleegers, Kristel and Badarinarayan, Nandini and Jakobsdottir, Johanna and Hamilton-Nelson, Kara L and Moreno-Grau, Sonia and Olaso, Robert and Raybould, Rachel and Chen, Yuning and Kuzma, Amanda B and Hiltunen, Mikko and Morgan, Taniesha and Ahmad, Shahzad and Vardarajan, Badri N and Epelbaum, Jacques and Hoffmann, Per and Boada, Merce and Beecham, Gary W and Garnier, Jean-Guillaume and Harold, Denise and Fitzpatrick, Annette L and Valladares, Otto and Moutet, Marie-Laure and Gerrish, Amy and Smith, Albert V and Qu, Liming and Bacq, Delphine and Denning, Nicola and Jian, Xueqiu and Zhao, Yi and Del Zompo, Maria and Fox, Nick C and Choi, Seung-Hoan and Mateo, Ignacio and Hughes, Joseph T and Adams, Hieab H and Malamon, John and Sanchez-Garcia, Florentino and Patel, Yogen and Brody, Jennifer A and Dombroski, Beth A and Naranjo, Maria Candida Deniz and Daniilidou, Makrina and Eiriksdottir, Gudny and Mukherjee, Shubhabrata and Wallon, David and Uphill, James and Aspelund, Thor and Cantwell, Laura B and Garzia, Fabienne and Galimberti, Daniela and Hofer, Edith and Butkiewicz, Mariusz and Fin, Bertrand and Scarpini, Elio and Sarnowski, Chloe and Bush, Will S and Meslage, Stéphane and Kornhuber, Johannes and White, Charles C and Song, Yuenjoo and Barber, Robert C and Engelborghs, Sebastiaan and Sordon, Sabrina and Voijnovic, Dina and Adams, Perrie M and Vandenberghe, Rik and Mayhaus, Manuel and Cupples, L. Adrienne and Albert, Marilyn S and De Deyn, Peter P and Gu, Wei and Himali, Jayanadra J and Beekly, Duane and Squassina, Alessio and Hartmann, Annette M and Orellana, Adelina and Blacker, Deborah and Rodriguez-Rodriguez, Eloy and Lovestone, Simon and Garcia, Melissa E and Doody, Rachelle S and Munoz-Fernadez, Carmen and Sussams, Rebecca and Lin, Honghuang and Fairchild, Thomas J and Benito, Yolanda A and ... and Alzheimer Disease Genetics Consortium (ADGC) and Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (CHARGE) and The European Alzheimer’s Disease Initiative (EADI) and Genetic and Environmental Risk in AD/Defining Genetic, Polygenic and Environmental Risk for Alzheimer’s Disease Consortium (GERAD/PERADES) and Cohorts Heart Aging Res Genomic Ep and Alzheimer Dis Genetics Consortium and European Alzheimers Dis Initiative and Genetic Environm Risk AD Defining and European Alzheimer’s Disease Initiative (EADI)
Nature genetics, ISSN 1546-1718, 2019, Volume 51, Issue 3, pp. 414 - 430
Journal Article
PLoS genetics, ISSN 1553-7404, 2014, Volume 10, Issue 10, p. e1004758
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2018, Volume 115, Issue 28, pp. E6640 - E6649
.... The strongest genetic risk factor for sporadic AD is the ε4 allele of Apolipoprotein E (ApoE4). Previous studies have shown that ApoE4 potentiates presymptomatic endosomal dysfunction and defective endocytic clearance of amyloid beta... 
Histone deacetylase | Trichostatin A | Amyloid beta | ApoE4 | exchanger | 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 | 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 | Astrocytes | Biological Sciences | PNAS Plus | H+ exchanger | Na+
Journal Article
Neuron (Cambridge, Mass.), ISSN 0896-6273, 2018, Volume 99, Issue 1, pp. 64 - 82.e7
Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer’s disease (AD) although definitive... 
systems biology | Roseolovirus | integrative genomics | human herpesvirus | multiscale networks | HHV-6B | HHV-7 | HHV-6A | network biology | Alzheimer's disease | AMYLOID PEPTIDE | READ ALIGNMENT | G-QUADRUPLEXES | TRANSFER-RNAS | IN-VIVO | DISEASE | POLY(ADP-RIBOSE) POLYMERASE-1 | EXPRESSION PROFILES | SIMPLEX INFECTION | NEUROSCIENCES | EPSTEIN-BARR-VIRUS | Amyloid Precursor Protein Secretases - genetics | Encephalitis, Viral - genetics | Encephalitis, Viral - virology | Genomics | Humans | Brain - virology | Gene Expression Profiling | Aspartic Acid Endopeptidases - genetics | Gene Regulatory Networks | Herpesvirus 7, Human | Case-Control Studies | Herpesvirus 6, Human | Viral Load | Alzheimer Disease - pathology | Brain - metabolism | Microbiota | Monomeric Clathrin Assembly Proteins - genetics | Tumor Suppressor Proteins - genetics | Amyloid beta-Protein Precursor - metabolism | Encephalitis, Viral - metabolism | Nuclear Proteins - genetics | Roseolovirus Infections - pathology | Clusterin - genetics | Roseolovirus Infections - genetics | Presenilin-1 - genetics | Mice, Transgenic | Roseolovirus Infections - metabolism | Mice, Knockout | Alzheimer Disease - virology | Animals | Adaptor Proteins, Signal Transducing - genetics | Alzheimer Disease - metabolism | Proteomics | Brain - pathology | Roseolovirus Infections - virology | Encephalitis, Viral - pathology | Mice | MicroRNAs - genetics | Alzheimer Disease - genetics | Cohort Studies | Brain | Medical colleges | Medical research | Genetic research | Medicine, Experimental | Development and progression | b-Site APP cleaving enzyme 1 | Neuropathology | Herpes simplex | Viruses | Gene expression | Neuromodulation | Protein turnover | Proteins | Brain research | Neurodegeneration | Autopsy | Data collection
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 | 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 | Proteins | Medical colleges | Alanine | Nervous system diseases | Neurosciences | Huntington's chorea | Neurons | Physiological aspects | Aspartate | Huntingtons disease | Phosphorylation | Neurodegeneration | Pathogenesis | Neuropathology | Rodents | Mutation
Journal Article
Molecular psychiatry, ISSN 1476-5578, 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 disease (AD) after APOE... 
Brain | Tau | BIN1 | Alzheimer | Drosophila | COMMON VARIANTS | PHOSPHORYLATION | PSYCHIATRY | BIOCHEMISTRY & MOLECULAR BIOLOGY | MODEL | brain | ENDOCYTOSIS | NEUROSCIENCES | IDENTIFIES VARIANTS | DISEASE | AMPHIPHYSIN-II | GENOME-WIDE ASSOCIATION | Endophenotypes | Gene Expression - genetics | Humans | Transcription Factors - deficiency | Nerve Degeneration - genetics | tau Proteins - metabolism | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Case-Control Studies | 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 | Cells, Cultured | Transcription Factors - genetics | Nerve Degeneration - pathology | Transcription Factors - metabolism | Carrier Proteins - genetics | Animals | 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 | Mice | Drosophila Proteins - genetics | Alzheimer Disease - genetics | Tumor Suppressor Proteins - biosynthesis | Physiological aspects | Complications and side effects | Genetic aspects | Alzheimer's disease | Risk factors | Amyloid beta-protein | Index Medicus | Original
Journal Article