Articles

Search Articles

Advanced search
Help

Catalogue

Articles

Databases

X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (1826) 1826
Conference Proceeding (277) 277
Book Review (173) 173
Publication (111) 111
Book Chapter (19) 19
Book / eBook (13) 13
Patent (8) 8
Dissertation (6) 6
Web Resource (1) 1
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
index medicus (1148) 1148
humans (1064) 1064
male (599) 599
neurosciences (597) 597
female (586) 586
genetics & heredity (439) 439
clinical neurology (410) 410
middle aged (370) 370
aged (359) 359
mutation (297) 297
alzheimer's disease (296) 296
dementia (265) 265
alzheimer disease - genetics (250) 250
adult (235) 235
animals (211) 211
genetic aspects (201) 201
pedigree (195) 195
biochemistry & molecular biology (186) 186
genotype (185) 185
genetics (174) 174
aged, 80 and over (171) 171
geriatrics & gerontology (157) 157
psychiatry (157) 157
neurology (156) 156
risk factors (145) 145
gene (142) 142
research (140) 140
alzheimers-disease (139) 139
analysis (139) 139
genes (126) 126
mutations (126) 126
genetic predisposition to disease (121) 121
pathology (121) 121
frontotemporal lobar degeneration (116) 116
frontotemporal dementia (115) 115
amyotrophic-lateral-sclerosis (111) 111
age of onset (108) 108
alleles (105) 105
phenotype (104) 104
molecular sequence data (102) 102
abridged index medicus (99) 99
chromosome mapping (98) 98
mice (96) 96
article (95) 95
disease (93) 93
cell biology (91) 91
cohort studies (91) 91
proteins (91) 91
dna mutational analysis (90) 90
amyotrophic lateral sclerosis (89) 89
genetic research (84) 84
association (81) 81
case-control studies (81) 81
risk (81) 81
nervous system diseases (80) 80
base sequence (78) 78
genetic linkage (78) 78
polymorphism, single nucleotide (78) 78
internal medicine (77) 77
charcot-marie-tooth disease - genetics (76) 76
apolipoproteins e - genetics (75) 75
locus (75) 75
linkage (74) 74
adolescent (73) 73
alzheimer disease - pathology (72) 72
diagnosis (72) 72
gene frequency (72) 72
genome-wide association (72) 72
alzheimers disease (71) 71
brain - pathology (69) 69
neurodegeneration (69) 69
amyotrophic lateral sclerosis - genetics (68) 68
genomics (68) 68
polymerase chain reaction (68) 68
amyloid beta-protein precursor - genetics (67) 67
genetic markers (67) 67
mental disorders (67) 67
polymorphism, genetic (67) 67
brain (66) 66
mutation - genetics (66) 66
expression (65) 65
membrane proteins - genetics (64) 64
presenilin-1 (64) 64
dementia - genetics (63) 63
medical research (61) 61
physiological aspects (61) 61
amino acid sequence (60) 60
amyloid precursor protein (60) 60
genetic predisposition to disease - genetics (60) 60
genetic variation (58) 58
biotechnology & applied microbiology (56) 56
alzheimer disease - metabolism (55) 55
haplotypes (55) 55
medicine & public health (55) 55
genome-wide association study (54) 54
bipolar disorder - genetics (53) 53
protein (53) 53
brain - metabolism (52) 52
health aspects (52) 52
neurodegenerative diseases (51) 51
more...
Library Location Library Location
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


1. Full Text C5 Molecular Genetics of frontotemporal lobar neurodegeneration
by Van Broeckhoven, C
Revue Neurologique, ISSN 0035-3787, 10/2009, Volume 165, Issue 10, p. 21
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
2. Full Text Pathological mechanisms underlying TDP-43 driven neurodegeneration in FTLDALS spectrum disorders
by Janssens, J and Van Broeckhoven, C
HUMAN MOLECULAR GENETICS, ISSN 0964-6906, 10/2013, Volume 22, pp. R77 - R87
Aggregation of misfolded TAR DNA-binding protein 43 (TDP-43) is a striking hallmark of neurodegenerative processes that are observed in several neurological... 
43 KDA TDP-43 | MOTOR-NEURON DEGENERATION | NUCLEIC-ACID BINDING | PRION-LIKE DOMAINS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETICS & HEREDITY | CASPASE 3 ACTIVATION | AMYOTROPHIC-LATERAL-SCLEROSIS | RNA RECOGNITION MOTIF | FRONTOTEMPORAL LOBAR DEGENERATION | DNA-BINDING PROTEIN | LENGTH POLYGLUTAMINE EXPANSIONS
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
3. Full Text Novel Alzheimer's disease risk genes: exhaustive investigation is paramount
by Sleegers, K and Van Broeckhoven, C
ACTA NEUROPATHOLOGICA, ISSN 0001-6322, 08/2019, Volume 138, Issue 2, pp. 171 - 172
IDENTIFIES VARIANTS | PATHOLOGY | CLU | NEUROSCIENCES | CLINICAL NEUROLOGY | GENOME-WIDE ASSOCIATION | Genetic research | Advertising executives | Alzheimer's disease | Genes | Genomics | Risk factors | Index Medicus
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
4. Full Text Locus‐specific mutation databases for neurodegenerative brain diseases
by Cruts, Marc and Theuns, Jessie and Van Broeckhoven, Christine
Human Mutation, ISSN 1059-7794, 09/2012, Volume 33, Issue 9, pp. 1340 - 1344
The Alzheimer disease and frontotemporal dementia (AD&FTLD) and Parkinson disease (PD) Mutation Databases make available curated information of sequence... 
neurodegenerative brain disease | Parkinson disease | locus‐specific | mutation database | Alzheimer disease | frontotemporal lobar degeneration | Mutation database | Frontotemporal lobar degeneration | Neurodegenerative brain disease | Locus-specific | MOLECULAR-GENETICS | APP | RESOURCES | ALZHEIMERS-DISEASE | FRONTOTEMPORAL DEMENTIA | PRESENILINS | GENES | GENETICS & HEREDITY | FRAGMENT | UPDATE | locus-specific | Genetic Predisposition to Disease | Genetic Association Studies | Humans | Databases, Genetic | Neurodegenerative Diseases - diagnosis | Neurodegenerative Diseases - genetics | Genetic Loci | Parkinson Disease - genetics | Alzheimer Disease - diagnosis | Frontotemporal Lobar Degeneration - diagnosis | Parkinson Disease - diagnosis | Frontotemporal Lobar Degeneration - genetics | Mutation | Alzheimer Disease - genetics | Genome, Human | Parkinson's disease | Molecular genetics | Alzheimer's disease | Analysis | Genes | Index Medicus | Databases
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
5. Full Text Evolutionary morphology of the lizard chemosensory system (vol 7, 10141, 2017)
by Baeckens, S and Herrel, A and Broeckhoven, C and Vasilopoulou-Kampitsi, M and Huyghe, K and Goyens, J and Van Damme, R
SCIENTIFIC REPORTS, ISSN 2045-2322, 12/2017, Volume 7
MULTIDISCIPLINARY SCIENCES
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
6. Full Text TDP-43 Transgenic Mice Develop Spastic Paralysis and Neuronal Inclusions Characteristic of ALS and Frontotemporal Lobar Degeneration
by Hans Wils and Gernot Kleinberger and Jonathan Janssens and Sandra Pereson and Geert Joris and Ivy Cuijt and Veerle Smits and Chantal Ceuterick-De Groote and Christine van Broeckhoven and Samir Kumar-Singh and Stanley Appel
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2010, Volume 107, Issue 8, pp. 3858 - 3863
Neuronal cytoplasmic and intranuclear aggregates of RNA-binding protein TDP-43 are a hallmark feature of neurodegenerative diseases such as amyotrophic lateral... 
Brain | Pathology | Nervous system diseases | Spinal cord | Neurons | Transgenic animals | Antibodies | Amyotrophic lateral sclerosis | Frontotemporal lobar degeneration | Mice | Protein aggregation | Neurodegeneration | FTLD | Motor neuron disease | Dementia | motor neuron disease | PROTEIN | NUCLEIC-ACID BINDING | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | neurodegeneration | UBIQUITIN IMMUNOHISTOCHEMISTRY | AMYOTROPHIC-LATERAL-SCLEROSIS | NEURODEGENERATIVE DISEASES | DROSOPHILA | CELLULAR TOXICITY | protein aggregation | dementia | MUTATIONS | AGGREGATION | Frontotemporal Lobar Degeneration - pathology | Amyotrophic Lateral Sclerosis - genetics | Humans | Mice, Transgenic | Paralysis - genetics | Mutation, Missense | Paralysis - pathology | DNA-Binding Proteins - genetics | Muscle Spasticity - pathology | DNA-Binding Proteins - metabolism | Amyotrophic Lateral Sclerosis - pathology | Inclusion Bodies - genetics | Animals | Frontotemporal Lobar Degeneration - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Frontotemporal Lobar Degeneration - genetics | Inclusion Bodies - metabolism | Muscle Spasticity - genetics | Development and progression | Nervous system | Genetic aspects | Degeneration | Paralysis | Binding proteins | Health aspects | Proteins | Neurosciences | Rodents | Mutation | Ribonucleic acid--RNA | Index Medicus | Biological Sciences
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
7. Full Text The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS
by Kohji Mori and Shih-Ming Weng and Thomas Arzberger and Stephanie May and Kristin Rentzsch and Elisabeth Kremmer and Bettina Schmid and Hans A. Kretzschmar and Marc Cruts and Christine Van Broeckhoven and Christian Haass and Dieter Edbauer
Science, ISSN 0036-8075, 3/2013, Volume 339, Issue 6125, pp. 1335 - 1338
Expansion of a GGGGCC hexanucleotide repeat upstream of the C9orf72 coding region is the most common cause of familial frontotemporal lobar degeneration and... 
Trucks | Pathology | Neurodegenerative diseases | REPORTS | Antibodies | Frontotemporal lobar degeneration | Immunoblotting | Amyotrophic lateral sclerosis | Cytoplasmic inclusions | Genetic mutation | Hippocampus | INITIATION | MULTIDISCIPLINARY SCIENCES | FRONTOTEMPORAL DEMENTIA | EXPANSION | FTD | ALS | AMYOTROPHIC-LATERAL-SCLEROSIS | IDENTIFICATION | HEXANUCLEOTIDE REPEAT | Frontotemporal Lobar Degeneration - pathology | Protein Biosynthesis | Sequestosome-1 Protein | Amyotrophic Lateral Sclerosis - genetics | Cerebellum - metabolism | Humans | Open Reading Frames | Hippocampus - pathology | Cerebellum - pathology | DNA-Binding Proteins - metabolism | Proteins - genetics | DNA Repeat Expansion | Hippocampus - metabolism | Amyotrophic Lateral Sclerosis - pathology | Proteins - metabolism | Frontotemporal Lobar Degeneration - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Heterozygote | C9orf72 Protein | Frontotemporal Lobar Degeneration - genetics | Adaptor Proteins, Signal Transducing - metabolism | Gene mutations | Nervous system | Genetic aspects | Degeneration | Nucleotides | Properties | Proteins | Genetics | Neurodegeneration | Dementia | Index Medicus | Cerebellum | Coding | Central nervous system | Links | Inclusions | Patients
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
8. Full Text GFRA2 in GRN-related frontotemporal lobar degeneration
by Wauters, Eline and Van Broeckhoven, Christine
The Lancet Neurology, ISSN 1474-4422, 06/2018, Volume 17, Issue 6, pp. 488 - 489
COMMON | CLINICAL NEUROLOGY | Frontotemporal Dementia | Genome-Wide Association Study | Progranulins | Humans | Age of Onset | Frontotemporal Lobar Degeneration - genetics | Mutation | Glial Cell Line-Derived Neurotrophic Factor Receptors - genetics | Index Medicus
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
9. Full Text The Use of Biomarkers and Genetic Screening to Diagnose Frontotemporal Dementia: Evidence and Clinical Implications
by Gossye, H and Van Broeckhoven, C and Engelborghs, S
FRONTIERS IN NEUROSCIENCE, 08/2019, Volume 13
Within the wide range of neurodegenerative brain diseases, the differential diagnosis of frontotemporal dementia (FTD) frequently poses a challenge. Often,... 
HEXANUCLEOTIDE REPEAT EXPANSION | DIFFERENTIAL-DIAGNOSIS | LOBAR DEGENERATION | MRI | ALZHEIMERS-DISEASE | frontotemporal dementia | AMYOTROPHIC-LATERAL-SCLEROSIS | biomarker | Alzheimer | NEUROSCIENCES | FRONTAL BEHAVIORAL INVENTORY | genetics | TRANSCRANIAL MAGNETIC STIMULATION | CEREBROSPINAL-FLUID BIOMARKERS | cerebrospinal fluid | dementia | NEUROFILAMENT LIGHT-CHAIN | PRIMARY PROGRESSIVE APHASIA
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
10. Full Text Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins
by Mori, Kohji and Arzberger, Thomas and Grässer, Friedrich A and Gijselinck, Ilse and May, Stephanie and Rentzsch, Kristin and Weng, Shih-Ming and Schludi, Martin H and van der Zee, Julie and Cruts, Marc and Van Broeckhoven, Christine and Kremmer, Elisabeth and Kretzschmar, Hans A and Haass, Christian and Edbauer, Dieter
Acta Neuropathologica, ISSN 0001-6322, 12/2013, Volume 126, Issue 6, pp. 881 - 893
Massive GGGGCC repeat expansion in the first intron of the gene C9orf72 is the most common known cause of familial frontotemporal lobar degeneration (FTLD) and... 
Pathology | Neurosciences | RAN translation | Medicine & Public Health | Neurodegeneration | FTLD | ALS | C9orf72 | DEMENTIA | AMYOTROPHIC-LATERAL-SCLEROSIS | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | CLINICAL NEUROLOGY | TDP-43 | EXPANSION | SPECTRUM | TDP-43-NEGATIVE INCLUSIONS | MOLECULAR-BASIS | GGGGCC REPEAT | Protein Biosynthesis | Amyotrophic Lateral Sclerosis - genetics | Humans | Amyotrophic Lateral Sclerosis - diagnosis | Brain - metabolism | Proteins - genetics | DNA Repeat Expansion | Proteins - metabolism | Frontotemporal Lobar Degeneration - metabolism | Frontotemporal Lobar Degeneration - diagnosis | Amyotrophic Lateral Sclerosis - metabolism | C9orf72 Protein | Frontotemporal Lobar Degeneration - genetics | Proteins | Brain | Biological products | RNA | Monoclonal antibodies | Amyotrophic lateral sclerosis | Glycine | Index Medicus
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
11. Full Text hnRNP A3 binds to GGGGCC repeats and is a constituent of p62-positive/TDP43-negative inclusions in the hippocampus of patients with C9orf72 mutations
by Mori, Kohji and Lammich, Sven and Mackenzie, Ian R. A and Forné, Ignasi and Zilow, Sonja and Kretzschmar, Hans and Edbauer, Dieter and Janssens, Jonathan and Kleinberger, Gernot and Cruts, Marc and Herms, Jochen and Neumann, Manuela and Van Broeckhoven, Christine and Arzberger, Thomas and Haass, Christian
Acta Neuropathologica, ISSN 0001-6322, 3/2013, Volume 125, Issue 3, pp. 413 - 423
Genetic analysis revealed the hexanucleotide repeat expansion GGGGCC within the regulatory region of the gene C9orf72 as the most common cause of familial... 
Pathology | hnRNP A3 | Neurosciences | Medicine & Public Health | Neurodegeneration | TDP-43 | FTLD | ALS | C9orf72 | DEMENTIA | PROTEIN | EXPANSIONS | AMYOTROPHIC-LATERAL-SCLEROSIS | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | MASS-SPECTROMETRY | CLINICAL NEUROLOGY | GENE | HEXANUCLEOTIDE REPEAT | Frontotemporal Lobar Degeneration - pathology | Gene Expression Regulation - genetics | Sequestosome-1 Protein | Amyotrophic Lateral Sclerosis - genetics | Humans | Repetitive Sequences, Nucleic Acid - physiology | Heterogeneous-Nuclear Ribonucleoprotein Group A-B - metabolism | Hippocampus - pathology | Chromatography, High Pressure Liquid | Mutation - genetics | DNA-Binding Proteins - metabolism | Proteins - genetics | Amyotrophic Lateral Sclerosis - pathology | Transfection | Frontotemporal Lobar Degeneration - metabolism | Mass Spectrometry | Amyotrophic Lateral Sclerosis - metabolism | HEK293 Cells | Inclusion Bodies - pathology | C9orf72 Protein | Frontotemporal Lobar Degeneration - genetics | Adaptor Proteins, Signal Transducing - metabolism | Inclusion Bodies - metabolism | RNA, Small Interfering - metabolism | Immunohistochemistry | Brain | RNA | Analysis | Physiological aspects | Amyotrophic lateral sclerosis | Genetic aspects | Binding proteins | Genetic translation | Protein binding | Index Medicus | Translation | Toxicity | Regulatory sequences | Metabolism | RNA-binding protein | Autopsy | Inclusion bodies | Genetic analysis | Mutation | Frontotemporal dementia | Hippocampus
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
12. Full Text Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease
by Sims, Rebecca and Van Der Lee, Sven J and Naj, Adam C and Bellenguez, Céline and Badarinarayan, Nandini and Jakobsdottir, Johanna and Kunkle, Brian W and Boland, Anne and Raybould, Rachel and Bis, Joshua C and Martin, Eden R and Grenier-Boley, Benjamin and Heilmann-Heimbach, Stefanie and Chouraki, Vincent and Kuzma, Amanda B and Sleegers, Kristel and Vronskaya, Maria and Ruiz, Agustin and Graham, Robert R and Olaso, Robert and Hoffmann, Per and Grove, Megan L and Vardarajan, Badri N and Hiltunen, Mikko and Nöthen, Markus M and White, Charles C and Hamilton-Nelson, Kara L and Epelbaum, Jacques and Maier, Wolfgang and Choi, Seung-Hoan and Beecham, Gary W and Dulary, Cécile and Herms, Stefan and Smith, Albert V and Funk, Cory C and Derbois, Céline and Forstner, Andreas J and Ahmad, Shahzad and Li, Hongdong and Bacq, Delphine and Harold, Denise and Satizabal, Claudia L and Valladares, Otto and Squassina, Alessio and Thomas, Rhodri and Brody, Jennifer A and Qu, Liming and Sánchez-Juan, Pascual and Morgan, Taniesha and Wolters, Frank J and Zhao, Yi and Garcia, Florentino Sanchez and Denning, Nicola and Fornage, Myriam and Malamon, John and Naranjo, Maria Candida Deniz and Majounie, Elisa and Mosley, Thomas H and Dombroski, Beth and Wallon, David and Lupton, Michelle K and Dupuis, Josée and Whitehead, Patrice and Fratiglioni, Laura and Medway, Christopher and Jian, Xueqiu and Mukherjee, Shubhabrata and Keller, Lina and Brown, Kristelle and Lin, Honghuang and Cantwell, Laura B and Panza, Francesco and McGuinness, Bernadette and Moreno-Grau, Sonia and Burgess, Jeremy D and Solfrizzi, Vincenzo and Proitsi, Petra and Adams, Hieab H and Allen, Mariet and Seripa, Davide and Pastor, Pau and Cupples, L Adrienne and Price, Nathan D and Hannequin, Didier and Frank-García, Ana and Levy, Daniel and Chakrabarty, Paramita and Caffarra, Paolo and Giegling, Ina and Beiser, Alexa S and Giedraitis, Vilmantas and Hampel, Harald and Garcia, Melissa E and Wang, Xue and Lannfelt, Lars and Mecocci, Patrizia and Eiriksdottir, Gudny and Crane, Paul K and Pasquier, Florence and Boccardi, Virginia and ... and EADI and GERAD PERADES and ARUKConsortium and CHARGE and ADGC and GERAD/PERADES, CHARGE, ADGC, EADI and ARUK Consortium and Stockholms universitet and Centrum för forskning om äldre och åldrande (ARC), (tills m KI) and Samhällsvetenskapliga fakulteten
Nature Genetics, ISSN 1061-4036, 09/2017, Volume 49, Issue 9, pp. 1373 - 1384
We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. In stage 1, we genotyped 34,174... 
COMMON VARIANTS | IDENTIFIES VARIANTS | METAANALYSIS | GENOTYPE IMPUTATION | LOW-FREQUENCY | SUSCEPTIBILITY | GENETICS & HEREDITY | RISK | LOCI | WAVE2 COMPLEX | GENOME-WIDE ASSOCIATION | Amino Acid Sequence | Microglia - metabolism | Genetic Predisposition to Disease - genetics | Gene Frequency | Humans | Immunity, Innate - genetics | Genotype | Gene Expression Profiling | Case-Control Studies | Linkage Disequilibrium | Membrane Glycoproteins - genetics | Sequence Homology, Amino Acid | Exome - genetics | Protein Interaction Maps - genetics | Adaptor Proteins, Signal Transducing - genetics | Phospholipase C gamma - genetics | Polymorphism, Single Nucleotide | Alzheimer Disease - genetics | Odds Ratio | Receptors, Immunologic - genetics | Immune response | Genetic variation | Physiological aspects | Development and progression | Genetic aspects | Research | Alzheimer's disease | Neurodegenerative diseases | Genes | Genomics | Health risks | Innate immunity | Genomes | Disease control | Immunity | Microglia | Proteins | Immune systems | Studies | Consortia | DNA microarrays | Genotyping | Gene frequency | DNA methylation | Alzheimers disease | Protein interaction | Bioinformatics | Genotypes | Index Medicus | Biological Sciences | Naturvetenskap | Natural Sciences | Biologiska vetenskaper
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights
13. Full Text Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease
by Lambert, Jean-Charles and Ibrahim-Verbaas, Carla A and Harold, Denise and Naj, Adam C and Sims, Rebecca and Bellenguez, Céline and Jun, Gyungah and DeStefano, Anita L and Bis, Joshua C and Beecham, Gary W and Grenier-Boley, Benjamin and Russo, Giancarlo and Thornton-Wells, Tricia A and Jones, Nicola and Smith, Albert V and Chouraki, Vincent and Thomas, Charlene and Ikram, M. Arfan and Zelenika, Diana and Vardarajan, Badri N and Kamatani, Yoichiro and Lin, Chiao-Feng and Gerrish, Amy and Schmidt, Helena and Kunkle, Brian and Fiévet, Nathalie and Amouyel, Philippe and Pasquier, Florence and Deramecourt, Vincent and De Bruijn, Renee F.A.G and Amin, Najaf and Hofman, Albert and Van Duijn, Cornelia M and Dunstan, Melanie L and Hollingworth, Paul and Owen, Michael J and O'Donovan, Michael C and Jones, Lesley and Holmans, Peter A and Moskvina, Valentina and Williams, Julie and Baldwin, Clinton and Farrer, Lindsay A and Choi, Seung-Hoan and Lunetta, Kathryn L and Fitzpatrick, Annette L and Harris, Tamara B and Psaty, Bruce M and Gilbert, John R and Hamilton-Nelson, Kara L and Martin, Eden R and Kunkle, Brian and Haines, Jonathan L and Gudnason, Vilmundur and Jonsson, Palmi V and Eiriksdottir, Gudny and Bihoreau, Marie-Thérèse and Lathrop, Mark and Valladares, Otto and Cantwell, Laura B and Wang, Li-San and Schellenberg, Gerard D and Ruiz, Agustin and Boada, Mercè and Reitz, Christiane and Mayeux, Richard and Ramirez, Alfredo and Maier, Wolfgang and Hanon, Olivier and Kukull, Walter A and Buxbaum, Joseph D and Campion, Dominique and Wallon, David and Hannequin, Didier and Crane, Paul K and Larson, Eric B and Becker, Tim and Cruchaga, Carlos and Goate, Alison M and Craig, David and Johnston, Janet A and Mc-Guinness, Bernadette and Todd, Stephen and Passmore, Peter and Berr, Claudine and Ritchie, Karen and Lopez, Oscar L and De Jager, Philip L and Evans, Denis and Lovestone, Simon and Proitsi, Petroula and Powell, John F and Letenneur, Luc and Barberger-Gateau, Pascale and Dufouil, Carole and Dartigues, Jean-François and Morón, Francisco J and Rubinsztein, David C and St. George-Hyslop, Peter and Sleegers, Kristel and ... and EADI and CHARGE and ADGC and GERAD and Cohorts for Heart and Aging Research in Genomic Epidemiology and Genetic and Environmental Risk in Alzheimer's Disease and Alzheimer's Disease Genetic Consortium and European Alzheimer's Disease Initiative (EADI) and Alzheimer's Disease Genetic Consortium (ADGC) and Genetic and Environmental Risk in Alzheimer's Disease (GERAD) and Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) and Stockholms universitet and Centrum för forskning om äldre och åldrande (ARC), (tills m KI) and Samhällsvetenskapliga fakulteten
Nature Genetics, ISSN 1061-4036, 12/2013, Volume 45, Issue 12, pp. 1452 - 1458
Eleven susceptibility loci for late-onset Alzheimer's disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this... 
GENOTYPES | COMMON VARIANTS | IMPUTATION | GENETIC RISK | SEQUENCE | GENETICS & HEREDITY | NEURONS | RECEPTOR | MUTATIONS | CD33 | GENOME-WIDE ASSOCIATION | Genetic Predisposition to Disease | Humans | Middle Aged | Male | Genetic Loci | Genome-Wide Association Study - statistics & numerical data | Case-Control Studies | Age of Onset | Aged, 80 and over | Alzheimer Disease - epidemiology | Female | Aged | Polymorphism, Single Nucleotide | Alzheimer Disease - genetics | Cohort Studies | Quantitative trait loci | Genetic aspects | Research | Genetic susceptibility | Alzheimer's disease | Identification and classification | Genealogy | Genomics | Genes | Quality control | Aging | Genomes | Alzheimers disease | Health risk assessment | Meta-analysis | Index Medicus | Genetik | Biological Sciences | Genetics | Naturvetenskap | Natural Sciences | Biologiska vetenskaper
Journal Article
Details down arrow
Digital rights down arrow
loading Loading Rights