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1. Full Text Phenotypic variability associated with progranulin haploinsufficiency in patients with the common 1477C→T (Arg493X) mutation: an international initiative
by Rademakers, Rosa, PhD and Baker, Matt, BSc and Gass, Jennifer, BS and Adamson, Jennifer, BS and Huey, Edward D, MD and Momeni, Parastoo, PhD and Spina, Salvatore, MD and Coppola, Giovanni, MD and Karydas, Anna M, BA and Stewart, Heather, PhD and Johnson, Nancy, PhD and Hsiung, Ging-Yuek, MD and Kelley, Brendan, MD and Kuntz, Karen, RN and Steinbart, Ellen, MA and Wood, Elisabeth McCarty, MS and Yu, Chang-En, PhD and Josephs, Keith, MD and Sorenson, Eric, MD and Womack, Kyle B, MD and Weintraub, Sandra, PhD and Pickering-Brown, Stuart M, PhD and Schofield, Peter R, DSc and Brooks, William S, MBBS and Van Deerlin, Vivianna M, MD and Snowden, Julie, PhD and Clark, Christopher M, MD and Kertesz, Andrew, MD and Boylan, Kevin, MD and Ghetti, Bernardino, MD and Neary, David, FRCP and Schellenberg, Gerard D, PhD and Beach, Thomas G, FRCPC and Mesulam, Marsel, MD and Mann, David, PhD and Grafman, Jordan, PhD and Mackenzie, Ian R, MD and Feldman, Howard, MD and Bird, Thomas, MD and Petersen, Ron, MD and Knopman, David, MD and Boeve, Bradley, MD and Geschwind, Dan H, MD and Miller, Bruce, MD and Wszolek, Zbigniew, MD and Lippa, Carol, MD and Bigio, Eileen H, MD and Dickson, Dennis, MD and Graff-Radford, Neill, FRCP and Hutton, Mike, PhD
Lancet Neurology, The, ISSN 1474-4422, 2007, Volume 6, Issue 10, pp. 857 - 868
Summary Background The progranulin gene ( GRN ) is mutated in 5–10% of patients with frontotemporal lobar degeneration (FTLD) and in about 20% of patients with... 
Neurology | MISSENSE | DEMENTIA | GENE | INCLUSIONS | TDP-43 | DISEASE | TAU | NEUROPATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | CLINICAL NEUROLOGY | FEATURES | Haplotypes | Neurons - pathology | Memory Disorders - genetics | Humans | Middle Aged | Ubiquitin - metabolism | Male | Dementia - epidemiology | Dementia - genetics | DNA-Binding Proteins - metabolism | Founder Effect | tau Proteins - genetics | Female | Retrospective Studies | Neurofibrillary Tangles - pathology | Memory Disorders - epidemiology | Dementia - pathology | Intercellular Signaling Peptides and Proteins - genetics | Aphasia, Primary Progressive - genetics | Genotype | Neurodegenerative Diseases - genetics | Phenotype | Apolipoproteins E - genetics | Age of Onset | Alleles | Inclusion Bodies - pathology | Heterozygote | Aged | Polymorphism, Single Nucleotide | Mutation | Alzheimer Disease - genetics | Neurodegenerative Diseases - epidemiology | Cohort Studies | Medical colleges | Neurosciences | Genetic aspects
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2. Full Text Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease
by Sims, Rebecca and Lee, Sven and Adams, Hieab and Reitz, Christiane and Hofman, A and Rivadeneira, F and Uitterlinden, Ané and Ikram, Arfan and Launer, Lenore and Amin, Najaf and Duijn, Cornelia 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
markdownabstractWe identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. In stage 1, we... 
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 | Studies | Consortia | DNA microarrays | Genotyping | Gene frequency | DNA methylation | Alzheimers disease | Protein interaction | Bioinformatics | Genotypes | Immune system | Biological Sciences | Naturvetenskap | Natural Sciences | Biologiska vetenskaper
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3. Full Text Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates A beta, tau, immunity and lipid processing
by Kunkle, BW and Grenier-Boley, B and Sims, R and Bis, JC and Damotte, V and Naj, AC and Boland, A and Vronskaya, M and van der Lee, SJ and Amlie-Wolf, A and Bellenguez, C and Frizatti, A and Chouraki, V and Martin, ER and Sleegers, K and Badarinarayan, N and Jakobsdottir, J and Hamilton-Nelson, KL and Moreno-Grau, S and Olaso, R and Raybould, R and Chen, YN and Kuzma, AB and Hiltunen, M and Morgan, T and Ahmad, S and Vardarajan, BN and Epelbaum, J and Hoffmann, P and Boada, M and Beecham, GW and Garnier, JG and Harold, D and Fitzpatrick, AL and Valladares, O and Moutet, ML and Gerrish, A and Smith, AV and Qu, LM and Bacq, D and Denning, N and Jian, XQ and Zhao, Y and Del Zompo, M and Fox, NC and Choi, SH and Mateo, I and Hughes, JT and Adams, HH and Malamon, J and Sanchez-Garcia, F and Patel, Y and Brody, JA and Dombroski, BA and Naranjo, MCD and Daniilidou, M and Eiriksdottir, G and Mukherjee, S and Wallon, D and Uphill, J and Aspelund, T and Cantwell, LB and Garzia, F and Galimberti, D and Hofer, E and Butkiewicz, M and Fin, B and Scarpini, E and Sarnowski, C and Bush, WS and Meslage, S and Kornhuber, J and White, CC and Song, Y and Barber, RC and Engelborghs, S and Sordon, S and Voijnovic, D and Adams, PM and Vandenberghe, R and Mayhaus, M and Cupples, LA and Albert, MS and De Deyn, PP and Gu, W and Himali, JJ and Beekly, D and Squassina, A and Hartmann, AM and Orellana, A and Blacker, D and Rodriguez-Rodriguez, E and Lovestone, S and Garcia, ME and Doody, RS and Munoz-Fernadez, C and Sussams, R and Lin, HH and Fairchild, TJ and Benito, YA and ... and Cohorts Heart Aging Res Genomic Ep and Alzheimer Dis Genetics Consortium and European Alzheimers Dis Initiative and Genetic Environm Risk AD Defining and Alzheimer Disease Genetics Consortium (ADGC) and Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (CHARGE) and 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 Stockholms universitet and Centrum för forskning om äldre och åldrande (ARC), (tills m KI) and Samhällsvetenskapliga fakulteten
NATURE GENETICS, ISSN 1061-4036, 03/2019, Volume 51, Issue 3, pp. 414 - 414
Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. To identify LOAD risk loci, we performed a large... 
COMMON VARIANTS | GENOTYPE IMPUTATION | AMYLOID-BETA | GENETICS & HEREDITY | DOMAIN-CONTAINING OXIDOREDUCTASE | MUTATIONS | ANGIOTENSIN-CONVERTING ENZYME | TRANSCRIPTION FACTOR | ONSET | GENOME-WIDE ASSOCIATION | APOLIPOPROTEIN-E | Genetic Predisposition to Disease - genetics | Lipids - genetics | Humans | Genetic Loci - genetics | Male | Genetic Testing - methods | Case-Control Studies | Haplotypes - genetics | tau Proteins - genetics | Amyloid beta-Peptides - genetics | Female | Lipid Metabolism - genetics | Aged | Alzheimer Disease - genetics | Genome-Wide Association Study - methods | Immunity - genetics | Ontology | Genomics | Genes | Lipids | Genomes | Mapping | Family medical history | Immunity | Risk factors | Protein turnover | Datasets | Proteins | Consortia | Genetic analysis | Dementia disorders | Genetics | Lipid metabolism | Alzheimer's disease | Age | ADAMTS-1 protein | Neurodegenerative diseases | Health risks | Metabolism | Risk analysis | Amyloid precursor protein | Meta-analysis | White blood cells | Genetic variance | Tau protein | Histocompatibility antigen HLA | Gene loci | Gene mapping | Alzheimers disease | Secretase | Dementia | Index Medicus | Basic Medicine | Medical Genetics | Medicinsk genetik | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper
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4. Full Text TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics
by Mackenzie, Ian R and Nicholson, Alexandra M and Sarkar, Mohona and Messing, James and Purice, Maria D and Pottier, Cyril and Annu, Kavya and Baker, Matt and Perkerson, Ralph B and Kurti, Aishe and Matchett, Billie J and Mittag, Tanja and Temirov, Jamshid and Hsiung, Ging-Yuek R and Krieger, Charles and Murray, Melissa E and Kato, Masato and Fryer, John D and Petrucelli, Leonard and Zinman, Lorne and Weintraub, Sandra and Mesulam, Marsel and Keith, Julia and Zivkovic, Sasha A and Hirsch-Reinshagen, Veronica and Roos, Raymond P and Züchner, Stephan and Graff-Radford, Neill R and Petersen, Ronald C and Caselli, Richard J and Wszolek, Zbigniew K and Finger, Elizabeth and Lippa, Carol and Lacomis, David and Stewart, Heather and Dickson, Dennis W and Kim, Hong Joo and Rogaeva, Ekaterina and Bigio, Eileen and Boylan, Kevin B and Taylor, J. Paul and Rademakers, Rosa
Neuron, ISSN 0896-6273, 08/2017, Volume 95, Issue 4, pp. 808 - 816.e9
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and... 
low-complexity domain | liquid-liquid phase separation | TDP-43 | T cell-restricted intracellular antigen-1 | stress granules | frontotemporal dementia | amyotrophic lateral sclerosis | membrane-less organelle | frontotemporal lobar degeneration | MULTISYSTEM PROTEINOPATHY | DISTAL MYOPATHY | MESSENGER-RNA | LIQUID DROPLETS | SEQUENCING DATA | HEXANUCLEOTIDE REPEAT | DOMAINS | C9ORF72 | NEUROSCIENCES | FAMILIAL ALS | Humans | Middle Aged | Family Health | Male | Green Fluorescent Proteins - genetics | DNA-Binding Proteins - metabolism | Transfection | Time Factors | Adult | Female | T-Cell Intracellular Antigen-1 | Frontotemporal Dementia - pathology | Frontotemporal Dementia - genetics | Stress, Physiological - physiology | Green Fluorescent Proteins - metabolism | Poly(A)-Binding Proteins - genetics | Amyotrophic Lateral Sclerosis - genetics | Heterogeneous-Nuclear Ribonucleoprotein Group A-B - metabolism | RNA-Binding Protein FUS - metabolism | Mutation - genetics | Heterogeneous Nuclear Ribonucleoprotein A1 | Microscopy, Confocal | Amyotrophic Lateral Sclerosis - pathology | Aged | HeLa Cells | Nervous system diseases | RNA | Analysis | Genetic research | Development and progression | Amyotrophic lateral sclerosis | Genetic aspects | T cells | Binding proteins | Protein binding | Dementia | Disease | Neurodegenerative diseases | Pathogenesis | Genes | Disorders | Lymphocytes T | Metabolism | Ribonucleic acid--RNA | Phase transitions | Proteins | Consortia | Pathology | DNA-binding protein | Etiology | Phase separation | Dementia disorders | Mutation | Frontotemporal dementia | Dismantling | Age | Deoxyribonucleic acid--DNA | Phase transition | T-cell-restricted intracellular antigen-1
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5. Full Text Evidence for a role of the rare p.A152T variant in mapt in increasing the risk for FTD-spectrum and Alzheimer's diseases
by Coppola, Giovanni and Chinnathambi, Subashchandrabose and Lee, Jason JiYong and Dombroski, Beth A and Baker, Matt C and Soto-ortolaza, Alexandra I and Lee, Suzee E and Klein, Eric and Huang, Alden Y and Sears, Renee and Lane, Jessica R and Karydas, Anna M and Kenet, Robert O and Biernat, Jacek and Wang, Li-San and Cotman, Carl W and Decarli, Charles S and Levey, Allan I and Ringman, John M and Mendez, Mario F and Chui, Helena C and Le ber, Isabelle and Brice, Alexis and Lupton, Michelle K and Preza, Elisavet and Lovestone, Simon and Powell, John and Graff-radford, Neill and Petersen, Ronald C and Boeve, Bradley F and Lippa, Carol F and Bigio, Eileen H and Mackenzie, Ian and Finger, Elizabeth and Kertesz, Andrew and Caselli, Richard J and Gearing, Marla and Juncos, Jorge L and Ghetti, Bernardino and Spina, Salvatore and Bordelon, Yvette M and Tourtellotte, Wallace W and Frosch, Matthew P and Vonsattel, Jean Paul G and Zarow, Chris and Beach, Thomas G and Albin, Roger L and Lieberman, Andrew P and Lee, Virginia M and Trojanowski, John Q and Van deerlin, Vivianna M and Bird, Thomas D and Galasko, Douglas R and Masliah, Eliezer and White, Charles L and Troncoso, Juan C and Hannequin, Didier and Boxer, Adam L and Geschwind, Michael D and Kumar, Satish and Mandelkow, Eva-Maria and Wszolek, Zbigniew K and Uitti, Ryan J and Dickson, Dennis W and Haines, Jonathan L and Mayeux, Richard and Pericak-vance, Margaret A and Farrer, Lindsay A and Apostolova, Liana G and Arnold, Steven E and Baldwin, Clinton T and Barber, Robert and Barmada, Michael M and Beach, Thomas and Beecham, Gary W and Beekly, Duane and Bennett, David A and Bigio, Eileen H and Bird, Thomas D and Blacker, Deborah and Boeve, Bradley F and Bowen, James D and Boxer, Adam and Burke, James R and Buros, Jacqueline and Buxbaum, Joseph D and Cairns, Nigel J and Cantwell, Laura B and Cao, Chuanhai and Carlson, Chris S and Carney, Regina M and Carrasquillo, Minerva M and Carroll, Steven L and Chui, Helena C and Clark, David G and Corneveaux, Jason and Cotman, Carl W and Crane, Paul K and Cruchaga, Carlos and Cummings, Jeffrey L and ... and Alzheimer's Dis Genetics Consortiu and Alzheimer's Disease Genetics Consortium
Human Molecular Genetics, ISSN 0964-6906, 2012, Volume 21, Issue 15, pp. 3500 - 3512
Tau p.A152T significantly increases the risk for both FTD-s (n 2139, OR 3.0, CI: 1.65.6, P 0.0005) and Alzheimers disease (AD) (n 3345, OR 2.3, CI: 1.34.2, P... 
TAU-PROTEIN | COMMON VARIANTS | PARKINSONISM | INCLUSIONS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | FRONTOTEMPORAL DEMENTIA | MUTATION | GENETICS & HEREDITY | HAPLOTYPE | ASSOCIATION | AGGREGATION | Frontotemporal Dementia - genetics | Haplotypes | Genetic Predisposition to Disease | Humans | Middle Aged | Genotype | Risk | Genetic Variation | tau Proteins - genetics | Alzheimer Disease - epidemiology | Aged | Alzheimer Disease - genetics | Frontotemporal Dementia - epidemiology | Association Studies
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6. Full Text Transethnic genome-wide scan identifies novel Alzheimer's disease loci
by Jun, Gyungah R and Chung, Jaeyoon and Mez, Jesse and Barber, Robert and Beecham, Gary W and Bennett, David A and Buxbaum, Joseph D and Byrd, Goldie S and Carrasquillo, Minerva M and Crane, Paul K and Cruchaga, Carlos and De Jager, Philip and Ertekin-Taner, Nilufer and Evans, Denis and Fallin, M. Danielle and Foroud, Tatiana M and Friedland, Robert P and Goate, Alison M and Graff-Radford, Neill R and Hendrie, Hugh and Hall, Kathleen S and Hamilton-Nelson, Kara L and Inzelberg, Rivka and Kamboh, M. Ilyas and Kauwe, John S.K and Kukull, Walter A and Kunkle, Brian W and Kuwano, Ryozo and Larson, Eric B and Logue, Mark W and Manly, Jennifer J and Martin, Eden R and Montine, Thomas J and Mukherjee, Shubhabrata and Naj, Adam and Reiman, Eric M and Reitz, Christiane and Sherva, Richard and St. George-Hyslop, Peter H and Thornton, Timothy and Younkin, Steven G and Vardarajan, Badri N and Wang, Li-San and Wendlund, Jens R and Winslow, Ashley R and Haines, Jonathan and Mayeux, Richard and Pericak-Vance, Margaret A and Schellenberg, Gerard and Lunetta, Kathryn L and Farrer, Lindsay A and Alzheimer's Dis Genetics and Alzheimer's Disease Genetics Consortium
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, ISSN 1552-5260, 2017, Volume 13, Issue 7, pp. 727 - 738
Abstract Introduction Genetic loci for Alzheimer's disease (AD) have been identified in whites of European ancestry, but the genetic architecture of AD among... 
Neurology | Genome-wide association | APOE interaction | Alzheimer's disease | Transethnic | PROTEIN | METAANALYSIS | SUSCEPTIBILITY LOCI | APOLIPOPROTEIN-E GENOTYPE | CLINICAL NEUROLOGY | GENE | MOUSE MODEL | BENZODIAZEPINE | APOE | ASSOCIATION | BINDING | Heparin-binding EGF-like Growth Factor - genetics | Genetic Predisposition to Disease | Genome-Wide Association Study | Apolipoprotein E4 - genetics | Receptors, GABA - genetics | Humans | Molecular Chaperones - genetics | NFI Transcription Factors - genetics | Membrane Glycoproteins - genetics | Peroxisomal Bifunctional Enzyme - genetics | Adaptor Proteins, Signal Transducing - genetics | Polymorphism, Single Nucleotide | GTPase-Activating Proteins - genetics | Alzheimer Disease - genetics | Genomics
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7. Full Text Association of Long Runs of Homozygosity With Alzheimer Disease Among African American Individuals
by Ghani, Mahdi and Reitz, Christiane and Cheng, Rong and Vardarajan, Badri Narayan and Jun, Gyungah and Sato, Christine and Naj, Adam and Rajbhandary, Ruchita and Wang, Li-San and Valladares, Otto and Lin, Chiao-Feng and Larson, Eric B and Graff-Radford, Neill R and Evans, Denis and De Jager, Philip L and Crane, Paul K and Buxbaum, Joseph D and Murrell, Jill R and Raj, Towfique and Ertekin-Taner, Nilufer and Logue, Mark and Baldwin, Clinton T and Green, Robert C and Barnes, Lisa L and Cantwell, Laura B and Fallin, M. Daniele and Go, Rodney C. P and Griffith, Patrick A and Obisesan, Thomas O and Manly, Jennifer J and Lunetta, Kathryn L and Kamboh, M. Ilyas and Lopez, Oscar L and Bennett, David A and Hendrie, Hugh and Hall, Kathleen S and Goate, Alison M and Byrd, Goldie S and Kukull, Walter A and Foroud, Tatiana M and Haines, Jonathan L and Farrer, Lindsay A and Pericak-Vance, Margaret A and Lee, Joseph H and Schellenberg, Gerard D and St. George-Hyslop, Peter and Mayeux, Richard and Rogaeva, Ekaterina and Alzheimer's Dis Genetics and Alzheimer’s Disease Genetics Consortium
JAMA Neurology, ISSN 2168-6149, 11/2015, Volume 72, Issue 11, pp. 1313 - 1323
IMPORTANCE: Mutations in known causal Alzheimer disease (AD) genes account for only 1% to 3% of patients and almost all are dominantly inherited. Recessive... 
POPULATION | DEMENTIA | VARIANTS | EXTENDED TRACTS | GENOTYPE | PROTEIN EXPRESSION | SECRETASE ACTIVITY | MUTATION | RISK | BRAIN | CLINICAL NEUROLOGY | African Americans - ethnology | Homozygote | Genome-Wide Association Study | Indiana - ethnology | Humans | Polymorphism, Single Nucleotide - genetics | Aged | Alzheimer Disease - genetics | Genes, Recessive | Case-Control Studies | Chicago - ethnology
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8. Full Text FUS Interacts with HSP60 to Promote Mitochondrial Damage
by Deng, Jianwen and Yang, Mengxue and Chen, Yanbo and Chen, Xiaoping and Liu, Jianghong and Sun, Shufeng and Cheng, Haipeng and Li, Yang and Bigio, Eileen H and Mesulam, Marsel and Xu, Qi and Du, Sidan and Fushimi, Kazuo and Zhu, Li and Wu, Jane Y
PLoS Genetics, ISSN 1553-7390, 2015, Volume 11, Issue 9, p. e1005357
FUS-proteinopathies, a group of heterogeneous disorders including ALS-FUS and FTLD-FUS, are characterized by the formation of inclusion bodies containing the... 
RNA-BINDING PROTEINS | OXIDATIVE STRESS | HEREDITARY SPASTIC PARAPLEGIA | DROSOPHILA-MELANOGASTER | BASOPHILIC INCLUSIONS | MOLECULAR CHAPERONES | IN-VIVO | MUTANT HUNTINGTIN | GENETICS & HEREDITY | AMYOTROPHIC-LATERAL-SCLEROSIS | FRONTOTEMPORAL LOBAR DEGENERATION | Reactive Oxygen Species - metabolism | Animals, Genetically Modified | Drosophila | Cells, Cultured | Mitochondria - metabolism | Drosophila Proteins - metabolism | Heterogeneous-Nuclear Ribonucleoprotein Group F-H - genetics | Heterogeneous-Nuclear Ribonucleoprotein Group F-H - metabolism | Phenotype | Animals | Protein Binding | Chaperonin 60 - metabolism | Neurons - metabolism | Drosophila Proteins - genetics | Heat shock proteins | Mitochondrial DNA | Observations | Health aspects | DNA damage | Amyotrophic lateral sclerosis | Mutation | Neurodegeneration | Genes | Rodents
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