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1. Full Text C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits
by Chew, Jeannie and Gendron, Tania F and Prudencio, Mercedes and Sasaguri, Hiroki and Zhang, Yong-Jie and Castanedes-Casey, Monica and Lee, Chris W and Jansen-West, Karen and Kurti, Aishe and Murray, Melissa E and Bieniek, Kevin F and Bauer, Peter O and Whitelaw, Ena C and Rousseau, Linda and Stankowski, Jeannette N and Stetler, Caroline and Daughrity, Lillian M and Perkerson, Emilie A and Desaro, Pamela and Johnston, Amelia and Overstreet, Karen and Edbauer, Dieter and Rademakers, Rosa and Boylan, Kevin B and Dickson, Dennis W and Fryer, John D and Petrucelli, Leonard
Science, ISSN 0036-8075, 06/2015, Volume 348, Issue 6239, pp. 1151 - 1154
The major genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis is a G(4)C(2) repeat expansion in C9ORF72. Efforts to combat... 
TRANSCRIPTS | INCLUSIONS | MULTIDISCIPLINARY SCIENCES | FRONTOTEMPORAL DEMENTIA | TOXICITY | PROTEINS | TRANSLATION | HEXANUCLEOTIDE REPEAT | GGGGCC REPEAT | RNA FOCI | FEATURES | Amyotrophic lateral sclerosis | Genetic aspects | Gene expression | Identification and classification | Dementia | Proteins | Brain | Genotype & phenotype | Neurology | Genetic disorders | Pathology | Animals | Abnormalities | Genetics | Viruses | Mathematical models | Mice
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2. 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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3. Full Text Dietary intervention rescues maternal obesity induced behavior deficits and neuroinflammation in offspring
by Kang, Silvia S and Kurti, Aishe and Fair, Damien A and Fryer, John D
Journal of Neuroinflammation, ISSN 1742-2094, 09/2014, Volume 11, Issue 1, pp. 156 - 156
Obesity induces a low-grade inflammatory state and has been associated with behavioral and cognitive alterations. Importantly, maternal environmental insults... 
ADHD | Maternal obesity | Neuroinflammation | ASD | Dietary intervention | Behavior | RETT-SYNDROME | HIGH-FAT DIET | BRAIN-DEVELOPMENT | NECROSIS-FACTOR-ALPHA | IMMUNOLOGY | NEUROSCIENCES | POSTOPERATIVE COGNITIVE DECLINE | IMMUNE-SYSTEM | CORE GUT MICROBIOME | ADIPOSITY PRIOR | BODY-MASS INDEX | WEIGHT-GAIN | Autism | Obesity | Inflammation | Attention-deficit hyperactivity disorder | Attention deficit disorder | Body mass index | Neurosciences | Laboratories | Rodents | Variance analysis
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4. Full Text C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins
by Zhang, Yong-Jie and Gendron, Tania F and Grima, Jonathan C and Sasaguri, Hiroki and Jansen-West, Karen and Xu, Ya-Fei and Katzman, Rebecca B and Gass, Jennifer and Murray, Melissa E and Shinohara, Mitsuru and Lin, Wen-Lang and Garrett, Aliesha and Stankowski, Jeannette N and Daughrity, Lillian and Tong, Jimei and Perkerson, Emilie A and Yue, Mei and Chew, Jeannie and Castanedes-Casey, Monica and Kurti, Aishe and Wang, Zizhao S and Liesinger, Amanda M and Baker, Jeremy D and Jiang, Jie and Lagier-Tourenne, Clotilde and Edbauer, Dieter and Cleveland, Don W and Rademakers, Rosa and Boylan, Kevin B and Bu, Guojun and Link, Christopher D and Dickey, Chad A and Rothstein, Jeffrey D and Dickson, Dennis W and Fryer, John D and Petrucelli, Leonard
Nature Neuroscience, ISSN 1097-6256, 05/2016, Volume 19, Issue 5, pp. 668 - 677
Neuronal inclusions of poly(GA), a protein unconventionally translated from G(4)C(2) repeat expansions in C9ORF72, are abundant in patients with frontotemporal... 
DIPEPTIDE-REPEAT PROTEINS | ANTISENSE TRANSCRIPTS | MOUSE MODEL | EXPANSION | DNA-REPAIR | NEURONAL LOSS | HEXANUCLEOTIDE REPEAT | NEUROSCIENCES | GGGGCC REPEAT | RNA FOCI | SQSTM1 MUTATIONS | Neurons - pathology | Gene Expression - genetics | Humans | Atrophy - pathology | Behavior, Animal | Brain - metabolism | DNA-Binding Proteins - metabolism | Frontotemporal Dementia - metabolism | Guanine Nucleotide Exchange Factors - metabolism | Brain - ultrastructure | C9orf72 Protein | Neurons - metabolism | Inclusion Bodies - metabolism | Ubiquitinated Proteins - metabolism | Frontotemporal Dementia - pathology | Inclusion Bodies - ultrastructure | Proteins - toxicity | Nerve Degeneration - pathology | Proteins - genetics | Amyotrophic Lateral Sclerosis - pathology | Animals | Carrier Proteins - metabolism | Proteins - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Brain - pathology | Mice | Mutation | Primary Cell Culture | Disease susceptibility | Genetic aspects | Open reading frames | Carrier proteins | Properties | Index Medicus
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5. Full Text Poly(GR) impairs protein translation and stress granule dynamics in C9orf72-associated frontotemporal dementia and amyotrophic lateral sclerosis
by Zhang, Yong-Jie and Gendron, Tania F and Ebbert, Mark T. W and O’Raw, Aliesha D and Yue, Mei and Jansen-West, Karen and Zhang, Xu and Prudencio, Mercedes and Chew, Jeannie and Cook, Casey N and Daughrity, Lillian M and Tong, Jimei and Song, Yuping and Pickles, Sarah R and Castanedes-Casey, Monica and Kurti, Aishe and Rademakers, Rosa and Oskarsson, Bjorn and Dickson, Dennis W and Hu, Wenqian and Gitler, Aaron D and Fryer, John D and Petrucelli, Leonard
Nature Medicine, ISSN 1078-8956, 08/2018, Volume 24, Issue 8, pp. 1136 - 1142
The major genetic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is a C9orf72 G(4)C(2) repeat expansion(1,2). Proposed... 
MEDICINE, RESEARCH & EXPERIMENTAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALS | TOXICITY | CELL BIOLOGY | C9FTD/ALS | C9ORF72 HEXANUCLEOTIDE REPEAT | DIPEPTIDE-REPEAT PROTEINS | ANTISENSE TRANSCRIPTS | EXPANSION | GGGGCC REPEAT | NUCLEOCYTOPLASMIC TRANSPORT | RNA FOCI | Cytoplasmic Granules - drug effects | Dipeptides - pharmacology | Humans | Mice, Inbred C57BL | Gene Expression Profiling | Ribosomal Proteins - metabolism | Behavior, Animal | Frontotemporal Dementia - metabolism | Animals | Cytoplasmic Granules - metabolism | Amyotrophic Lateral Sclerosis - metabolism | HEK293 Cells | Protein Biosynthesis - drug effects | C9orf72 Protein - metabolism | Stress, Physiological - drug effects | Cluster Analysis | Psychological aspects | Care and treatment | Rats as laboratory animals | Amyotrophic lateral sclerosis | Genetic aspects | Research | Frontotemporal dementia | Genetic translation | Stresses | Brain | Translation | Toxicity | Pathogenesis | Translation initiation | Homeostasis | Ribonucleic acid--RNA | Gene expression | Stress | Proteins | Atrophy | Ribosomal subunits | Neurodegeneration | Granular materials | Dementia disorders | Biocompatibility | Mice | Dismantling | Age | Dementia
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6. Full Text Diet and exercise orthogonally alter the gut microbiome and reveal independent associations with anxiety and cognition
by Kang, Silvia S and Jeraldo, Patricio R and Kurti, Aishe and Miller, Margret E. Berg and Cook, Marc D and Whitlock, Keith and Goldenfeld, Nigel and Woods, Jeffrey A and White, Bryan A and Chia, Nicholas and Fryer, John D
Molecular Neurodegeneration, ISSN 1750-1326, 09/2014, Volume 9, Issue 1, pp. 36 - 36
Background: The ingestion of a high-fat diet (HFD) and the resulting obese state can exert a multitude of stressors on the individual including anxiety and... 
Neuroscience | Exercise | Diet | Gut-brain axis | Anxiety | Cognition | Microbiome | HIGH-FAT DIET | BEHAVIOR | MOUSE | NEUROSCIENCES | ENERGY-BALANCE | HEART | OBESITY | EXPRESSION | BRAIN | EXPOSURE | PLASTICITY | Obesity - complications | Obesity - psychology | Mice, Inbred C57BL | Diet, High-Fat - adverse effects | Male | Physical Conditioning, Animal - physiology | Obesity - microbiology | Microbiota | Animals | Intestines - microbiology | Cognition - physiology | Physical Conditioning, Animal - psychology | Mice | Anxiety - etiology | Neurosciences | Analysis
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7. Full Text Heterochromatin anomalies and double-stranded RNA accumulation underlie C9orf72 poly(PR) toxicity
by Zhang, Yong-Jie and Guo, Lin and Guo, Lin and Gonzales, Patrick K and Gendron, Tania F and Wu, Yanwei and Jansen-West, Karen and O'Raw, Aliesha D and O’Raw, Aliesha D and Pickles, Sarah R and Prudencio, Mercedes and Carlomagno, Yari and Gachechiladze, Mariam A and Ludwig, Connor and Ludwig, Connor and Tian, Ruilin and Tian, Ruilin and Chew, Jeannie and DeTure, Michael and Lin, Wen-Lang and Tong, Jimei and Daughrity, Lillian M and Yue, Mei and Song, Yuping and Andersen, Jonathan W and Castanedes-Casey, Monica and Kurti, Aishe and Datta, Abhishek and Datta, Abhishek and Antognetti, Giovanna and McCampbell, Alexander and Rademakers, Rosa and Rademakers, Rosa and Oskarsson, Björn and Dickson, Dennis W and Kampmann, Martin and Kampmann, Martin and Ward, Michael E and Fryer, John D and Link, Christopher D and Link, Christopher D and Shorter, James and Petrucelli, Leonard
Science, ISSN 0036-8075, 02/2019, Volume 363, Issue 6428, pp. 707 - 707
How hexanucleotide GGGGCC (G(4)C(2)) repeat expansions in C9orf72 cause frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is not... 
PHASE-SEPARATION | ANTISENSE TRANSCRIPTS | MULTIDISCIPLINARY SCIENCES | EXPANSION | NEURODEGENERATION | DYSFUNCTION | PROTEINS | TRANSLATION | HEXANUCLEOTIDE REPEAT | GGGGCC REPEAT | FOCI | Amyotrophic lateral sclerosis | Chromatin | Genetic aspects | RNA | Frontotemporal dementia | Health aspects | Proteins | Nervous system diseases | Brain | Disease | Pathogenesis | Memory | Liquid phases | Gene sequencing | Neurodegeneration | Autopsy | Bioaccumulation | Biocompatibility | Expansion | Deoxyribonucleic acid--DNA | Neurodegenerative diseases | Abnormalities | Double-stranded RNA | Gene expression | Patients | Neurological diseases | Gene silencing | Pathology | Gliosis | Chromosome 9 | Stem cells | Mice | Disruption | Anomalies | Dementia | Transcription | Toxicity | Genes | Fluorescence | Tissues | Accumulation | Atrophy | Heterochromatin | Arginine | DNA methylation | Dementia disorders | Cell survival | Nucleotide sequence | Ribonucleic acid--RNA | Haploinsufficiency | Depletion | Green fluorescent protein | Fatalities | Methylation
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8. Full Text APOE ε2 is associated with increased tau pathology in primary tauopathy
by Zhao, Na and Liu, Chia-Chen and Van Ingelgom, Alexandra J and Linares, Cynthia and Kurti, Aishe and Knight, Joshua A and Heckman, Michael G and Diehl, Nancy N and Shinohara, Mitsuru and Martens, Yuka A and Attrebi, Olivia N and Petrucelli, Leonard and Fryer, John D and Wszolek, Zbigniew K and Graff-Radford, Neill R and Caselli, Richard J and Sanchez-Contreras, Monica Y and Rademakers, Rosa and Murray, Melissa E and Koga, Shunsuke and Dickson, Dennis W and Ross, Owen A and Bu, Guojun
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 4388 - 11
Apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease mainly by modulating amyloid-β pathology. APOE ε4 is... 
Apolipoprotein E4 - metabolism | Supranuclear Palsy, Progressive - pathology | Humans | Tauopathies - pathology | Apolipoprotein E2 - metabolism | Disease Progression | Alzheimer Disease - pathology | Tauopathies - metabolism | Animals | Alleles | Alzheimer Disease - metabolism | Supranuclear Palsy, Progressive - metabolism | Mice | Supranuclear Palsy, Progressive - genetics | Gene transfer | Neurodegenerative diseases | Abnormalities | Transgenic mice | Health risks | Viruses | Inflammation | Risk analysis | Risk factors | Pathology | Genotype & phenotype | Tau protein | Neurodegeneration | Apolipoprotein E | Progressive supranuclear palsy | Rodents | Degeneration | Paralysis | Genotypes
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9. Full Text Aberrant deposition of stress granule-resident proteins linked to C9orf72-associated TDP-43 proteinopathy
by Chew, Jeannie and Cook, Casey and Gendron, Tania F and Jansen-West, Karen and Del Rosso, Giulia and Daughrity, Lillian M and Castanedes-Casey, Monica and Kurti, Aishe and Stankowski, Jeannette N and Disney, Matthew D and Rothstein, Jeffrey D and Dickson, Dennis W and Fryer, John D and Zhang, Yong-Jie and Petrucelli, Leonard
Molecular neurodegeneration, ISSN 1750-1326, 02/2019, Volume 14, Issue 1, pp. 9 - 9
BackgroundA G(4)C(2) hexanucleotide repeat expansion in the noncoding region of C9orf72 is the major genetic cause of frontotemporal dementia and amyotrophic... 
Amyotrophic lateral sclerosis | Frontotemporal dementia | Neurodegeneration | Stress granules | TDP-43 | C9orf72 | PHASE-TRANSITIONS | AMYOTROPHIC-LATERAL-SCLEROSIS | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | IN-VITRO | C9ORF72 HEXANUCLEOTIDE REPEAT | DIPEPTIDE-REPEAT PROTEINS | ANTISENSE TRANSCRIPTS | EXPANSION | GGGGCC REPEAT | RNA FOCI | Proteins | Antisense RNA | Analysis | Dementia | Brain | Phenotypes | Toxicity | Neuropathology | Pathogenesis | Cognitive ability | Ribonucleic acid--RNA | Pathology | Gliosis | Inclusion bodies | Dementia disorders | Granules | Index Medicus
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10. Full Text ABCA7 deficiency accelerates amyloid-βgeneration and alzheimer’s neuronal pathology
by Sakae, Nobutaka and Liu, Chia-Chen and Shinohara, Mitsuru and Frisch-Daiello, Jessica and Ma, Li and Yamazaki, Yu and Tachibana, Masaya and Younkin, Linda and Kurti, Aishe and Carrasquillo, Minerva M and Zou, Fanggeng and Sevlever, Daniel and Bisceglio, Gina and Gan, Ming and Fol, Romain and Knight, Patrick and Wang, Miao and Han, Xianlin and Fryer, John D and Fitzgerald, Michael L and Ohyagi, Yasumasa and Younkin, Steven G and Bu, Guojun and Kanekiyo, Takahisa
Journal of Neuroscience, ISSN 0270-6474, 03/2016, Volume 36, Issue 13, pp. 3848 - 3859
BACE1 | APP | ABCA7 | Neuron | Cognitive function | Lipid homeostasis
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11. Full Text APOE4 CONDITIONALLY EXPRESSED IN CEREBROVASCULATURE IMPAIRS ENDOTHELIAL FUNCTIONS AND INDUCES COGNITIVE DEFICITS
by Yamazaki, Yu and Yamazaki, Akari and Liu, Chia-Chen and Oue, Hiroshi and Kurti, Aishe and Fryer, John D and Kanekiyo, Takahisa and Bu, Guojun
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, ISSN 1552-5260, 07/2018, Volume 14, Issue 7, pp. P1457 - P1458
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12. Full Text THE MOLECULAR CHAPERONE BRICHOS INHIBITS Aβ AGGREGATION AND OTHER NEUROPATHOLOGICAL PHENOTYPES IN A MOUSE MODEL OF Aβ AMYLOIDOSIS
by Kim, Jungsu and Kim, Chaeyoung and Dolfe, Lisa and Belmonte, Krystal and Flores, Luis and Kurti, Aishe and Fryer, John D and Presto, Jenny and Johansson, Jan
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, ISSN 1552-5260, 07/2017, Volume 13, Issue 7, pp. P1304 - P1305
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13. Full Text Behavioral and transcriptomic analysis of Trem2-null mice: not all knockout mice are created equal
by Kang, Silvia S and Kurti, Aishe and Baker, Kelsey E and Liu, Chia-Chen and Colonna, Marco and Ulrich, Jason D and Holtzman, David M and Bu, Guojun and Fryer, John D
Human Molecular Genetics, ISSN 0964-6906, 01/2018, Volume 27, Issue 2, pp. 211 - 223
Abstract It is clear that innate immune system status is altered in numerous neurodegenerative diseases. Human genetic studies have demonstrated that... 
SOLUBLE EPOXIDE HYDROLASE | IDENTIFIES VARIANTS | MICROGLIAL ACTIVATION | ONSET ALZHEIMERS-DISEASE | INFLAMMATORY RESPONSES | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | GENETICS & HEREDITY | MYELOID CELLS 2 | GENOME-WIDE ASSOCIATION | APOLIPOPROTEIN-E | PARKINSONS-DISEASE | Microglia - metabolism | Up-Regulation | Membrane Glycoproteins - metabolism | Mice, Inbred C57BL | Transcriptome | Behavior, Animal - physiology | Gene Expression Profiling - methods | Immunity, Innate | Membrane Glycoproteins - genetics | Mice, Knockout | Brain - metabolism | Animals | Cognition - physiology | Mice | Receptors, Immunologic - genetics | Receptors, Immunologic - metabolism | Disease Models, Animal
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