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1. Full Text Fibrillar Amyloid-β Burden in Cognitively Normal People at 3 Levels of Genetic Risk for Alzheimer's Disease
by Eric M. Reiman and Kewei Chen and Xiaofen Liu and Daniel Bandy and Meixiang Yu and Wendy Lee and Napatkamon Ayutyanont and Jennifer Keppler and Stephanie A. Reeder and Jessica B. S. Langbaum and Gene E. Alexander and William E. Klunk and Chester A. Mathis and Julie C. Price and Howard J. Aizenstein and Steven T. DeKosky and Richard J. Caselli and L. L. Iversen
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2009, Volume 106, Issue 16, pp. 6820 - 6825
Fibrillar amyloid-beta (Aβ) is found in the brains of many cognitively normal older people. Whether or not this reflects a predisposition to Alzheimer's... 
Homozygotes | Gene dosage | Imaging | Medical genetics | Predisposing factors | Alleles | Complex Systems: From Chemistry to Systems Biology Special Feature | Amyloids | Alzheimers disease | Positron emission tomography | Older adults | Apolipoprotein E | Pittsburgh compound B pet | DEPOSITION | MULTIDISCIPLINARY SCIENCES | HUMANS | APOLIPOPROTEIN-E GENOTYPE | EPSILON-4 ALLELE | PITTSBURGH COMPOUND-B | IMPAIRMENT | TYPE-4 ALLELE | apolipoprotein E | Pittsburgh Compound B PET | A-BETA | BRAIN | PET | Genetic Predisposition to Disease | Apolipoprotein E4 - genetics | Humans | Middle Aged | Cognition | Gene Dosage | Neuropsychological Tests | Homozygote | Magnetic Resonance Imaging | Amyloid beta-Peptides - metabolism | Brain Mapping | Heterozygote | Aged | Alzheimer Disease - genetics | Biological Sciences
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2. Full Text Amyloid Burden in Obstructive Sleep Apnea
by Yun, Chang-Ho and Lee, Ho-Young and Lee, Seung Ku and Kim, Hyun and Seo, Hyung Suk and Bang, Seong Ae and Kim, Sang Eun and Greve, Douglas N and Au, Rhoda and Shin, Chol and Thomas, Robert J
Journal of Alzheimer's Disease, ISSN 1387-2877, 2017, Volume 59, Issue 1, pp. 21 - 29
To test the hypothesis that excessive amyloid deposition is a biological link between obstructive sleep apnea (OSA) and Alzheimer's disease, we determined... 
sleep | cerebral cortex | positron-emission tomography | dementia | Alzheimer's disease | BRAIN STRUCTURAL-CHANGES | CORTICAL SURFACE | ALZHEIMERS-DISEASE | OLDER-ADULTS | INTERSTITIAL FLUID | MILD COGNITIVE IMPAIRMENT | CEREBROSPINAL-FLUID | EPSILON-4 ALLELE | NEUROSCIENCES | BETA DYNAMICS | CENTRAL-NERVOUS-SYSTEM | Brain - diagnostic imaging | Carbon Radioisotopes - pharmacokinetics | Humans | Middle Aged | Sleep Apnea, Obstructive - genetics | Independent Living | Male | Sleep Apnea, Obstructive - complications | Positron-Emission Tomography | Aniline Compounds - pharmacokinetics | Polysomnography | Sleep Apnea, Obstructive - pathology | Thiazoles - pharmacokinetics | Brain - metabolism | Neuropsychological Tests | Amyloid - metabolism | Apolipoproteins E - genetics | Female | Sleep Apnea, Obstructive - diagnostic imaging | Aged | Republic of Korea | Cohort Studies | Cerebellum | Neuroimaging | Brain | Cognitive ability | Spatial discrimination | Genomes | Sleep apnea | Substantia grisea | Epidemiology | Body mass index | Sleep disorders | Handedness | Apnea | Apolipoprotein E | Tomography | Deposition | Age | Cortex (temporal) | Genotypes | Hypertension | Cortex (cingulate) | Drinking behavior | Diabetes mellitus | Positron emission | Disease control | Sleep | Mood | Magnetic resonance imaging | Body mass | Body size | Alcoholic beverages | Positron emission tomography | Smoking | Indexing
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3. Full Text Germline MC1R status influences somatic mutation burden in melanoma
by Robles-Espinoza, Carla Daniela and Roberts, Nicola D and Chen, Shuyang and Leacy, Finbarr P and Alexandrov, Ludmil B and Pornputtapong, Natapol and Halaban, Ruth and Krauthammer, Michael and Cui, Rutao and Timothy Bishop, D and Adams, David J
Nature Communications, ISSN 2041-1723, 07/2016, Volume 7, Issue 1, pp. 12064 - 12064
The major genetic determinants of cutaneous melanoma risk in the general population are disruptive variants (R alleles) in the melanocortin 1 receptor (MC1R)... 
REPAIR | MULTIVARIATE IMPUTATION | VARIANTS | GENE | MULTIDISCIPLINARY SCIENCES | CUTANEOUS MELANOMA | DNA-DAMAGE | RISK | MELANOCORTIN 1 RECEPTOR | SKIN | RED HAIR | Mutation Accumulation | Skin Neoplasms - pathology | Genetic Predisposition to Disease | Neoplasm Invasiveness | Humans | Middle Aged | Receptor, Melanocortin, Type 1 - genetics | Male | Melanoma - pathology | Germ-Line Mutation - genetics | Genetic Variation | Hair Color | Melanoma - genetics | Skin Neoplasms - genetics | Alleles | Skin Pigmentation | Female | Head and Neck Neoplasms - genetics | Aged | Melanosis | Polymorphism, Single Nucleotide | Mutation | Cohort Studies | Index Medicus
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4. Full Text CR1 is associated with amyloid plaque burden and age‐related cognitive decline
by Chibnik, Lori B and Shulman, Joshua M and Leurgans, Sue E and Schneider, Julie A and Wilson, Robert S and Tran, Dong and Aubin, Cristin and Buchman, Aron S and Heward, Christopher B and Myers, Amanda J and Hardy, John A and Huentelman, Matthew J and Corneveaux, Jason J and Reiman, Eric M and Evans, Denis A and Bennett, David A and De Jager, Philip L
Annals of Neurology, ISSN 0364-5134, 03/2011, Volume 69, Issue 3, pp. 560 - 569
Objective Recently, genome‐wide association studies have identified 3 new susceptibility loci for Alzheimer's disease (AD), CLU, CR1, and PICALM. We leveraged... 
CONSORTIUM | OLDER PERSONS | IDENTIFIES VARIANTS | CEREBRAL INFARCTIONS | ESTABLISH | COHORT | CLU | NEUROSCIENCES | CLINICAL NEUROLOGY | GENOME-WIDE ASSOCIATION | ALZHEIMER-DISEASE PATHOLOGY | IMPAIRMENT | Age Factors | Humans | Middle Aged | Cognition Disorders - metabolism | Male | Alzheimer Disease - pathology | Brain - metabolism | Aged, 80 and over | Female | Genetic Predisposition to Disease | Genetic Association Studies | Plaque, Amyloid - pathology | Cognition Disorders - pathology | Genotype | Cognition Disorders - genetics | Plaque, Amyloid - genetics | Receptors, Complement 3b - metabolism | Analysis of Variance | Alleles | Alzheimer Disease - metabolism | Brain - pathology | Plaque, Amyloid - metabolism | Aged | Polymorphism, Single Nucleotide | Receptors, Complement 3b - genetics | Alzheimer Disease - genetics | Longitudinal Studies | Pathology | Genetics | Cognition & reasoning | Alzheimers disease | Religious orders
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5. Full Text KLOTHO heterozygosity attenuates APOE4-related amyloid burden in preclinical AD
by Erickson, Claire M and Schultz, Stephanie A and Oh, Jennifer M and Darst, Burcu F and Ma, Yue and Norton, Derek and Betthauser, Tobey and Gallagher, Catherine L and Carlsson, Cynthia M and Bendlin, Barbara B and Asthana, Sanjay and Hermann, Bruce P and Sager, Mark A and Blennow, Kaj and Zetterberg, Henrik and Engelman, Corinne D and Christian, Bradley T and Johnson, Sterling C and Dubal, Dena B and Okonkwo, Ozioma C and Sahlgrenska akademin and Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi and Göteborgs universitet and Gothenburg University and Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry and Sahlgrenska Academy
Neurology, ISSN 0028-3878, 04/2019, Volume 92, Issue 16, pp. e1878 - e1889
OBJECTIVETo examine whether the KLOTHO gene variant KL-VS attenuates APOE4-associated β-amyloid (Aβ) accumulation in a late-middle-aged cohort enriched with... 
COGNITIVE DECLINE | GENE | ALZHEIMERS-DISEASE | FUNCTIONAL VARIANT | RISK | APOE | EPSILON-4 ALLELE | ASSOCIATION | CLINICAL NEUROLOGY | APOLIPOPROTEIN-E | BETA | gene | epsilon-4 allele | apoe | association | apolipoprotein-e | Neurosciences & Neurology | Klinisk medicin | functional variant | Clinical Medicine | cognitive | decline | risk | beta | alzheimers-disease
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6. Full Text HLA Genetic Risk Burden in Multiple Sclerosis—Reply
by Isobe, Noriko and Oksenberg, Jorge R and Henry, Roland G
JAMA Neurology, ISSN 2168-6149, 12/2016, Volume 73, Issue 12, pp. 1501 - 1502
CLINICAL NEUROLOGY | Genetic Predisposition to Disease | HLA-DRB1 Chains | Humans | Risk Factors | Alleles | Genotype | Multiple Sclerosis - genetics | Polymorphism, Single Nucleotide
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7. Full Text Low JAK2V617F allele burden in primary myelofibrosis, compared to either a higher allele burden or unmutated status, is associated with inferior overall and leukemia-free survival
by Tefferi, A and Lasho, T.L and Huang, J and Finke, C and Mesa, R.A and Li, C.Y and Wu, W and Hanson, C.A and Pardanani, A
Leukemia, ISSN 0887-6924, 2008, Volume 22, Issue 4, pp. 756 - 761
The clinical relevance of JAK2V617F allele burden in primary myelofibrosis (PMF) has not been previously studied. Bone marrow-derived DNA from 199 patients... 
TRANSFORMATION | JAK2(V617F) | myelofibrosis | POLYCYTHEMIA-VERA | JAK2 V617F MUTATION | ESSENTIAL THROMBOCYTHEMIA | JAK2V617F | prognosis | TYROSINE KINASE MUTATION | EXON-12 MUTATIONS | MYELOPROLIFERATIVE-DISORDERS | ONCOLOGY | V617F | JAK2 | 617V-GREATER-THAN-F MUTATION | HEMATOLOGY | MYELOID METAPLASIA | Primary Myelofibrosis - mortality | Age Factors | Gene Frequency | Humans | Middle Aged | Janus Kinase 2 - genetics | Male | Survival Rate | Mutation, Missense | Bone Marrow Examination | Disease-Free Survival | Primary Myelofibrosis - genetics | Platelet Count | Primary Myelofibrosis - epidemiology | Alleles | Aged, 80 and over | Adult | Female | Aged | Polymerase chain reaction | Care and treatment | Usage | Myelofibrosis | Gene mutations | Genetic aspects | Research | Health aspects
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8. Full Text The relationship between sleep quality and brain amyloid burden
by Brown, Belinda M and Rainey-Smith, Stephanie R and Villemagne, Victor L and Weinborn, Michael and Bucks, Romola S and Sohrabi, Hamid R and Laws, Simon M and Taddei, Kevin and Macaulay, S. Lance and Ames, David and Fowler, Christopher and Maruff, Paul and Masters, Colin L and Rowe, Christopher C and Martins, Ralph N and AIBL Res Grp and AIBL Research Group and the AIBL Research Group
Sleep, ISSN 0161-8105, 05/2016, Volume 39, Issue 5, pp. 1063 - 1068
Study Objectives: To evaluate the association between self-reported sleep quality and levels of brain beta-amyloid (A beta) burden, and to determine the effect... 
Apolipoprotein ϵ4 allele | Sleep | Alzheimer disease | Sleep latency | Beta-amyloid | ALZHEIMER-DISEASE | sleep latency | GENOTYPE | DEPOSITION | apolipoprotein epsilon 4 allele | SELF-REPORTED SLEEP | NEUROSCIENCES | COGNITIVE FUNCTION | CLINICAL NEUROLOGY | IMPAIRMENT | beta-amyloid | sleep | BIOMARKERS | PHYSICAL-ACTIVITY | VALIDITY | DURATION | Apolipoprotein E4 - genetics | Cross-Sectional Studies | Humans | Self Report | Genotype | Linear Models | Male | Positron-Emission Tomography | Sleep - genetics | Brain - metabolism | Alleles | Amyloid beta-Peptides - metabolism | Amyloid beta-Peptides - analysis | Female | Heterozygote | Aged | Sleep - physiology | Index Medicus
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9. Full Text Mutation allele burden remains unchanged in chronic myelomonocytic leukaemia responding to hypomethylating agents
by Merlevede, Jane and Droin, Nathalie and Qin, Tingting and Meldi, Kristen and Yoshida, Kenichi and Morabito, Margot and Chautard, Emilie and Auboeuf, Didier and Fenaux, Pierre and Braun, Thorsten and Itzykson, Raphael and De Botton, Stéphane and Quesnel, Bruno and Commes, Thérèse and Jourdan, Eric and Vainchenker, William and Bernard, Olivier and Pata-Merci, Noemie and Solier, Stéphanie and Gayevskiy, Velimir and Dinger, Marcel E and Cowley, Mark J and Selimoglu-Buet, Dorothée and Meyer, Vincent and Artiguenave, François and Deleuze, Jean-François and Preudhomme, Claude and Stratton, Michael R and Alexandrov, Ludmil B and Padron, Eric and Ogawa, Seishi and Koscielny, Serge and Figueroa, Maria and Solary, Eric and Los Alamos National Lab. (LANL), Los Alamos, NM (United States)
Nature Communications, ISSN 2041-1723, 02/2016, Volume 7, Issue 1, p. 10767
The cytidine analogues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are commonly used to treat myelodysplastic syndromes, with or without a... 
GENE | SIGNATURES | CLONAL HEMATOPOIESIS | MULTIDISCIPLINARY SCIENCES | RECURRENT MUTATIONS | DEMETHYLATING AGENTS | TUMOR-SUPPRESSOR | ACUTE MYELOID-LEUKEMIA | CANCER | MYELODYSPLASTIC SYNDROMES | SOMATIC MUTATIONS | Cell Survival - drug effects | Humans | Leukemia, Myelomonocytic, Chronic - genetics | Middle Aged | Azacitidine - analogs & derivatives | Male | Leukemia, Myelomonocytic, Chronic - drug therapy | Sequence Analysis, DNA | Azacitidine - pharmacology | Antimetabolites, Antineoplastic - therapeutic use | Sequence Analysis, RNA | Alleles | HEK293 Cells | Aged, 80 and over | Antimetabolites, Antineoplastic - pharmacology | Female | Aged | Epigenesis, Genetic - drug effects | High-Throughput Nucleotide Sequencing | Gene Expression Regulation, Neoplastic - drug effects | Mutation | DNA Methylation - drug effects | Azacitidine - therapeutic use | cancer | genetics | BASIC BIOLOGICAL SCIENCES | biological sciences
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10. Full Text A prospective study of 338 patients with polycythemia vera: The impact of JAK2 (V617F) allele burden and leukocytosis on fibrotic or leukemic disease transformation and vascular complications
by Passamonti, F and Rumi, E and Pietra, D and Elena, C and Boveri, E and Arcaini, L and Roncoroni, E and Astori, C and Merli, M and Boggi, S and Pascutto, C and Lazzarino, M and Cazzola, M
Leukemia, ISSN 0887-6924, 2010, Volume 24, Issue 9, pp. 1574 - 1579
We studied the relationship between JAK2 (V617F) mutant allele burden and clinical phenotype, disease progression and survival in patients with polycythemia... 
polycythemia | myelofibrosis | thrombosis | JAK2 | prognosis | SURVIVAL | WILD-TYPE | JAK2(V617F) | RISK | ESSENTIAL THROMBOCYTHEMIA | PRIMARY MYELOFIBROSIS | JAK2V617F | ONCOLOGY | CHRONIC MYELOPROLIFERATIVE DISORDERS | 617V-GREATER-THAN-F MUTATION | HEMATOLOGY | EXPRESSION | Multivariate Analysis | Prospective Studies | Vascular Diseases - complications | Humans | Middle Aged | Janus Kinase 2 - genetics | Male | Polycythemia Vera - genetics | Polycythemia Vera - complications | Primary Myelofibrosis - genetics | Cell Transformation, Neoplastic - genetics | Alleles | Polymerase Chain Reaction | Female | Aged | Mutation | Polycythemia Vera - pathology | Leukocytosis - genetics | Leukemia - genetics | Complications and side effects | Polycythemia vera | Genetic aspects | Myelofibrosis | Research | Risk factors
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11. Full Text The effect of long-term ruxolitinib treatment on JAK2p.V617F allele burden in patients with myelofibrosis
by Deininger, Michael and Radich, Jerald and Burn, Timothy C and Huber, Reid and Paranagama, Dilan and Verstovsek, Srdan
Blood, ISSN 0006-4971, 09/2015, Volume 126, Issue 13, pp. 1551 - 1554
The JAK2 c.1849G>T (p.V617F) mutation leads to constitutive activation of Janus kinase (JAK)2 and contributes to dysregulated JAK signaling in myelofibrosis... 
SURVIVAL | POLYCYTHEMIA-VERA | IMPACT | EFFICACY | SAFETY | MYELOPROLIFERATIVE NEOPLASMS | MUTATIONS | JAK2 | HEMATOLOGY | INTERNATIONAL WORKING GROUP | AVAILABLE THERAPY | Primary Myelofibrosis - drug therapy | Pyrazoles - therapeutic use | Splenomegaly - drug therapy | Primary Myelofibrosis - complications | Splenomegaly - genetics | Humans | Janus Kinase 2 - genetics | Male | Spleen - drug effects | Primary Myelofibrosis - pathology | Splenomegaly - pathology | Point Mutation | Splenomegaly - complications | Primary Myelofibrosis - genetics | Spleen - metabolism | Alleles | Female | Spleen - pathology | Janus Kinase 2 - antagonists & inhibitors | Clinical Trials and Observations | Brief Report
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12. Full Text Vitamin D receptor deficiency enhances Wnt/β-catenin signaling and tumor burden in colon cancer
by Larriba, María Jesús and Ordóñez-Morán, Paloma and Chicote, Irene and Martín-Fernández, Génesis and Puig, Isabel and Muñoz, Alberto and Pálmer, Héctor G
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, p. e23524
Aberrant activation of the Wnt/beta-catenin pathway is critical for the initiation and progression of most colon cancers. This activation provokes the... 
STEM-CELLS | APC | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GROWTH | PHENOTYPE | E-CADHERIN | DIFFERENTIATION | BETA-CATENIN | WNT | EXPRESSION | Steroid Hydroxylases - metabolism | Colonic Neoplasms - genetics | Humans | Protein Transport - drug effects | Wnt Proteins - metabolism | Receptors, Calcitriol - genetics | Colonic Neoplasms - metabolism | Cell Nucleus - metabolism | RNA Interference | Cell Membrane - metabolism | Intestinal Neoplasms - genetics | Steroid Hydroxylases - genetics | Adenomatous Polyposis Coli Protein - genetics | Receptors, Calcitriol - deficiency | Signal Transduction | HCT116 Cells | Intestinal Neoplasms - metabolism | Vitamin D3 24-Hydroxylase | Tumor Burden | Reverse Transcriptase Polymerase Chain Reaction | beta Catenin - metabolism | Blotting, Western | Intestinal Neoplasms - pathology | Mice, Knockout | Gene Expression Regulation - drug effects | HT29 Cells | Animals | Calcitriol - pharmacology | Colonic Neoplasms - pathology | Cell Line, Tumor | Mice | Mutation | Phosphorylation | Transcription factors | Carcinoma | Wnt protein | Laboratories | Genes | Colorectal cancer | Calcitriol | Oncology | Genomes | Activation | Kinases | Small intestine | Nuclei | Accumulation | Proteins | β-catenin | Colon cancer | Vitamin D | Colon | Relocation | Phenotypes | Nutrient deficiency | Baldness | Breeding | Gene expression | Adenomatous polyposis coli | Signaling | Alleles | Stem cells | Ligands | Vitamin D receptors | Aberration | Tumors | Cancer
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13. Full Text HLA Genetic Risk Burden in Multiple Sclerosis
by Mühlau, Mark and Andlauer, Till F. M and Hemmer, Bernhard
JAMA Neurology, ISSN 2168-6149, 12/2016, Volume 73, Issue 12, pp. 1500 - 1501
ATROPHY | CLINICAL NEUROLOGY | Genetic Predisposition to Disease | HLA-DRB1 Chains | Humans | Risk Factors | Alleles | Genotype | Multiple Sclerosis - genetics | Polymorphism, Single Nucleotide
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14. Full Text Clinical correlates of JAK2V617F allele burden in essential thrombocythemia
by Kittur, Jaya and Knudson, Ryan A and Lasho, Terra L and Finke, Christy M and Gangat, Naseema and Wolanskyj, Alexandra P and Li, Chin‐Yang and Wu, Wenting and Ketterling, Rhett P and Pardanani, Animesh and Tefferi, Ayalew
Cancer, ISSN 0008-543X, 06/2007, Volume 109, Issue 11, pp. 2279 - 2284
BACKGROUND. JAK2V617F occurs in approximately 50% of patients with essential thrombocythemia (ET). Qualitative studies of mutation analysis have previously... 
JAK2 V617F | essential thrombocythemia | allele burden | Allele burden | Essential thrombocythemia | JAK2V617F | POLYCYTHEMIA-VERA | MYELOPROLIFERATIVE DISORDERS | RISK-FACTOR | ONCOLOGY | THROMBOSIS | TYROSINE KINASE JAK2 | JAK2 V617F MUTATION | HOMOZYGOUS JAK2(V617F) | LEUKOCYTOSIS | Venous Thrombosis - diagnosis | Humans | Middle Aged | Janus Kinase 2 - genetics | Male | Thrombocythemia, Essential - genetics | Phenotype | Platelet Count | Thrombocythemia, Essential - diagnosis | DNA Mutational Analysis | Bone Marrow - pathology | Adolescent | Alleles | Polymerase Chain Reaction | Aged, 80 and over | Adult | Female | Aged | DNA, Neoplasm - analysis | Venous Thrombosis - genetics | Thrombocythemia | Thrombocytosis | Genetic aspects | Research | Gene mutations
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