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Dennis Vance

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https://www.readbyqxmd.com/read/27694328/novel-role-for-matrix-metalloproteinase-9-in-modulation-of-cholesterol-metabolism
#1
Samuel Hernandez-Anzaldo, Vesna Brglez, Bianca Hemmeryckx, Dickson Leung, Janos G Filep, Jean E Vance, Dennis E Vance, Zamaneh Kassiri, Roger H Lijnen, Gérard Lambeau, Carlos Fernandez-Patron
BACKGROUND: The development of atherosclerosis is strongly linked to disorders of cholesterol metabolism. Matrix metalloproteinases (MMPs) are dysregulated in patients and animal models with atherosclerosis. Whether systemic MMP activity influences cholesterol metabolism is unknown. METHODS AND RESULTS: We examined MMP-9-deficient (Mmp9(-/-)) mice and found them to have abnormal lipid gene transcriptional responses to dietary cholesterol supplementation. As opposed to Mmp9(+/+) (wild-type) mice, Mmp9(-/-) mice failed to decrease the hepatic expression of sterol regulatory element binding protein 2 pathway genes, which control hepatic cholesterol biosynthesis and uptake...
September 30, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27080313/ccnf-mutations-in-amyotrophic-lateral-sclerosis-and-frontotemporal-dementia
#2
Kelly L Williams, Simon Topp, Shu Yang, Bradley Smith, Jennifer A Fifita, Sadaf T Warraich, Katharine Y Zhang, Natalie Farrawell, Caroline Vance, Xun Hu, Alessandra Chesi, Claire S Leblond, Albert Lee, Stephanie L Rayner, Vinod Sundaramoorthy, Carol Dobson-Stone, Mark P Molloy, Marka van Blitterswijk, Dennis W Dickson, Ronald C Petersen, Neill R Graff-Radford, Bradley F Boeve, Melissa E Murray, Cyril Pottier, Emily Don, Claire Winnick, Emily P McCann, Alison Hogan, Hussein Daoud, Annie Levert, Patrick A Dion, Jun Mitsui, Hiroyuki Ishiura, Yuji Takahashi, Jun Goto, Jason Kost, Cinzia Gellera, Athina Soragia Gkazi, Jack Miller, Joanne Stockton, William S Brooks, Karyn Boundy, Meraida Polak, José Luis Muñoz-Blanco, Jesús Esteban-Pérez, Alberto Rábano, Orla Hardiman, Karen E Morrison, Nicola Ticozzi, Vincenzo Silani, Jacqueline de Belleroche, Jonathan D Glass, John B J Kwok, Gilles J Guillemin, Roger S Chung, Shoji Tsuji, Robert H Brown, Alberto García-Redondo, Rosa Rademakers, John E Landers, Aaron D Gitler, Guy A Rouleau, Nicholas J Cole, Justin J Yerbury, Julie D Atkin, Christopher E Shaw, Garth A Nicholson, Ian P Blair
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are overlapping, fatal neurodegenerative disorders in which the molecular and pathogenic basis remains poorly understood. Ubiquitinated protein aggregates, of which TDP-43 is a major component, are a characteristic pathological feature of most ALS and FTD patients. Here we use genome-wide linkage analysis in a large ALS/FTD kindred to identify a novel disease locus on chromosome 16p13.3. Whole-exome sequencing identified a CCNF missense mutation at this locus...
2016: Nature Communications
https://www.readbyqxmd.com/read/26797396/pioglitazone-attenuates-hepatic-inflammation-and-fibrosis-in-phosphatidylethanolamine-n-methyltransferase-deficient-mice
#3
Jelske N van der Veen, Susanne Lingrell, Xia Gao, Ariel D Quiroga, Abhijit Takawale, Edward A Armstrong, Jerome Y Yager, Zamaneh Kassiri, Richard Lehner, Dennis E Vance, René L Jacobs
Phosphatidylethanolamine N-methyltransferase (PEMT) is an important enzyme in hepatic phosphatidylcholine (PC) biosynthesis. Pemt(-/-) mice are protected against high-fat diet (HFD)-induced obesity and insulin resistance; however, these mice develop nonalcoholic fatty liver disease (NAFLD). We hypothesized that peroxisomal proliferator-activated receptor-γ (PPARγ) activation by pioglitazone might stimulate adipocyte proliferation, thereby directing lipids from the liver toward white adipose tissue. Pioglitazone might also act directly on PPARγ in the liver to improve NAFLD...
April 1, 2016: American Journal of Physiology. Gastrointestinal and Liver Physiology
https://www.readbyqxmd.com/read/26603903/lack-of-phosphatidylethanolamine-n-methyltransferase-in-mice-does-not-promote-fatty-acid-oxidation-in-skeletal-muscle
#4
Guergana Tasseva, Jelske N van der Veen, Susanne Lingrell, René L Jacobs, Dennis E Vance, Jean E Vance
Phosphatidylethanolamine N-methyltransferase (PEMT) converts phosphatidylethanolamine (PE) to phosphatidylcholine (PC) in the liver. Mice lacking PEMT are protected from high-fat diet-induced obesity and insulin resistance, and exhibit increased whole-body energy expenditure and oxygen consumption. Since skeletal muscle is a major site of fatty acid oxidation and energy utilization, we determined if rates of fatty acid oxidation/oxygen consumption in muscle are higher in Pemt(-/-) mice than in Pemt(+/+) mice...
February 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/26391255/lack-of-phosphatidylethanolamine-n-methyltransferase-alters-hepatic-phospholipid-composition-and-induces-endoplasmic-reticulum-stress
#5
Xia Gao, Jelske N van der Veen, Jean E Vance, Aducio Thiesen, Dennis E Vance, René L Jacobs
BACKGROUND & AIMS: Endoplasmic reticulum (ER) stress is associated with development of steatohepatitis. Phosphatidylethanolamine N-methyltransferase (PEMT) is a hepatic enzyme located on the ER and mitochondria-associated membranes and catalyzes phosphatidylcholine (PC) synthesis via methylation of phosphatidylethanolamine (PE). We hypothesized that PEMT deficiency in mice alters ER phospholipid content, thereby inducing ER stress and sensitizing the mice to diet-induced steatohepatitis...
December 2015: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/26269184/induction-of-heme-oxygenase-1-deficiency-and-associated-glutamate-mediated-neurotoxicity-is-a-highly-conserved-hiv-phenotype-of-chronic-macrophage-infection-that-is-resistant-to-antiretroviral-therapy
#6
Alexander J Gill, Colleen E Kovacsics, Patricia J Vance, Ronald G Collman, Dennis L Kolson
UNLABELLED: Expression of the cytoprotective enzyme heme oxygenase-1 (HO-1) is significantly reduced in the brain prefrontal cortex of HIV-positive individuals with HIV-associated neurocognitive disorders (HAND). Furthermore, this HO-1 deficiency correlates with brain viral load, markers of macrophage activation, and type I interferon responses. In vitro, HIV replication in monocyte-derived macrophages (MDM) selectively reduces HO-1 protein and RNA expression and induces production of neurotoxic levels of glutamate; correction of this HO-1 deficiency reduces neurotoxic glutamate production without an effect on HIV replication...
October 2015: Journal of Virology
https://www.readbyqxmd.com/read/26113536/insufficient-glucose-supply-is-linked-to-hypothermia-upon-cold-exposure-in-high-fat-diet-fed-mice-lacking-pemt
#7
Xia Gao, Jelske N van der Veen, Carlos Fernandez-Patron, Jean E Vance, Dennis E Vance, René L Jacobs
Mice that lack phosphatidylethanolamine N-methyltransferase (Pemt(-/-) mice) are protected from high-fat (HF) diet-induced obesity. HF-fed Pemt(-/-) mice show higher oxygen consumption and heat production, indicating that more energy might be utilized for thermogenesis and might account for the resistance to diet-induced weight gain. To test this hypothesis, HF-fed Pemt(-/-) and Pemt(+/+) mice were challenged with acute cold exposure at 4°C. Unexpectedly, HF-fed Pemt(-/-) mice developed hypothermia within 3 h of cold exposure...
September 2015: Journal of Lipid Research
https://www.readbyqxmd.com/read/26079275/clinical-mrsa-isolates-from-skin-and-soft-tissue-infections-show-increased-in%C3%A2-vitro-production-of-phenol-soluble-modulins
#8
Nicholas R Berlon, Robert Qi, Batu K Sharma-Kuinkel, Hwang-Soo Joo, Lawrence P Park, Dennis George, Joshua T Thaden, Julia A Messina, Stacey A Maskarinec, Manica Mueller-Premru, Eugene Athan, Pierre Tattevin, Juan M Pericas, Christopher W Woods, Michael Otto, Vance G Fowler
BACKGROUND: Phenol-soluble modulins (PSMs) are amphipathic, pro-inflammatory proteins secreted by most Staphylococcus aureus isolates. This study tested the hypothesis that in vitro PSM production levels are associated with specific clinical phenotypes. METHODS: 177 methicillin-resistant S. aureus (MRSA) isolates from infective endocarditis (IE), skin and soft tissue infection (SSTI), and hospital-acquired/ventilator-associated pneumonia (HAP) were matched by geographic origin, then genotyped using spa-typing...
October 2015: Journal of Infection
https://www.readbyqxmd.com/read/25667419/functional-characterization-of-enzymes-catalyzing-ceramide-phosphoethanolamine-biosynthesis-in-mice
#9
Andreas Bickert, Christina Ginkel, Matthijs Kol, Katharina vom Dorp, Holger Jastrow, Joachim Degen, René L Jacobs, Dennis E Vance, Elke Winterhager, Xian-Cheng Jiang, Peter Dörmann, Pentti Somerharju, Joost C M Holthuis, Klaus Willecke
Besides bulk amounts of SM, mammalian cells produce small quantities of the SM analog ceramide phosphoethanolamine (CPE). Little is known about the biological role of CPE or enzymes responsible for CPE production. Heterologous expression studies revealed that SM synthase (SMS)2 is a bifunctional enzyme producing both SM and CPE, whereas SMS-related protein (SMSr) serves as monofunctional CPE synthase. Acute disruption of SMSr catalytic activity in cultured cells causes a rise in endoplasmic reticulum (ER) ceramides, fragmentation of ER exit sites, and induction of mitochondrial apoptosis...
April 2015: Journal of Lipid Research
https://www.readbyqxmd.com/read/25663231/park10-is-a-major-locus-for-sporadic-neuropathologically-confirmed-parkinson-disease
#10
Gary W Beecham, Dennis W Dickson, William K Scott, Eden R Martin, Gerard Schellenberg, Karen Nuytemans, Eric B Larson, Joseph D Buxbaum, John Q Trojanowski, Vivianna M Van Deerlin, Howard I Hurtig, Deborah C Mash, Thomas G Beach, Juan C Troncoso, Olga Pletnikova, Matthew P Frosch, Bernardino Ghetti, Tatiana M Foroud, Lawrence S Honig, Karen Marder, Jean Paul Vonsattel, Samuel M Goldman, Harry V Vinters, Owen A Ross, Zbigniew K Wszolek, Liyong Wang, Derek M Dykxhoorn, Margaret A Pericak-Vance, Thomas J Montine, James B Leverenz, Ted M Dawson, Jeffery M Vance
OBJECTIVE: To minimize pathologic heterogeneity in genetic studies of Parkinson disease (PD), the Autopsy-Confirmed Parkinson Disease Genetics Consortium conducted a genome-wide association study using both patients with neuropathologically confirmed PD and controls. METHODS: Four hundred eighty-four cases and 1,145 controls met neuropathologic diagnostic criteria, were genotyped, and then imputed to 3,922,209 variants for genome-wide association study analysis...
March 10, 2015: Neurology
https://www.readbyqxmd.com/read/25531812/rarity-of-the-alzheimer-disease-protective-app-a673t-variant-in-the-united-states
#11
MULTICENTER STUDY
Li-San Wang, Adam C Naj, Robert R Graham, Paul K Crane, Brian W Kunkle, Carlos Cruchaga, Josue D Gonzalez Murcia, Lisa Cannon-Albright, Clinton T Baldwin, Henrik Zetterberg, Kaj Blennow, Walter A Kukull, Kelley M Faber, Nicole Schupf, Maria C Norton, JoAnn T Tschanz, Ronald G Munger, Christopher D Corcoran, Ekaterina Rogaeva, Chiao-Feng Lin, Beth A Dombroski, Laura B Cantwell, Amanda Partch, Otto Valladares, Hakon Hakonarson, Peter St George-Hyslop, Robert C Green, Alison M Goate, Tatiana M Foroud, Regina M Carney, Eric B Larson, Timothy W Behrens, John S K Kauwe, Jonathan L Haines, Lindsay A Farrer, Margaret A Pericak-Vance, Richard Mayeux, Gerard D Schellenberg, Marilyn S Albert, Roger L Albin, Liana G Apostolova, Steven E Arnold, Robert Barber, Michael Barmada, Lisa L Barnes, Thomas G Beach, James T Becker, Gary W Beecham, Duane Beekly, David A Bennett, Eileen H Bigio, Thomas D Bird, Deborah Blacker, Bradley F Boeve, James D Bowen, Adam Boxer, James R Burke, Joseph D Buxbaum, Nigel J Cairns, Chuanhai Cao, Chris S Carlson, Steven L Carroll, Helena C Chui, David G Clark, David H Cribbs, Elizabeth A Crocco, Charles DeCarli, Steven T DeKosky, F Yesim Demirci, Malcolm Dick, Dennis W Dickson, Ranjan Duara, Nilufer Ertekin-Taner, Kenneth B Fallon, Martin R Farlow, Steven Ferris, Matthew P Frosch, Douglas R Galasko, Mary Ganguli, Marla Gearing, Daniel H Geschwind, Bernardino Ghetti, John R Gilbert, Jonathan D Glass, Neill R Graff-Radford, John H Growdon, Ronald L Hamilton, Kara L Hamilton-Nelson, Lindy E Harrell, Elizabeth Head, Lawrence S Honig, Christine M Hulette, Bradley T Hyman, Gail P Jarvik, Gregory A Jicha, Lee-Way Jin, Gyungah Jun, Gyungah Jun, M Ilyas Kamboh, Anna Karydas, Jeffrey A Kaye, Ronald Kim, Edward H Koo, Neil W Kowall, Joel H Kramer, Frank M LaFerla, James J Lah, James B Leverenz, Allan I Levey, Gei Li, Andrew P Lieberman, Oscar L Lopez, Kathryn L Lunetta, Constantine G Lyketsos, Wendy J Mack, Daniel C Marson, Eden R Martin, Frank Martiniuk, Deborah C Mash, Eliezer Masliah, Wayne C McCormick, Susan M McCurry, Andrew N McDavid, Ann C McKee, W Marsel Mesulam, Bruce L Miller, Carol A Miller, Joshua W Miller, Thomas J Montine, John C Morris, Jill R Murrell, John M Olichney, Joseph E Parisi, William Perry, Elaine Peskind, Ronald C Petersen, Aimee Pierce, Wayne W Poon, Huntington Potter, Joseph F Quinn, Ashok Raj, Murray Raskind, Eric M Reiman, Barry Reisberg, Christiane Reitz, John M Ringman, Erik D Roberson, Howard J Rosen, Roger N Rosenberg, Mary Sano, Andrew J Saykin, Julie A Schneider, Lon S Schneider, William W Seeley, Amanda G Smith, Joshua A Sonnen, Salvatore Spina, Robert A Stern, Rudolph E Tanzi, Tricia A Thornton-Wells, John Q Trojanowski, Juan C Troncoso, Debby W Tsuang, Vivianna M Van Deerlin, Linda J Van Eldik, Badri N Vardarajan, Harry V Vinters, Jean Paul Vonsattel, Sandra Weintraub, Kathleen A Welsh-Bohmer, Jennifer Williamson, Sarah Wishnek, Randall L Woltjer, Clinton B Wright, Steven G Younkin, Chang-En Yu, Lei Yu
IMPORTANCE: Recently, a rare variant in the amyloid precursor protein gene (APP) was described in a population from Iceland. This variant, in which alanine is replaced by threonine at position 673 (A673T), appears to protect against late-onset Alzheimer disease (AD). We evaluated the frequency of this variant in AD cases and cognitively normal controls to determine whether this variant will significantly contribute to risk assessment in individuals in the United States. OBJECTIVE: To determine the frequency of the APP A673T variant in a large group of elderly cognitively normal controls and AD cases from the United States and in 2 case-control cohorts from Sweden...
February 2015: JAMA Neurology
https://www.readbyqxmd.com/read/25463480/decreased-lipogenesis-in-white-adipose-tissue-contributes-to-the-resistance-to-high-fat-diet-induced-obesity-in-phosphatidylethanolamine-n-methyltransferase-deficient-mice
#12
Xia Gao, Jelske N van der Veen, Martin Hermansson, Marta Ordoñez, Antonio Gomez-Muñoz, Dennis E Vance, René L Jacobs
Mice lacking phosphatidylethanolamine N-methyltransferase (PEMT, Pemt(-/-) mice) are resistant to high-fat diet (HFD)-induced obesity (DIO) but develop non-alcoholic steatohepatitis. PEMT expression is strongly induced during differentiation of 3T3-L1 adipocytes. Hence, we hypothesized that white adipose tissue (WAT) might be a key player in the protection against DIO in Pemt(-/-) mice. We fed Pemt(-/-) and Pemt(+/+) mice the HFD for 2 weeks, after which we examined adipocyte differentiation, adipogenesis and lipolysis in WAT...
February 2015: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/25433161/vagus-nerve-contributes-to-the-development-of-steatohepatitis-and-obesity-in-phosphatidylethanolamine-n-methyltransferase-deficient-mice
#13
Xia Gao, Jelske N van der Veen, Linfu Zhu, Todd Chaba, Marta Ordoñez, Susanne Lingrell, Debby P Y Koonen, Jason R B Dyck, Antonio Gomez-Muñoz, Dennis E Vance, René L Jacobs
BACKGROUND & AIMS: Phosphatidylethanolamine N-methyltransferase (PEMT), a liver enriched enzyme, is responsible for approximately one third of hepatic phosphatidylcholine biosynthesis. When fed a high-fat diet (HFD), Pemt(-/-) mice are protected from HF-induced obesity; however, they develop steatohepatitis. The vagus nerve relays signals between liver and brain that regulate peripheral adiposity and pancreas function. Here we explore a possible role of the hepatic branch of the vagus nerve in the development of diet induced obesity and steatohepatitis in Pemt(-/-) mice...
April 2015: Journal of Hepatology
https://www.readbyqxmd.com/read/25421547/association-between-intervertebral-disc-degeneration-and-endplate-perfusion-studied-by-dce-mri
#14
L Tugan Muftuler, Joshua P Jarman, Hon J Yu, Vance O Gardner, Dennis J Maiman, Volkan Emre Arpinar
PURPOSE: The goal of this study was to study the association between solute transport mechanisms in cartilaginous disc endplates and the degeneration of intervertebral discs. Intervertebral disc degeneration is a multi-factorial process. It is suspected that poor nutrient delivery to discs might be a factor leading to degeneration. Several studies suggest that defects in disc endplates could lead to poor transport of nutrients. An imaging technique assessing endplate perfusion could be a valuable tool in investigating disc degeneration...
April 2015: European Spine Journal
https://www.readbyqxmd.com/read/25324900/association-of-mapt-haplotypes-with-alzheimer-s-disease-risk-and-mapt-brain-gene-expression-levels
#15
Mariet Allen, Michaela Kachadoorian, Zachary Quicksall, Fanggeng Zou, High Seng Chai, Curtis Younkin, Julia E Crook, V Shane Pankratz, Minerva M Carrasquillo, Siddharth Krishnan, Thuy Nguyen, Li Ma, Kimberly Malphrus, Sarah Lincoln, Gina Bisceglio, Christopher P Kolbert, Jin Jen, Shubhabrata Mukherjee, John K Kauwe, Paul K Crane, Jonathan L Haines, Richard Mayeux, Margaret A Pericak-Vance, Lindsay A Farrer, Gerard D Schellenberg, Joseph E Parisi, Ronald C Petersen, Neill R Graff-Radford, Dennis W Dickson, Steven G Younkin, Nilüfer Ertekin-Taner
INTRODUCTION: MAPT encodes for tau, the predominant component of neurofibrillary tangles that are neuropathological hallmarks of Alzheimer's disease (AD). Genetic association of MAPT variants with late-onset AD (LOAD) risk has been inconsistent, although insufficient power and incomplete assessment of MAPT haplotypes may account for this. METHODS: We examined the association of MAPT haplotypes with LOAD risk in more than 20,000 subjects (n-cases = 9,814, n-controls = 11,550) from Mayo Clinic (n-cases = 2,052, n-controls = 3,406) and the Alzheimer's Disease Genetics Consortium (ADGC, n-cases = 7,762, n-controls = 8,144)...
2014: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/25281863/acid-sphingomyelinase-ceramide-system-in-steatohepatitis-a-novel-target-regulating-multiple-pathways
#16
REVIEW
Carmen Garcia-Ruiz, Jose M Mato, Dennis Vance, Neil Kaplowitz, José C Fernández-Checa
Steatohepatitis (SH) is an intermediate stage of fatty liver disease and is one of the most common causes of chronic liver disease worldwide that may progress to cirrhosis and liver cancer. SH encompasses alcoholic and non-alcoholic steatohepatitis, the latter being of particular concern as it is associated with obesity and insulin resistance and has become a major cause of liver transplantation. The molecular mechanisms governing the transition from steatosis to SH are not fully understood. Here we discuss emerging data indicating that the acid sphingomyelinase (ASMase), a specific mechanism of ceramide generation, is required for the activation of key pathways that regulate steatosis, fibrosis and lipotoxicity, including endoplasmic reticulum stress, autophagy and lysosomal membrane permeabilization...
January 2015: Journal of Hepatology
https://www.readbyqxmd.com/read/25202977/heme-oxygenase-1-deficiency-accompanies-neuropathogenesis-of-hiv-associated-neurocognitive-disorders
#17
Alexander J Gill, Colleen E Kovacsics, Stephanie A Cross, Patricia J Vance, Lorraine L Kolson, Kelly L Jordan-Sciutto, Benjamin B Gelman, Dennis L Kolson
Heme oxygenase-1 (HO-1) is an inducible, detoxifying enzyme that is critical for limiting oxidative stress, inflammation, and cellular injury within the CNS and other tissues. Here, we demonstrate a deficiency of HO-1 expression in the brains of HIV-infected individuals. This HO-1 deficiency correlated with cognitive dysfunction, HIV replication in the CNS, and neuroimmune activation. In vitro analysis of HO-1 expression in HIV-infected macrophages, a primary CNS HIV reservoir along with microglia, demonstrated a decrease in HO-1 as HIV replication increased...
October 2014: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/25199842/effects-of-multiple-genetic-loci-on-age-at-onset-in-late-onset-alzheimer-disease-a-genome-wide-association-study
#18
Adam C Naj, Gyungah Jun, Christiane Reitz, Brian W Kunkle, William Perry, Yo Son Park, Gary W Beecham, Ruchita A Rajbhandary, Kara L Hamilton-Nelson, Li-San Wang, John S K Kauwe, Matthew J Huentelman, Amanda J Myers, Thomas D Bird, Bradley F Boeve, Clinton T Baldwin, Gail P Jarvik, Paul K Crane, Ekaterina Rogaeva, M Michael Barmada, F Yesim Demirci, Carlos Cruchaga, Patricia L Kramer, Nilufer Ertekin-Taner, John Hardy, Neill R Graff-Radford, Robert C Green, Eric B Larson, Peter H St George-Hyslop, Joseph D Buxbaum, Denis A Evans, Julie A Schneider, Kathryn L Lunetta, M Ilyas Kamboh, Andrew J Saykin, Eric M Reiman, Philip L De Jager, David A Bennett, John C Morris, Thomas J Montine, Alison M Goate, Deborah Blacker, Debby W Tsuang, Hakon Hakonarson, Walter A Kukull, Tatiana M Foroud, Eden R Martin, Jonathan L Haines, Richard P Mayeux, Lindsay A Farrer, Gerard D Schellenberg, Margaret A Pericak-Vance, Marilyn S Albert, Roger L Albin, Liana G Apostolova, Steven E Arnold, Robert Barber, Lisa L Barnes, Thomas G Beach, James T Becker, Duane Beekly, Eileen H Bigio, James D Bowen, Adam Boxer, James R Burke, Nigel J Cairns, Laura B Cantwell, Chuanhai Cao, Chris S Carlson, Regina M Carney, Minerva M Carrasquillo, Steven L Carroll, Helena C Chui, David G Clark, Jason Corneveaux, David H Cribbs, Elizabeth A Crocco, Charles DeCarli, Steven T DeKosky, Malcolm Dick, Dennis W Dickson, Ranjan Duara, Kelley M Faber, Kenneth B Fallon, Martin R Farlow, Steven Ferris, Matthew P Frosch, Douglas R Galasko, Mary Ganguli, Marla Gearing, Daniel H Geschwind, Bernardino Ghetti, John R Gilbert, Jonathan D Glass, John H Growdon, Ronald L Hamilton, Lindy E Harrell, Elizabeth Head, Lawrence S Honig, Christine M Hulette, Bradley T Hyman, Gregory A Jicha, Lee-Way Jin, Anna Karydas, Jeffrey A Kaye, Ronald Kim, Edward H Koo, Neil W Kowall, Joel H Kramer, Frank M LaFerla, James J Lah, James B Leverenz, Allan I Levey, Ge Li, Andrew P Lieberman, Chiao-Feng Lin, Oscar L Lopez, Constantine G Lyketsos, Wendy J Mack, Frank Martiniuk, Deborah C Mash, Eliezer Masliah, Wayne C McCormick, Susan M McCurry, Andrew N McDavid, Ann C McKee, Marsel Mesulam, Bruce L Miller, Carol A Miller, Joshua W Miller, Jill R Murrell, John M Olichney, Vernon S Pankratz, Joseph E Parisi, Henry L Paulson, Elaine Peskind, Ronald C Petersen, Aimee Pierce, Wayne W Poon, Huntington Potter, Joseph F Quinn, Ashok Raj, Murray Raskind, Barry Reisberg, John M Ringman, Erik D Roberson, Howard J Rosen, Roger N Rosenberg, Mary Sano, Lon S Schneider, William W Seeley, Amanda G Smith, Joshua A Sonnen, Salvatore Spina, Robert A Stern, Rudolph E Tanzi, Tricia A Thornton-Wells, John Q Trojanowski, Juan C Troncoso, Otto Valladares, Vivianna M Van Deerlin, Linda J Van Eldik, Badri N Vardarajan, Harry V Vinters, Jean Paul Vonsattel, Sandra Weintraub, Kathleen A Welsh-Bohmer, Jennifer Williamson, Sarah Wishnek, Randall L Woltjer, Clinton B Wright, Steven G Younkin, Chang-En Yu, Lei Yu
IMPORTANCE: Because APOE locus variants contribute to risk of late-onset Alzheimer disease (LOAD) and to differences in age at onset (AAO), it is important to know whether other established LOAD risk loci also affect AAO in affected participants. OBJECTIVES: To investigate the effects of known Alzheimer disease risk loci in modifying AAO and to estimate their cumulative effect on AAO variation using data from genome-wide association studies in the Alzheimer Disease Genetics Consortium...
November 2014: JAMA Neurology
https://www.readbyqxmd.com/read/25188341/genome-wide-association-meta-analysis-of-neuropathologic-features-of-alzheimer-s-disease-and-related-dementias
#19
Gary W Beecham, Kara Hamilton, Adam C Naj, Eden R Martin, Matt Huentelman, Amanda J Myers, Jason J Corneveaux, John Hardy, Jean-Paul Vonsattel, Steven G Younkin, David A Bennett, Philip L De Jager, Eric B Larson, Paul K Crane, M Ilyas Kamboh, Julia K Kofler, Deborah C Mash, Linda Duque, John R Gilbert, Harry Gwirtsman, Joseph D Buxbaum, Patricia Kramer, Dennis W Dickson, Lindsay A Farrer, Matthew P Frosch, Bernardino Ghetti, Jonathan L Haines, Bradley T Hyman, Walter A Kukull, Richard P Mayeux, Margaret A Pericak-Vance, Julie A Schneider, John Q Trojanowski, Eric M Reiman, Gerard D Schellenberg, Thomas J Montine
Alzheimer's disease (AD) and related dementias are a major public health challenge and present a therapeutic imperative for which we need additional insight into molecular pathogenesis. We performed a genome-wide association study and analysis of known genetic risk loci for AD dementia using neuropathologic data from 4,914 brain autopsies. Neuropathologic data were used to define clinico-pathologic AD dementia or controls, assess core neuropathologic features of AD (neuritic plaques, NPs; neurofibrillary tangles, NFTs), and evaluate commonly co-morbid neuropathologic changes: cerebral amyloid angiopathy (CAA), Lewy body disease (LBD), hippocampal sclerosis of the elderly (HS), and vascular brain injury (VBI)...
September 2014: PLoS Genetics
https://www.readbyqxmd.com/read/24855646/the-epigenetic-drug-5-azacytidine-interferes-with-cholesterol-and-lipid-metabolism
#20
Steve Poirier, Samaneh Samami, Maya Mamarbachi, Annie Demers, Ta Yuan Chang, Dennis E Vance, Grant M Hatch, Gaétan Mayer
DNA methylation and histone acetylation inhibitors are widely used to study the role of epigenetic marks in the regulation of gene expression. In addition, several of these molecules are being tested in clinical trials or already in use in the clinic. Antimetabolites, such as the DNA-hypomethylating agent 5-azacytidine (5-AzaC), have been shown to lower malignant progression to acute myeloid leukemia and to prolong survival in patients with myelodysplastic syndromes. Here we examined the effects of DNA methylation inhibitors on the expression of lipid biosynthetic and uptake genes...
July 4, 2014: Journal of Biological Chemistry
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