Search

Your search keyword '"Gill, Michael"' showing total 21 results
Start Over Author "Gill, Michael" Journal plos one
21 results on '"Gill, Michael"'

4. Gene-based analysis in HRC imputed genome wide association data identifies three novel genes for Alzheimer’s disease.

Author

Baker, Emily, Sims, Rebecca, Leonenko, Ganna, Frizzati, Aura, Harwood, Janet C., Grozeva, Detelina, null, null, Morgan, Kevin, Passmore, Peter, Holmes, Clive, Powell, John, Brayne, Carol, Gill, Michael, Mead, Simon, Bossù, Paola, Spalletta, Gianfranco, Goate, Alison M., Cruchaga, Carlos, Maier, Wolfgang, and Heun, Reinhard

Subjects
ALZHEIMER'S disease, SINGLE nucleotide polymorphisms, GENES, CIRCADIAN rhythms, MOLECULAR genetics, CHOLESTEROL metabolism
Abstract

Late onset Alzheimer’s disease is the most common form of dementia for which about 30 susceptibility loci have been reported. The aim of the current study is to identify novel genes associated with Alzheimer’s disease using the largest up-to-date reference single nucleotide polymorphism (SNP) panel, the most accurate imputation software and a novel gene-based analysis approach which tests for patterns of association within genes, in the powerful genome-wide association dataset of the International Genomics of Alzheimer’s Project Consortium, comprising over 7 million genotypes from 17,008 Alzheimer’s cases and 37,154 controls. In addition to earlier reported genes, we detected three novel gene-wide significant loci PPARGC1A (p = 2.2 × 10−6), RORA (p = 7.4 × 10−7) and ZNF423 (p = 2.1 × 10−6). PPARGC1A and RORA are involved in circadian rhythm; circadian disturbances are one of the earliest symptoms of Alzheimer’s disease. PPARGC1A is additionally linked to energy metabolism and the generation of amyloid beta plaques. RORA is involved in a variety of functions apart from circadian rhythm, such as cholesterol metabolism and inflammation. The ZNF423 gene resides in an Alzheimer’s disease-specific protein network and is likely involved with centrosomes and DNA damage repair. [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

6. DNA Methylation of the Serotonin Transporter Gene in Peripheral Cells and Stress-Related Changes in Hippocampal Volume: A Study in Depressed Patients and Healthy Controls

Author

Booij, Linda, primary, Szyf, Moshe, additional, Carballedo, Angela, additional, Frey, Eva-Maria, additional, Morris, Derek, additional, Dymov, Sergiy, additional, Vaisheva, Farida, additional, Ly, Victoria, additional, Fahey, Ciara, additional, Meaney, James, additional, Gill, Michael, additional, and Frodl, Thomas, additional

Published
2015
Full Text
View/download PDF

10. Cause-Specific Mortality in HIV-Positive Patients Who Survived Ten Years after Starting Antiretroviral Therapy.

Author

Trickey, Adam, May, Margaret T., Vehreschild, Janne, Obel, Niels, Gill, Michael John, Crane, Heidi, Boesecke, Christoph, Samji, Hasina, Grabar, Sophie, Cazanave, Charles, Cavassini, Matthias, Shepherd, Leah, d’Arminio Monforte, Antonella, Smit, Colette, Saag, Michael, Lampe, Fiona, Hernando, Vicky, Montero, Marta, Zangerle, Robert, and Justice, Amy C.

Subjects
HIV infections, THERAPEUTICS, ANTIRETROVIRAL agents, DEATH rate, VIRAL replication, CD4 lymphocyte count
Abstract

Objectives: To estimate mortality rates and prognostic factors in HIV-positive patients who started combination antiretroviral therapy between 1996–1999 and survived for more than ten years. Methods: We used data from 18 European and North American HIV cohort studies contributing to the Antiretroviral Therapy Cohort Collaboration. We followed up patients from ten years after start of combination antiretroviral therapy. We estimated overall and cause-specific mortality rate ratios for age, sex, transmission through injection drug use, AIDS, CD4 count and HIV-1 RNA. Results: During 50,593 person years 656/13,011 (5%) patients died. Older age, male sex, injecting drug use transmission, AIDS, and low CD4 count and detectable viral replication ten years after starting combination antiretroviral therapy were associated with higher subsequent mortality. CD4 count at ART start did not predict mortality in models adjusted for patient characteristics ten years after start of antiretroviral therapy. The most frequent causes of death (among 340 classified) were non-AIDS cancer, AIDS, cardiovascular, and liver-related disease. Older age was strongly associated with cardiovascular mortality, injecting drug use transmission with non-AIDS infection and liver-related mortality, and low CD4 and detectable viral replication ten years after starting antiretroviral therapy with AIDS mortality. Five-year mortality risk was <5% in 60% of all patients, and in 30% of those aged over 60 years. Conclusions: Viral replication, lower CD4 count, prior AIDS, and transmission via injecting drug use continue to predict higher all-cause and AIDS-related mortality in patients treated with combination antiretroviral therapy for over a decade. Deaths from AIDS and non-AIDS infection are less frequent than deaths from other non-AIDS causes. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

12. Genomewide Association Scan of Suicidal Thoughts and Behaviour in Major Depression

Author

Schosser, Alexandra, primary, Butler, Amy W., additional, Ising, Marcus, additional, Perroud, Nader, additional, Uher, Rudolf, additional, Ng, Mandy Y., additional, Cohen-Woods, Sarah, additional, Craddock, Nick, additional, Owen, Michael J., additional, Korszun, Ania, additional, Jones, Lisa, additional, Jones, Ian, additional, Gill, Michael, additional, Rice, John P., additional, Maier, Wolfgang, additional, Mors, Ole, additional, Rietschel, Marcella, additional, Lucae, Susanne, additional, Binder, Elisabeth B., additional, Preisig, Martin, additional, Perry, Julia, additional, Tozzi, Federica, additional, Muglia, Pierandrea, additional, Aitchison, Katherine J., additional, Breen, Gerome, additional, Craig, Ian W., additional, Farmer, Anne E., additional, Müller-Myhsok, Bertram, additional, McGuffin, Peter, additional, and Lewis, Cathryn M., additional

Published
2011
Full Text
View/download PDF

13. Correction: Genetic Evidence Implicates the Immune System and Cholesterol Metabolism in the Aetiology of Alzheimer's Disease

Author

Jones, Lesley, primary, Holmans, Peter A., additional, Hamshere, Marian L., additional, Harold, Denise, additional, Moskvina, Valentina, additional, Ivanov, Dobril, additional, Pocklington, Andrew, additional, Abraham, Richard, additional, Hollingworth, Paul, additional, Sims, Rebecca, additional, Gerrish, Amy, additional, Pahwa, Jaspreet Singh, additional, Jones, Nicola, additional, Stretton, Alexandra, additional, Morgan, Angharad R., additional, Lovestone, Simon, additional, Powell, John, additional, Proitsi, Petroula, additional, Lupton, Michelle K., additional, Brayne, Carol, additional, Rubinsztein, David C., additional, Gill, Michael, additional, Lawlor, Brian, additional, Lynch, Aoibhinn, additional, Morgan, Kevin, additional, Brown, Kristelle S., additional, Passmore, Peter A., additional, Craig, David, additional, McGuinness, Bernadette, additional, Todd, Stephen, additional, Holmes, Clive, additional, Mann, David, additional, Smith, A. David, additional, Love, Seth, additional, Kehoe, Patrick G., additional, Mead, Simon, additional, Fox, Nick, additional, Rossor, Martin, additional, Collinge, John, additional, Maier, Wolfgang, additional, Jessen, Frank, additional, Schürmann, Britta, additional, van den Bussche, Hendrik, additional, Heuser, Isabella, additional, Peters, Oliver, additional, Kornhuber, Johannes, additional, Wiltfang, Jens, additional, Dichgans, Martin, additional, Frölich, Lutz, additional, Hampel, Harald, additional, Hüll, Michael, additional, Rujescu, Dan, additional, Goate, Alison M., additional, Kauwe, John S. K., additional, Cruchaga, Carlos, additional, Nowotny, Petra, additional, Morris, John C., additional, Mayo, Kevin, additional, Livingston, Gill, additional, Bass, Nicholas J., additional, Gurling, Hugh, additional, McQuillin, Andrew, additional, Gwilliam, Rhian, additional, Deloukas, Panos, additional, Al-Chalabi, Ammar, additional, Shaw, Christopher E., additional, Singleton, Andrew B., additional, Guerreiro, Rita, additional, Mühleisen, Thomas W., additional, Nöthen, Markus M., additional, Moebus, Susanne, additional, Jöckel, Karl-Heinz, additional, Klopp, Norman, additional, Wichmann, H.-Erich, additional, Rüther, Eckhard, additional, Carrasquillo, Minerva M., additional, Pankratz, V. Shane, additional, Younkin, Steven G., additional, Hardy, John, additional, O'Donovan, Michael C., additional, Owen, Michael J., additional, and Williams, Julie, additional

Published
2011
Full Text
View/download PDF

14. Genetic Evidence Implicates the Immune System and Cholesterol Metabolism in the Aetiology of Alzheimer's Disease

Author

Jones, Lesley, primary, Holmans, Peter A., additional, Hamshere, Marian L., additional, Harold, Denise, additional, Moskvina, Valentina, additional, Ivanov, Dobril, additional, Pocklington, Andrew, additional, Abraham, Richard, additional, Hollingworth, Paul, additional, Sims, Rebecca, additional, Gerrish, Amy, additional, Pahwa, Jaspreet Singh, additional, Jones, Nicola, additional, Stretton, Alexandra, additional, Morgan, Angharad R., additional, Lovestone, Simon, additional, Powell, John, additional, Proitsi, Petroula, additional, Lupton, Michelle K., additional, Brayne, Carol, additional, Rubinsztein, David C., additional, Gill, Michael, additional, Lawlor, Brian, additional, Lynch, Aoibhinn, additional, Morgan, Kevin, additional, Brown, Kristelle S., additional, Passmore, Peter A., additional, Craig, David, additional, McGuinness, Bernadette, additional, Todd, Stephen, additional, Holmes, Clive, additional, Mann, David, additional, Smith, A. David, additional, Love, Seth, additional, Kehoe, Patrick G., additional, Mead, Simon, additional, Fox, Nick, additional, Rossor, Martin, additional, Collinge, John, additional, Maier, Wolfgang, additional, Jessen, Frank, additional, Schürmann, Britta, additional, van den Bussche, Hendrik, additional, Heuser, Isabella, additional, Peters, Oliver, additional, Kornhuber, Johannes, additional, Wiltfang, Jens, additional, Dichgans, Martin, additional, Frölich, Lutz, additional, Hampel, Harald, additional, Hüll, Michael, additional, Rujescu, Dan, additional, Goate, Alison M., additional, Kauwe, John S. K., additional, Cruchaga, Carlos, additional, Nowotny, Petra, additional, Morris, John C., additional, Mayo, Kevin, additional, Livingston, Gill, additional, Bass, Nicholas J., additional, Gurling, Hugh, additional, McQuillin, Andrew, additional, Gwilliam, Rhian, additional, Deloukas, Panos, additional, Al-Chalabi, Ammar, additional, Shaw, Christopher E., additional, Singleton, Andrew B., additional, Guerreiro, Rita, additional, Mühleisen, Thomas W., additional, Nöthen, Markus M., additional, Moebus, Susanne, additional, Jöckel, Karl-Heinz, additional, Klopp, Norman, additional, Wichmann, H.-Erich, additional, Rüther, Eckhard, additional, Carrasquillo, Minerva M., additional, Pankratz, V. Shane, additional, Younkin, Steven G., additional, Hardy, John, additional, O'Donovan, Michael C., additional, Owen, Michael J., additional, and Williams, Julie, additional

Published
2010
Full Text
View/download PDF

19. DNA Variation in the SNAP25 Gene Confers Risk to ADHD and Is Associated with Reduced Expression in Prefrontal Cortex.

Author

Hawi, Ziarih, Matthews, Natasha, Wagner, Joseph, Wallace, Robyn H., Butler, Tim J., Vance, Alasdair, Kent, Lindsey, Gill, Michael, and Bellgrove, Mark A.

Subjects
RISK factors of attention-deficit hyperactivity disorder, GENE expression, PREFRONTAL cortex, LABORATORY mice, PHENOTYPES, POLYMERASE chain reaction, DNA, BIOLOGICAL variation, MENTAL health
Abstract

Background: The Coloboma mouse carries a ∼2 cM deletion encompassing the SNAP25 gene and has a hyperactive phenotype similar to that of ADHD. Such mice are 3 fold more active compared to their control littermates. Genetic association studies support a role for allelic variants of the human SNAP25 gene in predisposing to ADHD. Methods/Principal Findings: We performed association analysis across the SNAP25 gene in 1,107 individuals (339 ADHD trios). To assess the functional relevance of the SNAP25-ADHD associated allele, we performed quantitative PCR on post-mortem tissue derived from the inferior frontal gyrus of 89 unaffected adults. Significant associations with the A allele of SNP rs362990 (χ2 = 10, p-corrected = 0.019, OR = 1.5) and three marker haplotypes (rs6108461, rs362990 and rs362998) were observed. Furthermore, a significant additive decrease in the expression of the SNAP25 transcript as a function of the risk allele was also observed. This effect was detected at the haplotype level, where increasing copies of the ADHD-associated haplotype reduced the expression of the transcript. Conclusions: Our data show that DNA variation at SNAP25 confers risk to ADHD and reduces the expression of the transcript in a region of the brain that is critical for the regulation of attention and inhibition. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

20. Genetic Classification of Populations Using Supervised Learning.

Author

Bridges, Michael, Heron, Elizabeth A., O'Dushlaine, Colm, Segurado, Ricardo, Morris, Derek, Corvin, Aiden, Gill, Michael, and Pinto, Carlos

Subjects
ECOLOGICAL genetics, POPULATION, SUPERVISED learning, CASE-control method, GENOTYPE-environment interaction, PRINCIPAL components analysis
Abstract

There are many instances in genetics in which we wish to determine whether two candidate populations are distinguishable on the basis of their genetic structure. Examples include populations which are geographically separated, case-control studies and quality control (when participants in a study have been genotyped at different laboratories). This latter application is of particular importance in the era of large scale genome wide association studies, when collections of individuals genotyped at different locations are being merged to provide increased power. The traditional method for detecting structure within a population is some form of exploratory technique such as principal components analysis. Such methods, which do not utilise our prior knowledge of the membership of the candidate populations. are termed unsupervised. Supervised methods, on the other hand are able to utilise this prior knowledge when it is available. In this paper we demonstrate that in such cases modern supervised approaches are a more appropriate tool for detecting genetic differences between populations. We apply two such methods, (neural networks and support vector machines) to the classification of three populations (two from Scotland and one from Bulgaria). The sensitivity exhibited by both these methods is considerably higher than that attained by principal components analysis and in fact comfortably exceeds a recently conjectured theoretical limit on the sensitivity of unsupervised methods. In particular, our methods can distinguish between the two Scottish populations, where principal components analysis cannot. We suggest, on the basis of our results that a supervised learning approach should be the method of choice when classifying individuals into pre-defined populations, particularly in quality control for large scale genome wide association studies. [ABSTRACT FROM AUTHOR]

Published
2011
Full Text
View/download PDF

21. Gene-wide analysis detects two new susceptibility genes for Alzheimer's disease.

Author

Escott-Price V, Bellenguez C, Wang LS, Choi SH, Harold D, Jones L, Holmans P, Gerrish A, Vedernikov A, Richards A, DeStefano AL, Lambert JC, Ibrahim-Verbaas CA, Naj AC, Sims R, Jun G, Bis JC, Beecham GW, Grenier-Boley B, Russo G, Thornton-Wells TA, Denning N, Smith AV, Chouraki V, Thomas C, Ikram MA, Zelenika D, Vardarajan BN, Kamatani Y, Lin CF, Schmidt H, Kunkle B, Dunstan ML, Vronskaya M, Johnson AD, Ruiz A, Bihoreau MT, Reitz C, Pasquier F, Hollingworth P, Hanon O, Fitzpatrick AL, Buxbaum JD, Campion D, Crane PK, Baldwin C, Becker T, Gudnason V, Cruchaga C, Craig D, Amin N, Berr C, Lopez OL, De Jager PL, Deramecourt V, Johnston JA, Evans D, Lovestone S, Letenneur L, Hernández I, Rubinsztein DC, Eiriksdottir G, Sleegers K, Goate AM, Fiévet N, Huentelman MJ, Gill M, Brown K, Kamboh MI, Keller L, Barberger-Gateau P, McGuinness B, Larson EB, Myers AJ, Dufouil C, Todd S, Wallon D, Love S, Rogaeva E, Gallacher J, George-Hyslop PS, Clarimon J, Lleo A, Bayer A, Tsuang DW, Yu L, Tsolaki M, Bossù P, Spalletta G, Proitsi P, Collinge J, Sorbi S, Garcia FS, Fox NC, Hardy J, Naranjo MC, Bosco P, Clarke R, Brayne C, Galimberti D, Scarpini E, Bonuccelli U, Mancuso M, Siciliano G, Moebus S, Mecocci P, Zompo MD, Maier W, Hampel H, Pilotto A, Frank-García A, Panza F, Solfrizzi V, Caffarra P, Nacmias B, Perry W, Mayhaus M, Lannfelt L, Hakonarson H, Pichler S, Carrasquillo MM, Ingelsson M, Beekly D, Alvarez V, Zou F, Valladares O, Younkin SG, Coto E, Hamilton-Nelson KL, Gu W, Razquin C, Pastor P, Mateo I, Owen MJ, Faber KM, Jonsson PV, Combarros O, O'Donovan MC, Cantwell LB, Soininen H, Blacker D, Mead S, Mosley TH Jr, Bennett DA, Harris TB, Fratiglioni L, Holmes C, de Bruijn RF, Passmore P, Montine TJ, Bettens K, Rotter JI, Brice A, Morgan K, Foroud TM, Kukull WA, Hannequin D, Powell JF, Nalls MA, Ritchie K, Lunetta KL, Kauwe JS, Boerwinkle E, Riemenschneider M, Boada M, Hiltunen M, Martin ER, Schmidt R, Rujescu D, Dartigues JF, Mayeux R, Tzourio C, Hofman A, Nöthen MM, Graff C, Psaty BM, Haines JL, Lathrop M, Pericak-Vance MA, Launer LJ, Van Broeckhoven C, Farrer LA, van Duijn CM, Ramirez A, Seshadri S, Schellenberg GD, Amouyel P, and Williams J

Subjects
Case-Control Studies, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Receptors, Antigen, B-Cell genetics, Alzheimer Disease genetics, Carrier Proteins genetics, Heat-Shock Proteins genetics
Abstract

Background: Alzheimer's disease is a common debilitating dementia with known heritability, for which 20 late onset susceptibility loci have been identified, but more remain to be discovered. This study sought to identify new susceptibility genes, using an alternative gene-wide analytical approach which tests for patterns of association within genes, in the powerful genome-wide association dataset of the International Genomics of Alzheimer's Project Consortium, comprising over 7 m genotypes from 25,580 Alzheimer's cases and 48,466 controls., Principal Findings: In addition to earlier reported genes, we detected genome-wide significant loci on chromosomes 8 (TP53INP1, p = 1.4×10-6) and 14 (IGHV1-67 p = 7.9×10-8) which indexed novel susceptibility loci., Significance: The additional genes identified in this study, have an array of functions previously implicated in Alzheimer's disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimer's disease.

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results