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1. No evidence that extended tracts of homozygosity are associated with Alzheimerʼs disease

Author

Sims, Rebecca, Dwyer, Sarah, Harold, Denise, Gerrish, Amy, Hollingworth, Paul, Chapman, Jade, Jones, Nicola, Abraham, Richard, Ivanov, Dobril, Pahwa, Jaspreet Singh, Moskvina, Valentina, Dowzell, Kimberley, Thomas, Charlene, Stretton, Alexandra, Lovestone, Simon, Powell, John, Proitsi, Petroula, Lupton, Michelle K., Brayne, Carol, Rubinsztein, David C., Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, Morgan, Kevin, Brown, Kristelle S., Passmore, Peter A., Craig, David, McGuiness, Bernadette, Todd, Stephen, Johnston, Janet A., Holmes, Clive, Mann, David, Smith, David A., Love, Seth, Kehoe, Patrick G., Hardy, John, Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Livingston, Gill, Bass, Nicholas J., Gurling, Hugh, McQuillin, Andrew, Jones, Lesley, Holmans, Peter A., OʼDonovan, Michael, Owen, Michael J., and Williams, Julie

Published
2011
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3. Quantitative Interaction Proteomics of Neurodegenerative Disease Proteins

Author

Hosp, Fabian, Vossfeldt, Hannes, Lannfelt, Lars, Holmans, Peter, O'Donovan, Michael, Owen, Michael J., Williams, Julie, Ingelsson, Martin, Lalowski, Maciej, Voigt, Aaron, Selbach, Matthias, Harold, Denise, Abraham, Richard, Hollingworth, Paul, Sims, Rebecca, Gerrish, Amy, Heinig, Matthias, Chapman, Jade, Russo, Giancarlo, Hamshere, Marian, Pahwa, Jaspreet Singh, Escott-Price, Valentina, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Stretton, Alexandra, Vasiljevic, Djordje, Morgan, Angharad, Lovestone, Simon, Powell, John, Proitsi, Petroula, Lupton, Michelle K., Brayne, Carol, Rubinsztein, David C., Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, Arumughan, Anup, Morgan, Kevin, Brown, Kristelle, Passmore, Peter, Craig, David, McGuinness, Bernadette, Todd, Stephen, Johnston, Janet, Holmes, Clive, Mann, David, Smith, A. David, Wyler, Emanuel, Love, Seth, Kehoe, Patrick G., Hardy, John, Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Maier, Wolfgang, Jessen, Frank, Heun, Reiner, Genetic and Environmental Risk for Alzheimer's Disease GERAD1 Consortium, Schürmann, Britta, Ramirez, Alfredo, Becker, Tim, Herold, Christine, Lacour, André, Drichel, Dmitriy, van den Bussche, Hendrik, Heuser, Isabella, Kornhuber, Johannes, Wiltfang, Jens, Landthaler, Markus, Dichgans, Martin, Frölich, Lutz, Hampel, Harald, Hüll, Michael, Rujescu, Dan, Goate, Alison, Kauwe, John S. K., Cruchaga, Carlos, Nowotny, Petra, Morris, John C., Hubner, Norbert, Mayo, Kevin, Livingston, Gill, Bass, Nicholas J., Gurling, Hugh, McQuillin, Andrew, Gwilliam, Rhian, Deloukas, Panagiotis, Al-Chalabi, Ammar, Shaw, Christopher E., Singleton, Andrew B., Wanker, Erich E., Guerreiro, Rita, Mühleisen, Thomas W., Nöthen, Markus M., Moebus, Susanne, Jöckel, Karl-Heinz, Klopp, Norman, Wichmann, H-Erich, Carrasquillo, Minerva M., Pankratz, V. Shane, and Younkin, Steven G.

Subjects
Proteomics, Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy), Neurodegenerative Diseases, nervous system diseases, Phenotype, lcsh:Biology (General), Cardiovascular and Metabolic Diseases, Tandem Mass Spectrometry, mental disorders, Animals, Humans, Immunoprecipitation, Function and Dysfunction of the Nervous System, lcsh:QH301-705.5, Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci), Chromatography, Liquid, Genome-Wide Association Study
Abstract

SummarySeveral proteins have been linked to neurodegenerative disorders (NDDs), but their molecular function is not completely understood. Here, we used quantitative interaction proteomics to identify binding partners of Amyloid beta precursor protein (APP) and Presenilin-1 (PSEN1) for Alzheimer’s disease (AD), Huntingtin (HTT) for Huntington’s disease, Parkin (PARK2) for Parkinson’s disease, and Ataxin-1 (ATXN1) for spinocerebellar ataxia type 1. Our network reveals common signatures of protein degradation and misfolding and recapitulates known biology. Toxicity modifier screens and comparison to genome-wide association studies show that interaction partners are significantly linked to disease phenotypes in vivo. Direct comparison of wild-type proteins and disease-associated variants identified binders involved in pathogenesis, highlighting the value of differential interactome mapping. Finally, we show that the mitochondrial protein LRPPRC interacts preferentially with an early-onset AD variant of APP. This interaction appears to induce mitochondrial dysfunction, which is an early phenotype of AD.

Published
2015
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4. Common polygenic variation enhances risk prediction for Alzheimer's disease

Author

Escott-Price, Valentina, Sims, Rebecca, Passmore, Peter, ODonovan, Michael, Owen, Michael J, Holmes, Clive, Powell, John, Brayne, Carol, Gill, Michael, Mead, Simon, Goate, Alison, Cruchaga, Carlos, Lambert, Jean-Charles, van Duijn, Cornelia, Bannister, Christian, Maier, Wolfgang, Ramirez, Alfredo, Holmans, Peter, Jones, Lesley, Hardy, John, Seshadri, Sudha, Schellenberg, Gerard D, Amouyel, Philippe, Williams, Julie, Abraham, Richard, Harold, Denise, Hollingworth, Paul, Gerrish, Amy, Chapman, Jade, Russo, Giancarlo, Hamshere, Marian, Pahwa, Jaspreet Singh, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Vronskaya, Maria, Stretton, Alexandra, Morgan, Angharad, Taylor, Sarah, Lovestone, Simon, Proitsi, Petroula, Lupton, Michelle K, Rubinsztein, David C, Lawlor, Brian, Lynch, Aoibhinn, Brown, Kristelle, Majounie, Elisa, Craig, David, McGuinness, Bernadette, Todd, Stephen, Johnston, Janet, Mann, David, Smith, A David, Love, Seth, Kehoe, Patrick G, Fox, Nick, Rossor, Martin, Badarinarayan, Nandini, Collinge, John, Jessen, Frank, Heun, Reiner, Schürmann, Britta, Becker, Tim, Herold, Christine, Lacour, Andre, Drichel, Dmitriy, van den Bussche, Hendrik, Heuser, Isabella, GERAD/PERADES, Kornhuber, Johannes, Wiltfang, Jens, Dichgans, Martin, Frölich, Lutz, Hampel, Harald, Hüll, Michael, Rujescu, Dan, Kauwe, John S K, Nowotny, Petra, Morris, John C, consortia, IGAP, Mayo, Kevin, Livingston, Gill, Bass, Nicholas J, Gurling, Hugh, McQuillin, Andrew, Gwilliam, Rhian, Deloukas, Panagiotis, Al-Chalabi, Ammar, Shaw, Christopher E, Singleton, Andrew B, Morgan, Kevin, Guerreiro, Rita, Mühleisen, Thomas W, Nöthen, Markus M., Moebus, Susanne, Jöckel, Karl-Heinz, Klopp, Norman, Wichmann, H-Erich, Carrasquillo, Minerva M, Pankratz, V Shane, Younkin, Steven G, and Epidemiology

Subjects
Apolipoprotein E, Oncology, Risk, Multifactorial Inheritance, medicine.medical_specialty, Genotype, genetics [Alzheimer Disease], Bioinformatics, Logistic regression, Apolipoproteins E, Alzheimer Disease, Positive predicative value, Internal medicine, medicine, Humans, Genetic Predisposition to Disease, ddc:610, Genetic Testing, genetics [Genetic Predisposition to Disease], genetics [Multifactorial Inheritance], Alleles, Receiver operating characteristic, Case-control study, Genetic Variation, Original Articles, medicine.disease, Confidence interval, genetics [Genetic Variation], Logistic Models, ROC Curve, Case-Control Studies, genetics [Apolipoproteins E], Neurology (clinical), Alzheimer's disease, Psychology, Genome-Wide Association Study
Abstract

The identification of subjects at high risk for Alzheimer's disease is important for prognosis and early intervention. We investigated the polygenic architecture of Alzheimer's disease and the accuracy of Alzheimer's disease prediction models, including and excluding the polygenic component in the model. This study used genotype data from the powerful dataset comprising 17 008 cases and 37 154 controls obtained from the International Genomics of Alzheimer's Project (IGAP). Polygenic score analysis tested whether the alleles identified to associate with disease in one sample set were significantly enriched in the cases relative to the controls in an independent sample. The disease prediction accuracy was investigated in a subset of the IGAP data, a sample of 3049 cases and 1554 controls (for whom APOE genotype data were available) by means of sensitivity, specificity, area under the receiver operating characteristic curve (AUC) and positive and negative predictive values. We observed significant evidence for a polygenic component enriched in Alzheimer's disease (P = 4.9 × 10(-26)). This enrichment remained significant after APOE and other genome-wide associated regions were excluded (P = 3.4 × 10(-19)). The best prediction accuracy AUC = 78.2% (95% confidence interval 77-80%) was achieved by a logistic regression model with APOE, the polygenic score, sex and age as predictors. In conclusion, Alzheimer's disease has a significant polygenic component, which has predictive utility for Alzheimer's disease risk and could be a valuable research tool complementing experimental designs, including preventative clinical trials, stem cell selection and high/low risk clinical studies. In modelling a range of sample disease prevalences, we found that polygenic scores almost doubles case prediction from chance with increased prediction at polygenic extremes.

Published
2015
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5. A genome-wide association study for late-onset Alzheimer's disease using DNA pooling

Author

Hillmer Axel M, Cichon Sven, Dowzell Kimberley, Georgieva Lyudmila, Morgan Angharad, Hollingworth Paul, Sims Rebecca, Moskvina Valentina, Abraham Richard, O'Donovan Michael C, Williams Julie, Owen Michael J, and Kirov George

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Late-onset Alzheimer's disease (LOAD) is an age related neurodegenerative disease with a high prevalence that places major demands on healthcare resources in societies with increasingly aged populations. The only extensively replicable genetic risk factor for LOAD is the apolipoprotein E gene. In order to identify additional genetic risk loci we have conducted a genome-wide association (GWA) study in a large LOAD case – control sample, reducing costs through the use of DNA pooling. Methods DNA samples were collected from 1,082 individuals with LOAD and 1,239 control subjects. Age at onset ranged from 60 to 95 and Controls were matched for age (mean = 76.53 years, SD = 33), gender and ethnicity. Equimolar amounts of each DNA sample were added to either a case or control pool. The pools were genotyped using Illumina HumanHap300 and Illumina Sentrix HumanHap240S arrays testing 561,494 SNPs. 114 of our best hit SNPs from the pooling data were identified and then individually genotyped in the case – control sample used to construct the pools. Results Highly significant association with LOAD was observed at the APOE locus confirming the validity of the pooled genotyping approach. For 109 SNPs outside the APOE locus, we obtained uncorrected p-values ≤ 0.05 for 74 after individual genotyping. To further test these associations, we added control data from 1400 subjects from the 1958 Birth Cohort with the evidence for association increasing to 3.4 × 10-6 for our strongest finding, rs727153. rs727153 lies 13 kb from the start of transcription of lecithin retinol acyltransferase (phosphatidylcholine – retinol O-acyltransferase, LRAT). Five of seven tag SNPs chosen to cover LRAT showed significant association with LOAD with a SNP in intron 2 of LRAT, showing greatest evidence of association (rs201825, p-value = 6.1 × 10-7). Conclusion We have validated the pooling method for GWA studies by both identifying the APOE locus and by observing a strong enrichment for significantly associated SNPs. We provide evidence for LRAT as a novel candidate gene for LOAD. LRAT plays a prominent role in the Vitamin A cascade, a system that has been previously implicated in LOAD.

Published
2008
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6. Genetic predisposition to increased blood cholesterol and triglyceride lipid levels and risk of Alzheimer disease: a Mendelian randomization analysis

Author

Proitsi, Petroula, Lupton, Michelle K, Velayudhan, Latha, Newhouse, Stephen, Fogh, Isabella, Tsolaki, Magda, Daniilidou, Makrina, Pritchard, Megan, Kloszewska, Iwona, Soininen, Hilkka, Mecocci, Patrizia, Vellas, Bruno, Williams, Julie, Harold, Denise, Sims, Rebecca, Gerrish, Amy, Chapman, Jade, Escott-Price, Valentina, Abraham, Richard, Hollingworth, Paul, Hamshere, Marian, Singh Pahwa, Jaspreet, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Stretton, Alexandra, Morgan, Angharad R, Williams, Kate, Lovestone, Simon, Powell, John F, Brayne, Carol, Rubinsztein, David C, Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, Morgan, Kevin, Brown, Kristelle S, Passmore, Peter, Craig, David, Mcguinness, Bernadette, Johnston, Janet A., Todd, Stephen, Holmes, Clive, Mann, David, Smith, A David, Love, Seth, Kehoe, Patrick G, Hardy, John, Guerreiro, Rita, Singleton, Andrew B, Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Maier, Wolfgang, Jessen, Frank, Heun, Reiner, Schürmann, Britta, Ramirez, Alfredo, Becker, Tim, Herold, Christine, Lacour, André, Drichel, Dmitriy, van den Bussche, Hendrik, Heuser, Isabella, Kornhuber, Johannes, Wiltfang, Jens, Dichgans, Martin, Frölich, Lutz, Hampel, Harald, Hüll, Michael, Rujescu, Dan, Goate, Alison M, Kauwe, John S K, Cruchaga, Carlos, Nowotny, Petra, Morris, John C, Mayo, Kevin, Livingston, Gill, Bass, Nicholas J, Gurling, Hugh, McQuillin, Andrew, Gwilliam, Rhian, Deloukas, Panagiotis, Nöthen, Markus M, Holmans, Peter A, O'Donovan, Michael C, Owen, Michael J, Stewart, Robert C, Sham, Pak, Proitsi, Petroula [0000-0002-2553-6974], Velayudhan, Latha [0000-0002-7712-930X], Newhouse, Stephen [0000-0002-1843-9842], Fogh, Isabella [0000-0002-6266-8933], Tsolaki, Magda [0000-0002-2072-8010], Pritchard, Megan [0000-0001-8872-3614], Mecocci, Patrizia [0000-0003-0729-5246], Williams, Julie [0000-0002-4069-0259], Stewart, Robert [0000-0002-4435-6397], Lovestone, Simon [0000-0003-0473-4565], and Apollo - University of Cambridge Repository

Subjects
Male, Epidemiology, genetics [Triglycerides], Blood lipids, Physiology, Genome-wide association study, genetics [Alzheimer Disease], genetics [Cholesterol], Bioinformatics, methods [Genome-Wide Association Study], Biochemistry, methods [Mendelian Randomization Analysis], Risk Factors, Medicine and Health Sciences, Longitudinal Studies, genetics [Genetic Predisposition to Disease], blood [Cholesterol], Aged, 80 and over, education.field_of_study, Research Support, Non-U.S. Gov't, diagnosis [Alzheimer Disease], Mendelian Randomization Analysis, General Medicine, 3. Good health, Cholesterol, genetics [Polymorphism, Single Nucleotide], Medicine, Female, Biotechnology, Research Article, Population, Biology, Polymorphism, Single Nucleotide, blood [Alzheimer Disease], Research Support, N.I.H., Extramural, Alzheimer Disease, blood [Triglycerides], Mendelian randomization, Journal Article, Genetics, Genetic predisposition, Humans, Genetic Predisposition to Disease, ddc:610, education, Molecular Biology, Triglycerides, Aged, Biology and Life Sciences, Lipid metabolism, Cell Biology, Odds ratio, Geriatrics, RC0321, Research Support, U.S. Gov't, Non-P.H.S, Neuroscience, Genome-Wide Association Study
Abstract

In this study, Proitsi and colleagues use a Mendelian randomization approach to dissect the causal nature of the association between circulating lipid levels and late onset Alzheimer's Disease (LOAD) and find that genetic predisposition to increased plasma cholesterol and triglyceride lipid levels is not associated with elevated LOAD risk. Please see later in the article for the Editors' Summary, Background Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported. We have used a Mendelian randomization approach to dissect the causal nature of the association between circulating lipid levels and late onset AD (LOAD) and test the hypothesis that genetically raised lipid levels increase the risk of LOAD. Methods and Findings We included 3,914 patients with LOAD, 1,675 older individuals without LOAD, and 4,989 individuals from the general population from six genome wide studies drawn from a white population (total n = 10,578). We constructed weighted genotype risk scores (GRSs) for four blood lipid phenotypes (high-density lipoprotein cholesterol [HDL-c], low-density lipoprotein cholesterol [LDL-c], triglycerides, and total cholesterol) using well-established SNPs in 157 loci for blood lipids reported by Willer and colleagues (2013). Both full GRSs using all SNPs associated with each trait at p, Editors' Summary Background Currently, about 44 million people worldwide have dementia, a group of brain disorders characterized by an irreversible decline in memory, communication, and other “cognitive” functions. Dementia mainly affects older people and, because people are living longer, experts estimate that more than 135 million people will have dementia by 2050. The commonest form of dementia is Alzheimer disease. In this type of dementia, protein clumps called plaques and neurofibrillary tangles form in the brain and cause its degeneration. The earliest sign of Alzheimer disease is usually increasing forgetfulness. As the disease progresses, affected individuals gradually lose their ability to deal with normal daily activities such as dressing. They may become anxious or aggressive or begin to wander. They may also eventually lose control of their bladder and of other physical functions. At present, there is no cure for Alzheimer disease although some of its symptoms can be managed with drugs. Most people with the disease are initially cared for at home by relatives and other unpaid carers, but many patients end their days in a care home or specialist nursing home. Why Was This Study Done? Several lines of evidence suggest that lipid metabolism (how the body handles cholesterol and other fats) is altered in patients whose Alzheimer disease develops after the age of 60 years (late onset Alzheimer disease, LOAD). In particular, epidemiological studies (observational investigations that examine the patterns and causes of disease in populations) have found an association between high amounts of cholesterol in the blood in midlife and the risk of LOAD. However, observational studies cannot prove that abnormal lipid metabolism (dyslipidemia) causes LOAD. People with dyslipidemia may share other characteristics that cause both dyslipidemia and LOAD (confounding) or LOAD might actually cause dyslipidemia (reverse causation). Here, the researchers use “Mendelian randomization” to examine whether lifetime changes in lipid metabolism caused by genes have a causal impact on LOAD risk. In Mendelian randomization, causality is inferred from associations between genetic variants that mimic the effect of a modifiable risk factor and the outcome of interest. Because gene variants are inherited randomly, they are not prone to confounding and are free from reverse causation. So, if dyslipidemia causes LOAD, genetic variants that affect lipid metabolism should be associated with an altered risk of LOAD. What Did the Researchers Do and Find? The researchers investigated whether genetic predisposition to raised lipid levels increased the risk of LOAD in 10,578 participants (3,914 patients with LOAD, 1,675 elderly people without LOAD, and 4,989 population controls) using data collected in six genome wide studies looking for gene variants associated with Alzheimer disease. The researchers constructed a genotype risk score (GRS) for each participant using genetic risk markers for four types of blood lipids on the basis of the presence of single nucleotide polymorphisms (SNPs, a type of gene variant) in their DNA. When the researchers used statistical methods to investigate the association between the GRS and LOAD among all the study participants, they found no association between the GRS and LOAD. What Do These Findings Mean? These findings suggest that the genetic predisposition to raised blood levels of four types of lipid is not causally associated with LOAD risk. The accuracy of this finding may be affected by several limitations of this study, including the small proportion of lipid variance explained by the GRS and the validity of several assumptions that underlie all Mendelian randomization studies. Moreover, because all the participants in this study were white, these findings may not apply to people of other ethnic backgrounds. Given their findings, the researchers suggest that the observed epidemiological associations between abnormal lipid levels in the blood and variation in lipid levels for reasons other than genetics, or to LOAD risk could be secondary to variation in lipid levels for reasons other than genetics, or to LOAD, a possibility that can be investigated by studying blood lipid levels and other markers of lipid metabolism over time in large groups of patients with LOAD. Importantly, however, these findings provide new information about the role of lipids in LOAD development that may eventually lead to new therapeutic and public-health interventions for Alzheimer disease. Additional Information Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001713. The UK National Health Service Choices website provides information (including personal stories) about Alzheimer's disease The UK not-for-profit organization Alzheimer's Society provides information for patients and carers about dementia, including personal experiences of living with Alzheimer's disease The US not-for-profit organization Alzheimer's Association also provides information for patients and carers about dementia and personal stories about dementia Alzheimer's Disease International is the international federation of Alzheimer disease associations around the world; it provides links to individual associations, information about dementia, and links to World Alzheimer Reports MedlinePlus provides links to additional resources about Alzheimer's disease (in English and Spanish) Wikipedia has a page on Mendelian randomization (note: Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)

Published
2014
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7. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease (vol 41, pg 1088, 2009)

Author

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

Subjects
Medicine(all), Alzheimer's disease
Published
2013

8. Linking Protective GAB2 Variants, Increased Cortical GAB2 Expression and Decreased Alzheimer's Disease Pathology

Author

Zou, Fanggeng, Belbin, Olivia, Petersen, Ronald C, disease, Genetic and Environmental Risk for Alzheimer’s, Morgan, Kevin, Younkin, Steven G, Harold, Denise, Sims, Rebecca, Gerrish, Amy, Chapman, Jade, Moskvina, Valentina, Abraham, Richard, Carrasquillo, Minerva M, Hollingworth, Paul, Hamshere, Marian, Pahwa, Jaspreet Singh, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Stretton, Alexandra, Morgan, Angharad, Williams, Kate, Culley, Oliver J, Lovestone, Simon, Powell, John, Proitsi, Petroula, Lupton, Michelle K, Brayne, Carol, Rubinsztein, David C, Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, Hunter, Talisha A, Brown, Kristelle, Passmore, Peter, Craig, David, McGuinness, Bernadette, Johnston, Janet A, Todd, Stephen, Holmes, Clive, Mann, David, Smith, A David, Love, Seth, Ma, Li, Kehoe, Patrick G, Hardy, John, Guerreiro, Rita, Singleton, Andrew, Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Maier, Wolfgang, Jessen, Frank, Bisceglio, Gina D, Heun, Reiner, Schürmann, Britta, Ramirez, Alfredo, Herold, Christine, Lacour, André, Drichel, Dmitriy, van den Bussche, Hendrik, Heuser, Isabella, Kornhuber, Johannes, Wiltfang, Jens, Allen, Mariet, Dichgans, Martin, Frölich, Lutz, Hampel, Harald, Hüll, Michael, Rujescu, Dan, Goate, Alison, Kauwe, John S K, Cruchaga, Carlos, Nowotny, Petra, Morris, John C, Dickson, Dennis W, Mayo, Kevin, Livingston, Gill, Bass, Nicholas J, Gurling, Hugh, McQuillin, Andrew, Gwilliam, Rhian, Deloukas, Panagiotis, Nöthen, Markus M, Holmans, Peter, O'Donovan, Michael, Graff-Radford, Neill R, Owen, Michael J, Williams, Julie, and Wiltfang, Jens (Beitragende*r)

Subjects
Male, Pathology, Heredity, Medizin, lcsh:Medicine, Gene Expression, genetics [Alzheimer Disease], pathology [Alzheimer Disease], 0302 clinical medicine, Polymorphism (computer science), Risk Factors, genetics [Adaptor Proteins, Signal Transducing], Senile plaques, lcsh:Science, 0303 health sciences, Multidisciplinary, Temporal Lobe, Neurology, genetics [Polymorphism, Single Nucleotide], Medicine, Female, Alzheimer's disease, Research Article, medicine.medical_specialty, Genotypes, genetics [Genetic Loci], Biology, metabolism [RNA, Messenger], Polymorphism, Single Nucleotide, metabolism [Temporal Lobe], Cell Line, Molecular Genetics, 03 medical and health sciences, metabolism [Adaptor Proteins, Signal Transducing], genetics [RNA, Messenger], Genetic Heterogeneity, Apolipoproteins E, Meta-Analysis as Topic, Alzheimer Disease, genetics [Haplotypes], medicine, GAB2 protein, human, Genetics, Humans, Genetic Predisposition to Disease, ddc:610, RNA, Messenger, Allele, Genetic Association Studies, 030304 developmental biology, Adaptor Proteins, Signal Transducing, Aged, Evolutionary Biology, Population Biology, Genetic heterogeneity, lcsh:R, Case-control study, Computational Biology, Neurofibrillary tangle, pathology [Temporal Lobe], Human Genetics, Epistasis, Genetic, Odds ratio, medicine.disease, R1, Haplotypes, Genetic Loci, Case-Control Studies, Postmortem Changes, Genetics of Disease, North America, Genetic Polymorphism, Epistasis, genetics [Apolipoproteins E], lcsh:Q, Dementia, 030217 neurology & neurosurgery, Population Genetics
Abstract

GRB-associated binding protein 2 (GAB2) represents a compelling genome-wide association signal for late-onset Alzheimer's disease (LOAD) with reported odds ratios (ORs) ranging from 0.75-0.85. We tested eight GAB2 variants in four North American Caucasian case-control series (2,316 LOAD, 2,538 controls) for association with LOAD. Meta-analyses revealed ORs ranging from (0.61-1.20) with no significant association (all p>0.32). Four variants were hetergeneous across the populations (all p

Published
2013
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9. Erratum: Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease

Author

Harold, Denise, primary, Abraham, Richard, additional, Hollingworth, Paul, additional, Sims, Rebecca, additional, Gerrish, Amy, additional, Hamshere, Marian L, additional, Pahwa, Jaspreet Singh, additional, Moskvina, Valentina, additional, Dowzell, Kimberley, additional, Williams, Amy, additional, Jones, Nicola, additional, Thomas, Charlene, 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, Hardy, John, additional, Mead, Simon, additional, Fox, Nick, additional, Rossor, Martin, additional, Collinge, John, additional, Maier, Wolfgang, additional, Jessen, Frank, additional, Schürmann, Britta, additional, Heun, Reinhard, additional, van den Bussche, Hendrik, additional, Heuser, Isabella, 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, Sleegers, Kristel, additional, Bettens, Karolien, additional, Engelborghs, Sebastiaan, additional, De Deyn, Peter P, additional, Van Broeckhoven, Christine, additional, Livingston, Gill, additional, Bass, Nicholas J, additional, Gurling, Hugh, additional, McQuillin, Andrew, additional, Gwilliam, Rhian, additional, Deloukas, Panagiotis, additional, Al-Chalabi, Ammar, additional, Shaw, Christopher E, additional, Tsolaki, Magda, 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, Carrasquillo, Minerva M, additional, Pankratz, V Shane, additional, Younkin, Steven G, additional, Holmans, Peter A, additional, O'Donovan, Michael, additional, Owen, Michael J, additional, and Williams, Julie, additional

Published
2013
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10. The Role of Variation at AβPP, PSEN1, PSEN2, and MAPT in Late Onset Alzheimer's Disease

Author

Gerrish, Amy, primary, Russo, Giancarlo, additional, Richards, Alexander, additional, Moskvina, Valentina, additional, Ivanov, Dobril, additional, Harold, Denise, additional, Sims, Rebecca, additional, Abraham, Richard, additional, Hollingworth, Paul, additional, Chapman, Jade, additional, Hamshere, Marian, additional, Pahwa, Jaspreet Singh, additional, Dowzell, Kimberley, additional, Williams, Amy, additional, Jones, Nicola, additional, Thomas, Charlene, 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, Johnston, Janet A., additional, Holmes, Clive, additional, Mann, David, additional, Smith, A. David, additional, Love, Seth, additional, Kehoe, Patrick G., additional, Hardy, John, additional, Mead, Simon, additional, Fox, Nick, additional, Rossor, Martin, additional, Collinge, John, additional, Maier, Wolfgang, additional, Jessen, Frank, additional, Kölsch, Heike, additional, Heun, Reinhard, additional, Schürmann, Britta, additional, Bussche, Hendrik van den, additional, Heuser, Isabella, 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, Panagiotis, additional, Davies, Gail, additional, Harris, Sarah E., additional, Starr, John M., additional, Deary, Ian J., additional, Al-Chalabi, Ammar, additional, Shaw, Christopher E., additional, Tsolaki, Magda, 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, Carrasquillo, Minerva M, additional, Pankratz, V Shane, additional, Younkin, Steven G., additional, Jones, Lesley, additional, Holmans, Peter A, additional, O'Donovan, Michael C., additional, Owen, Michael J., additional, and Williams, Julie, additional

Published
2012
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11. Education, occupation and retirement age effects on the age of onset of Alzheimer's disease

Author

Lupton, Michelle K, primary, Stahl, Daniel, additional, Archer, Nicola, additional, Foy, Catherine, additional, Poppe, Michaela, additional, Lovestone, Simon, additional, Hollingworth, Paul, additional, Williams, Julie, additional, Owen, Micheal J, additional, Dowzell, Kimberley, additional, Abraham, Richard, additional, Sims, Rebecca, additional, Brayne, Carol, additional, Rubinsztein, David, additional, Gill, Michael, additional, Lawlor, Brian, additional, Lynch, Aoibhinn, additional, and Powell, John F, additional

Published
2009
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12. Erratum: Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease

Author

Harold, Denise, primary, Abraham, Richard, additional, Hollingworth, Paul, additional, Sims, Rebecca, additional, Gerrish, Amy, additional, Hamshere, Marian L, additional, Pahwa, Jaspreet Singh, additional, Moskvina, Valentina, additional, Dowzell, Kimberley, additional, Williams, Amy, additional, Jones, Nicola, additional, Thomas, Charlene, 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, Hardy, John, 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, 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, Sleegers, Kristel, additional, Bettens, Karolien, additional, Engelborghs, Sebastiaan, additional, De Deyn, Peter P, additional, Van Broeckhoven, Christine, additional, Livingston, Gill, additional, Bass, Nicholas J, additional, Gurling, Hugh, additional, McQuillin, Andrew, additional, Gwilliam, Rhian, additional, Deloukas, Panagiotis, additional, Al-Chalabi, Ammar, additional, Shaw, Christopher E, additional, Tsolaki, Magda, 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, Carrasquillo, Minerva M, additional, Pankratz, V Shane, additional, Younkin, Steven G, additional, Holmans, Peter A, additional, O'Donovan, Michael, additional, Owen, Michael J, additional, and Williams, Julie, additional

Published
2009
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13. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease

Author

Harold, Denise, primary, Abraham, Richard, additional, Hollingworth, Paul, additional, Sims, Rebecca, additional, Gerrish, Amy, additional, Hamshere, Marian L, additional, Pahwa, Jaspreet Singh, additional, Moskvina, Valentina, additional, Dowzell, Kimberley, additional, Williams, Amy, additional, Jones, Nicola, additional, Thomas, Charlene, 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, Hardy, John, additional, Mead, Simon, additional, Fox, Nick, additional, Rossor, Martin, additional, Collinge, John, additional, Maier, Wolfgang, additional, Jessen, Frank, additional, Schürmann, Britta, additional, Heun, Reinhard, additional, van den Bussche, Hendrik, additional, Heuser, Isabella, 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, Sleegers, Kristel, additional, Bettens, Karolien, additional, Engelborghs, Sebastiaan, additional, De Deyn, Peter P, additional, Van Broeckhoven, Christine, additional, Livingston, Gill, additional, Bass, Nicholas J, additional, Gurling, Hugh, additional, McQuillin, Andrew, additional, Gwilliam, Rhian, additional, Deloukas, Panagiotis, additional, Al-Chalabi, Ammar, additional, Shaw, Christopher E, additional, Tsolaki, Magda, 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, Carrasquillo, Minerva M, additional, Pankratz, V Shane, additional, Younkin, Steven G, additional, Holmans, Peter A, additional, O'Donovan, Michael, additional, Owen, Michael J, additional, and Williams, Julie, additional

Published
2009
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14. A genome-wide association study for late-onset Alzheimer's disease using DNA pooling

Author

Abraham, Richard, primary, Moskvina, Valentina, additional, Sims, Rebecca, additional, Hollingworth, Paul, additional, Morgan, Angharad, additional, Georgieva, Lyudmila, additional, Dowzell, Kimberley, additional, Cichon, Sven, additional, Hillmer, Axel M, additional, O'Donovan, Michael C, additional, Williams, Julie, additional, Owen, Michael J, additional, and Kirov, George, additional

Published
2008
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15. P3‐265: Testing for association between Alzheimer's disease with psychosis and variants identified as influencing risk of schizophrenia

Author

Sims, Rebecca, primary, Hollingworth, Paul, additional, Morgan, Angharad, additional, Dowzell, Kimberley, additional, Stretton, Alexandra, additional, Jones, Laura, additional, Norton, Nadine, additional, Williams, Hywel, additional, Georgieva, Lyudmila, additional, Moskvina, Valentina, additional, Nikolov, Ivan, additional, Hamshere, Marian, additional, Holmans, Peter, additional, Lovestone, Simon, additional, Brayne, Carol, additional, Rubinsztein, David C., additional, Williams, Nigel M., additional, Kirov, George, additional, Craddock, Nick, additional, O'Donovan, Michael, additional, Owen, Michael, additional, Williams, Julie, additional, and Abraham, Richard, additional

Published
2008
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16. P3-016: The APOE-ϵ4 allele does not affect rate of cognitive and functional decline in late-onset Alzheimer's disease (AD): Findings from the U.K. Medical Research Council (MRC) genetic resource for AD

Author

Hollingworth, Paul, primary, Dowzell, Kimberley, additional, Williams, Amy, additional, Keates, Sophie, additional, Abraham, Richard, additional, Morgan, Angharad, additional, Foy, Catherine, additional, Archer, Nicola, additional, Powell, John, additional, Lovestone, Simon, additional, O'Donavan, Michael, additional, Owen, Michael J., additional, and Williams, Julie, additional

Published
2008
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17. P1-335: A powerful association analysis of 496 SNPs in 80 positional candidate genes in a linked region on chromosome 10 for association with late onset Alzheimer's disease

Author

Abraham, Richard, primary, Morgan, Angharad R., additional, Jehu, Luke, additional, Turic, Dragana, additional, Hamilton, Gillian, additional, Hollingworth, Paul, additional, Moore, Pamela, additional, Dowzell, Kimberley, additional, Holmans, Peter, additional, Moskvina, Valentina, additional, Cope, Natalie, additional, Powell, John, additional, Lovestone, Simon, additional, Brayne, Carol, additional, Rubinsztein, David C., additional, O'Donovan, Michael, additional, Owen, Michael J., additional, and Williams, Julie, additional

Published
2006
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18. P1-219: Three components describe behavioural symptoms in 1120 individuals with late-onset Alzheimer's disease

Author

Hamshere, Marian L., primary, Hollingworth, Paul, additional, Moskvina, Valentina, additional, Dowzell, Kimberley, additional, Foy, Catherine, additional, Archer, Nicola, additional, Lynch, Aoibhinn, additional, Lovestone, Simon, additional, Brayne, Carol, additional, Rubinsztein, David, additional, Lawlor, Brian, additional, Gill, Michael, additional, Owen, Michael, additional, and Williams, Julie, additional

Published
2006
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19. P1–328: Association analysis of 22 positional/functional candidate genes on chromosome 10 with late onset Alzheimer's disease

Author

Morgan, Angharad R., primary, Jehu, Luke, additional, Turic, Dragana, additional, Harold, Denise, additional, Hamilton, Gillian, additional, Hollingworth, Paul, additional, Moore, Pamela, additional, Dowzell, Kimberley, additional, Moskvina, Valentina, additional, Jones, Lesley, additional, Powell, John, additional, Lovestone, Simon, additional, Brayne, Carol, additional, Rubinsztein, David C., additional, O'Donovan, Michael, additional, Owen, Mike J., additional, and Williams, Julie, additional

Published
2006
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20. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease.

Author

Hollingworth, Paul, Harold, Denise, Sims, Rebecca, Gerrish, Amy, Lambert, Jean-Charles, Carrasquillo, Minerva M., Abraham, Richard, Hamshere, Marian L., Pahwa, Jaspreet Singh, Moskvina, Valentina, Dowzell, Kimberley, Jones, Nicola, Stretton, Alexandra, Thomas, Charlene, Richards, Alex, Ivanov, Dobril, Widdowson, Caroline, Chapman, Jade, Lovestone, Simon, and Powell, John

Subjects
GENETICS of Alzheimer's disease, GENES, APOLIPOPROTEIN E, CLUSTERIN, GENOMICS, DISEASE susceptibility
Abstract

We sought to identify new susceptibility loci for Alzheimer's disease through a staged association study (GERAD+) and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium (ADGC) in a companion paper. We undertook a combined analysis of four genome-wide association datasets (stage 1) and identified ten newly associated variants with P ≤ 1 × 10−5. We tested these variants for association in an independent sample (stage 2). Three SNPs at two loci replicated and showed evidence for association in a further sample (stage 3). Meta-analyses of all data provided compelling evidence that ABCA7 (rs3764650, meta P = 4.5 × 10−17; including ADGC data, meta P = 5.0 × 10−21) and the MS4A gene cluster (rs610932, meta P = 1.8 × 10−14; including ADGC data, meta P = 1.2 × 10−16) are new Alzheimer's disease susceptibility loci. We also found independent evidence for association for three loci reported by the ADGC, which, when combined, showed genome-wide significance: CD2AP (GERAD+, P = 8.0 × 10−4; including ADGC data, meta P = 8.6 × 10−9), CD33 (GERAD+, P = 2.2 × 10−4; including ADGC data, meta P = 1.6 × 10−9) and EPHA1 (GERAD+, P = 3.4 × 10−4; including ADGC data, meta P = 6.0 × 10−10). [ABSTRACT FROM AUTHOR]

Published
2011
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21. Education, occupation and retirement age effects on the age of onset of Alzheimer's disease.

Author

Lupton, Michelle K, Stahl, Daniel, Archer, Nicola, Foy, Catherine, Poppe, Michaela, Lovestone, Simon, Hollingworth, Paul, Williams, Julie, Owen, Micheal J, Dowzell, Kimberley, Abraham, Richard, Sims, Rebecca, Brayne, Carol, Rubinsztein, David, Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, and Powell, John F

Subjects
ALZHEIMER'S patients, AGE factors in cognition disorders, RETIREMENT & psychology, COGNITION disorder risk factors
Abstract

Objective To determine the effects of early life education, mid life employment and later life retirement age on the age of onset (AOO) of Alzheimer's disease (AD). Methods Multiple regression analyses were carried out using data for 1320 probable AD cases, of which 382 were males with employment and retirement age data, using informant based information on education and employment. Results No relation was found between years of education, best qualification obtained, or employment variables in males and the AOO of AD. A significant effect of later retirement age in delaying the AOO of AD was seen in males. Conclusions In this study no effect of education or employment was seen, although this may be due to limited variance in the study population. The significant effect of retirement age may have several explanations, the most interesting of which would be the suggestion that active employment later in life allows an individual to prolong their cognitive assets above the threshold for dementia. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2010
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22. No consistent evidence for association between mtDNA variants and Alzheimer disease

Author

Hudson, G., Sims, R., Harold, D., Chapman, J., Hollingworth, P., Gerrish, A., Russo, G., Hamshere, M., Moskvina, V., Jones, N., Thomas, C., Stretton, A., Holmans, P.A., O'Donovan, M.C., Owen, M.J., Williams, J., Chinnery, P.F., Harold, Denise, Abraham, Richard, Hollingworth, Paul, Sims, Rebecca, Gerrish, Amy, Chapman, Jade, Russo, Giancarlo, Hamshere, Marian, Pahwa, Jaspreet Singh, Moskvina, Valentina, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Stretton, Alexandra, Morgan, Angharad, Lovestone, Simon, Powell, John, Proitsi, Petroula, Lupton, Michelle K, Brayne, Carol, Rubinsztein, David C., Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, Morgan, Kevin, Brown, Kristelle, Passmore, Peter, Craig, David, McGuinness, Bernadette, Todd, Stephen, Johnston, Janet, Holmes, Clive, Mann, David, Smith, A. David, Love, Seth, Kehoe, Patrick G., Hardy, John, Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Maier, Wolfgang, Jessen, Frank, Heun, Reiner, Kölsch, Heike, Schürmann, Britta, van den Bussche, Hendrik, Heuser, Isabella, Kornhuber, Johannes, Wiltfang, Jens, Dichgans, Martin, Frölich, Lutz, Hampel, Harald, Hüll, Michael, Rujescu, Dan, Goate, Alison, Kauwe, John S.K., Cruchaga, Carlos, Nowotny, Petra, Morris, John C., Mayo, Kevin, Livingston, Gill, Bass, Nicholas J., Gurling, Hugh, McQuillin, Andrew, Gwilliam, Rhian, Deloukas, Panagiotis, Holmans, Peter, O'Donovan, Michael, Owen, Michael J., and Williams, Julie

Abstract

Although several studies have described an association between Alzheimer disease (AD) and genetic variation of mitochondrial DNA (mtDNA), each has implicated different mtDNA variants, so the role of mtDNA in the etiology of AD remains uncertain.

Published
2012
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23. Quantitative interaction proteomics of neurodegenerative disease proteins

Author

Hosp, Fabian, Vossfeldt, Hannes, Heinig, Matthias, Vasiljevic, Djordje, Arumughan, Anup, Wyler, Emanuel, Genetic And Environmental Risk For Alzheimer's Disease GERAD1 Consortium, Landthaler, Markus, Hubner, Norbert, Wanker, Erich E., Lannfelt, Lars, Ingelsson, Martin, Lalowski, Maciej, Voigt, Aaron, Selbach, Matthias, Harold, Denise, Abraham, Richard, Hollingworth, Paul, Sims, Rebecca, Gerrish, Amy, Chapman, Jade, Russo, Giancarlo, Hamshere, Marian, Pahwa, Jaspreet Singh, Escott-Price, Valentina, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Stretton, Alexandra, Morgan, Angharad, Lovestone, Simon, Powell, John, Proitsi, Petroula, Lupton, Michelle K., Brayne, Carol, Rubinsztein, David C., Gill, Michael, Lawlor, Brian, Lynch, Aoibhinn, Morgan, Kevin, Brown, Kristelle, Passmore, Peter, Craig, David, McGuinness, Bernadette, Todd, Stephen, Johnston, Janet, Holmes, Clive, Mann, David, Smith, A. David, Love, Seth, Kehoe, Patrick G., Hardy, John, Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Maier, Wolfgang, Jessen, Frank, Heun, Reiner, Schürmann, Britta, Ramirez, Alfredo, Becker, Tim, Herold, Christine, Lacour, André, Drichel, Dmitriy, Van Den Bussche, Hendrik, Heuser, Isabella, Kornhuber, Johannes, Wiltfang, Jens, Dichgans, Martin, Frölich, Lutz, Hampel, Harald, Hüll, Michael, Rujescu, Dan, Goate, Alison, Kauwe, John S. K., Cruchaga, Carlos, Nowotny, Petra, Morris, John C., Mayo, Kevin, Livingston, Gill, Bass, Nicholas J., Gurling, Hugh, McQuillin, Andrew, Gwilliam, Rhian, Deloukas, Panagiotis, Al-Chalabi, Ammar, Shaw, Christopher E., Singleton, Andrew B., Guerreiro, Rita, Mühleisen, Thomas W., Nöthen, Markus M., Moebus, Susanne, Jöckel, Karl-Heinz, Klopp, Norman, Wichmann, H-Erich, Carrasquillo, Minerva M., Pankratz, V. Shane, Younkin, Steven G., Holmans, Peter, O'Donovan, Michael, Owen, Michael J., and Williams, Julie

Subjects
3. Good health
Abstract

Cell Rep 11(7), 1134-1146 (2015). doi:10.1016/j.celrep.2015.04.030, Published by Cell Press, Maryland Heights, MO

24. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease.

Author

Harold, Denise, Abraham, Richard, Hollingworth, Paul, Sims, Rebecca, Gerrish, Amy, Hamshere, Marian L, Pahwa, Jaspreet Singh, Moskvina, Valentina, Dowzell, Kimberley, Williams, Amy, Jones, Nicola, Thomas, Charlene, Stretton, Alexandra, Morgan, Angharad R, Lovestone, Simon, Powell, John, Proitsi, Petroula, Lupton, Michelle K, Brayne, Carol, and Rubinsztein, David C

Subjects
ALZHEIMER'S disease, GENOMES
Abstract

A correction to the article "Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease," that appeared in the September 6, 2009 issue is presented.

Published
2013
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