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2. A novel role for the late-onset Alzheimer’s disease (LOAD)-associated protein Bin1 in regulating postsynaptic trafficking and glutamatergic signaling

Author

Schürmann, Britta, Bermingham, Daniel P., Kopeikina, Katherine J., Myczek, Kristoffer, Yoon, Sehyoun, Horan, Katherine E., Kelly, Crystle J., Martin-de-Saavedra, Maria Dolores, Forrest, Marc P., Fawcett-Patel, Jessica M., Smith, Katharine R., Gao, Ruoqi, Bach, Anthony, Burette, Alain C., Rappoport, Joshua Z., Weinberg, Richard J., Martina, Marco, and Penzes, Peter

Published
2020
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5. Structured illumination microscopy (SIM) imaging of Bin1 colocalization with trafficking markers in cultured rat cortical neurons

Author

Schürmann, Britta, Bermingham, Daniel P., Kopeikina, Katherine J., Myczek, Kristoffer, Yoon, Sehyoun, Horan, Katherine E., Kelly, Crystle J., Martin-de-Saavedra, Maria Dolores, Forrest, Marc P., Fawcett-Patel, Jessica M., Smith, Katharine R., Gao, Ruoqi, Bach, Anthony, Burette, Alain C., Rappoport, Joshua Z., Weinberg, Richard J., Martina, Marco, and Penzes, Peter

Published
2020
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11. Genome-Wide Association Study of Vascular Dementia

Author

Schrijvers, Elisabeth M.C., Schürmann, Britta, Koudstaal, Peter J., van den Bussche, Hendrik, Van Duijn, Cornelia M., Hentschel, Frank, Heun, Reinhard, Hofman, Albert, Jessen, Frank, Kölsch, Heike, Kornhuber, Johannes, Peters, Oliver, Rivadeneira, Fernando, Rüther, Eckart, Uitterlinden, André G., Riedel-Heller, Steffi, Dichgans, Martin, Wiltfang, Jens, Maier, Wolfgang, Breteler, Monique M.B., and Ikram, M. Arfan

Published
2012
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12. Efficacy of Δ9 -Tetrahydrocannabinol (THC) Alone or in Combination With a 1:1 Ratio of Cannabidiol (CBD) in Reversing the Spatial Learning Deficits in Old Mice.

Author

Nidadavolu, Prakash, Bilkei-Gorzo, Andras, Krämer, Michael, Schürmann, Britta, Palmisano, Michela, Beins, Eva C., Madea, Burkhard, and Zimmer, Andreas

Subjects
AGE factors in cognition, CANNABIDIOL, TETRAHYDROCANNABINOL, COGNITIVE aging, CANNABINOID receptors, MICE
Abstract

Decline in cognitive performance, an aspect of the normal aging process, is influenced by the endocannabinoid system (ECS). Cannabinoid receptor 1 (CB1) signaling diminishes with advancing age in specific brain regions that regulate learning and memory and abolishing CB1 receptor signaling accelerates cognitive aging in mice. We recently demonstrated that prolonged exposure to low dose (3 mg/kg/day) Δ9-tetrahydrocannabinol (THC) improved the cognitive performances in old mice on par with young untreated mice. Here we investigated the potential influence of cannabidiol (CBD) on this THC effect, because preclinical and clinical studies indicate that the combination of THC and CBD often exhibits an enhanced therapeutic effect compared to THC alone. We first tested the effectiveness of a lower dose (1 mg/kg/day) THC, and then the efficacy of the combination of THC and CBD in 1:1 ratio, same as in the clinically approved medicine Sativex®. Our findings reveal that a 1 mg/kg/day THC dose still effectively improved spatial learning in aged mice. However, a 1:1 combination of THC and CBD failed to do so. The presence of CBD induced temporal changes in THC metabolism ensuing in a transient elevation of blood THC levels. However, as CBD metabolizes, the inhibitory effect on THC metabolism was alleviated, causing a rapid clearance of THC. Thus, the beneficial effects of THC seemed to wane off more swiftly in the presence of CBD, due to these metabolic effects. The findings indicate that THC-treatment alone is more efficient to improve spatial learning in aged mice than the 1:1 combination of THC and CBD. [ABSTRACT FROM AUTHOR]

Published
2021
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13. A novel role for the late-onset Alzheimer’s disease (LOAD)-associated protein Bin1 in regulating postsynaptic trafficking and glutamatergic signaling

Author

Schürmann, Britta, primary, Bermingham, Daniel P., additional, Kopeikina, Katherine J., additional, Myczek, Kristoffer, additional, Yoon, Sehyoun, additional, Horan, Katherine E., additional, Kelly, Crystle J., additional, Martin-de-Saavedra, Maria Dolores, additional, Forrest, Marc P., additional, Fawcett-Patel, Jessica M., additional, Smith, Katharine R., additional, Gao, Ruoqi, additional, Bach, Anthony, additional, Burette, Alain C., additional, Rappoport, Joshua Z., additional, Weinberg, Richard J., additional, Martina, Marco, additional, and Penzes, Peter, additional

Published
2019
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14. 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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15. 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

17. Molecular dynamics simulations of ordered alkane chains physisorbed on graphite.

Author

Hentschke, Reinhard, Schürmann, Britta L., and Rabe, Jürgen P.

Subjects
*MOLECULAR dynamics, *ALKANES, *GRAPHITE
Abstract

Scanning tunneling microscopy (STM) studies at the interface between the basal plane of graphite and organic solutions or melts of long chain alkanes and alkyl derivatives reveal that the molecules order in lamellae with the main molecular axes oriented parallel to the substrate. Here we employ molecular dynamics (MD) simulations to obtain more details on the molecular order and dynamics within the alkane lamellae as a function of density. We find that the orientation of the molecular carbon zigzag planes relative to the graphite is governed by a subtle interplay of packing and entropic effects. In addition, we consider multiple layer adsorption and investigate the rapid loss of order with increasing distance from the interface. Finally, we study the diffusive behavior of an isolated long chain alkane, C350H702, on graphite, which is of interest in the context of STM imaging of isolated macromolecules at interfaces. The sensitive dependence on atomic parameters renders MD simulations a valuable complementary tool for the detailed interpretation of STM data. [ABSTRACT FROM AUTHOR]

Published
1992
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18. 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

19. 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

20. 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

22. 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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23. P4-084: Genome-wide association study using cerebrospinal fluid biomarkers beta-amyloid-42 and pTau181 in German samples of Alzheimer's disease

Author

Ramirez, Alfredo, primary, Herold, Christine, additional, Lewczuk, Piotr, additional, Lacour, André, additional, Drichel, Dmitriy, additional, Schürmann, Britta, additional, Kornhuber, Johannes, additional, Peters, Oliver, additional, Heun, Reiner, additional, Hampel, Harald, additional, Frölich, Lutz, additional, Hüll, Michael, additional, Hoffmann, Per, additional, Vogt, Stefani, additional, Kölsch, Heike, additional, Heneka, Michael, additional, Alferink, Judith, additional, Rüther, Eckart, additional, Wiltfang, Jens, additional, Dichgans, Martin, additional, Baur, Max, additional, Jessen, Frank, additional, Maier, Wolfgang, additional, Becker, Tim, additional, and Nöthen, Markus, additional

Published
2012
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24. 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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26. 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
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27. 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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28. 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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29. The Opioid Peptides Enkephalin and β-Endorphin in Alcohol Dependence

Author

Racz, Ildiko, primary, Schürmann, Britta, additional, Karpushova, Anna, additional, Reuter, Martin, additional, Cichon, Sven, additional, Montag, Christian, additional, Fürst, Robert, additional, Schütz, Christian, additional, Franke, Petra E., additional, Strohmaier, Jana, additional, Wienker, Thomas F., additional, Terenius, Lars, additional, Ösby, Urban, additional, Gunnar, Agneta, additional, Maier, Wolfgang, additional, Bilkei-Gorzó, Andras, additional, Nöthen, Markus, additional, and Zimmer, Andreas, additional

Published
2008
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38. Dynorphins Regulate Fear Memory: from Mice to Men.

Author

Bilkei-Gorzo, Andras, Erk, Susanne, Schürmann, Britta, Mauer, Daniela, Michel, Kerstin, Boecker, Henning, Scheef, Lukas, Walter, Henrik, and Zimmer, Andreas

Subjects
DYNORPHINS, FEAR, MEMORY, COGNITIVE therapy, NEUROPHYSIOLOGY, AMYGDALOID body, PREFRONTAL cortex, LABORATORY mice
Abstract

Reexposure to trauma reminders is an integral element of trauma-focused cognitive behavioral therapy (Roberts et al., 2009), but little is known about the physiological processes underlying the therapeutic progress. While it is well established that amygdala, prefrontal cortex and hippocampus are key brain structures in fear memory processing (McGaugh, 2004; Herry et al., 2008; Likhtik et al., 2008), it is not well known which neurotransmitters or neuromodulators are involved. Here with a translational approach we investigated the role of dynorphins in the formation and extinction of fear memories in mice and in humans. Mice lacking dynorphin showed an enhanced cue-dependent fear conditioning, as well as delayed extinction in contextual conditioning/extinction paradigms. The pharmacological blockade of k-opioid receptors before the extinction trials but not before or after the conditioning produced a similar effect. Analysis of neuronal activity, using the immediate early gene c-fos, demonstrated a reduced neuronal activity in key limbic structures during extinction in the absence of dynorphin. Translating these findings into thehumandomain, fear conditioning and extinction, coupled with functional MRI was then performed in volunteers preselected for a functionally relevant polymorphism in the dynorphin gene. Human volunteers bearing the (T) allele of PDYN (prodynorphin) at rs1997794 showed reduced fear extinction and a significantly diminished functional connectivity between amygdala and ventromedial prefrontal cortex. Our findings establish a role of dynorphin k-opioid receptor signaling in fear extinction. [ABSTRACT FROM AUTHOR]

Published
2012
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39. Genome-wide association study using cerebrospinal fluid biomarkers beta-amyloid-42 and pTau181 in German samples of Alzheimer's disease

Author

Ramirez, Alfredo, Herold, Christine, Lewczuk, Piotr, Lacour, André, Drichel, Dmitriy, Schürmann, Britta, Kornhuber, Johannes, Peters, Oliver, Heun, Reiner, Hampel, Harald, Frölich, Lutz, Hüll, Michael, Hoffmann, Per, Vogt, Stefani, Kölsch, Heike, Heneka, Michael, Alferink, Judith, Rüther, Eckart, Wiltfang, Jens, Dichgans, Martin, Baur, Max, Jessen, Frank, Maier, Wolfgang, Becker, Tim, and Nöthen, Markus

Published
2012
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40. The Oral Antidiabetic Pioglitazone Protects from Neurodegeneration and Amyotrophic Lateral Sclerosis-Like Symptoms in Superoxide Dismutase-G93A Transgenic Mice.

Author

Schütz, Burkhard, Reimann, Jens, Dumitrescu-Ozimek, Lucia, Kappes-Horn, Karin, Landreth, Gary E., Schürmann, Britta, Zimmer, Andreas, and Heneka, Michael T.

Subjects
MOTOR neurons, NEURONS, DEGENERATION (Pathology), PEROXISOMES, MICROGLIA, ASTROCYTES, TRANSGENIC mice
Abstract

Amyotrophic lateral sclerosis (ALS) represents a fatal neurodegenerative disorder characterized by progressive death of the upper and lower motor neurons. Because accompanying inflammation may interact with and promote neurodegeneration, anti-inflammatory treatment strategies are being evaluated. Because peroxisome proliferator-activated receptor γ (PPARγ) agonists act as potent anti-inflammatory drugs, we tested whether superoxide dismutase (SOD1)-G93A transgenic mice, a mouse model of ALS, benefit from oral treatment with the PPARγ agonist pioglitazone (Pio). Pio-treated transgenic mice revealed improved muscle strength and body weight, exhibited a delayed disease onset, and survived significantly longer than nontreated SOD1-G93A mice. Quantification of motor neurons of the spinal cord at day 90 revealed complete neuroprotection by Pio, whereas nontreated SOD1-G93A mice had lost 30% of motor neurons. This was paralleled by preservation of the median fiber diameter of the quadriceps muscle, indicating not only morphological but also functional protection of motor neurons by Pio. Activated microglia were significantly reduced at sites of neurodegeneration in Pio-treated SOD1-G93A mice, as were the protein levels of cyclooxygenase 2 and inducible nitric oxide synthase. Interestingly, mRNA levels of the suppressor of cytokine signaling 1 and 3 genes were increased by Pio, whereas both the mRNA and protein levels of endogenous mouse SOD1 and of transgenic human SOD1 remained unaffected. [ABSTRACT FROM AUTHOR]

Published
2005
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41. 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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45. AbinitioSCF and MRD-CI description of the A2A′ – X2A″ transition of the as yet unknown HNCl molecule

Author

Schürmann, Britta L. and Buenker, Robert J.

Abstract

Abinitiopotential curves of the X2A″ ground state and the first excited A2A′ state (2Π in linear geometry) of HNCl are calculated employing multi-reference single- and double-excitation configuration interaction in order to aid in the search for this system experimentally. A vibrational analysis (frequencies and Franck–Condon factors) of the A2A′ – X2A″ transition is undertaken by neglecting coupling between the various modes. Diagonal and off-diagonal force constants together with the fundamental frequencies have been calculated by including mode coupling for both electronic states, and oscillator strengths and radiative lifetimes are also obtained. Comparison with theoretical and experimental results for other isovalent systems is also made in order to establish trends in this group of HAB systems.

Published
1985
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46. 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

47. A novel Alzheimer disease locus located near the gene encoding tau protein

Author

Herold, Christine, Bird, Thomas D, Destefano, Hanon, Tárraga, Levey, Allan I, Vinters, Harry V, Frölich, Lutz, Rujescu, Reisberg, Barry, Martiniuk, Frank, Raskind, Murray, Clarke, Germanou, Antonia, Mosley, Mead, Miller, Carol A, Kehoe, Patrick G, Apostolova, Liana G, Roberson, Erik D, Hamilton, Ronald L, Welsh-Bohmer, Kathleen A, Reiman, Larson, Baldwin, Clinton T, Schneider, Julie A, Dunstan, Letenneur, Corneveaux, Jason, DeKosky, Steven T, Pickering-Brown, Stuart, Schellenberg, Owen, Michael J, Escott-Price, Rossor, Martin, Farrer, Nalls, Turton, James, Smith, Amanda G, Royall, Donald R, McQuillin, Andrew, Mukherjee, Shubhabrata, Vonsattel, Jean Paul, Dartigues, Wang, Seshadri, Leverenz, James B, Oldham, Harriet, Masliah, Eliezer, Glass, Jonathan D, Dick, Malcolm, Ben-Shlomo, Yoav, Yu, Lei, Kamboh, Faber, Kelley M, Ringman, John M, Russo, Giancarlo, Tanzi, Rudolph E, Schott, Jonathan M, Jöckel, Karl-Heinz, Crocco, Elizabeth A, Vronskaya, Tzourio, Lin, Chiao-Feng, Lord, Jenny, Lynch, Aoibhinn, Powell, Bigio, Eileen H, Buxbaum, Ma, Li, Ortega-Cubero, Sara, Riedel-Heller, Steffi, Emilsson, Barmada, Michjael M, Albin, Roger L, Gill, DeCarli, Charles, Wendland, Partch, Amanda, Collinge, John, Hooper, Nigel M, Cao, Chuanhai, Heuser, Isabella, Koo, Edward H, Adams, Perrie M, Miller, Joshua W, Miller, Bruce L, Murrell, Jill R, Stern, Robert A, Stretton, Alexandra, Wilhelmsen, Galasko, Douglas R, Moebus, Susanne, Kukull, Gkatzima, Olymbia, Hardy, John, Rosenberg, Roger N, Perry, William, McDavid, Andrew N, Schürmann, Britta, Albert, Marilyn S, Gwilliam, Rhian, Chui, Helena C, Tsolaki, Magda, Gilbert, John R, Brown, Kristelle, McCurry, Susan M, Lupton, Michelle, Farlow, Martin R, Mash, Deborah C, Carlson, Chris S, De Jager, Paulson, Henry L, Dichgans, Martin, Petersen, Ronald C, Hulette, Christine M, Head, Elizabeth, Hampel, Chouraki, Asthana, Sanjay, Lawlor, Brian, Schmidt, O'Bryant, Sid, Kauwe, John S. K., Brayne, Raj, Ashok, Kim, Ronald, Burke, James R, Gudnason, Li, Ge, Williamson, Jennifer, Klopp, Norman, Warden, Donald, Gerrish, Amy, Denning, Love, Rotter, Cruchaga, Carlos, Ghetti, Bernardino, Chung, Ryan, Natalie, Parisi, Joseph E, Ferris, Steven, Nöthen, Psaty, Wright, Clinton B, Jin, Lee-Way, Ibrahim-Verbaas, Cairns, Nigel J, Thomas, Charlene, Naj, Barnes, Lisa L, Boada, Shaw, Christopher E, Arnold, Steven E, Blacker, Deborah, Van Broeckhoven, Heun, Reiner, Karydas, Anna, Hofman, Sano, Mary, Vardy, Emma, Pankratz, Vernon S, Graff-Radford, Neill R, Warren, Jason D, Gearing, Marla, Winslow, McKee, Ann C, Choi, Laza, Jonsson, Bisceglio, Gina, Kamatani, Seeley, William W, Al-Chalabi, Ammar, St George-Hyslop, Beekly, Sager, Mark A, Holmes, Reitz, Christiane, Huentelman, Matthew J, Bayer, Anthony, Lyketsos, Constantine G, Doody, Rachelle S, Mayo, Kevin, Eiriksdottir, Lacour, André, Van Eldik, Linda J, Fairchild, Thomas J, Launer, Makrina, Daniilidou, Jun, Tsuang, Debby W, LaFerla, Frank M, Maier, Yesim Demirci, Woltjer, Randall L, Amouyel, Mann, David, Honig, Lawrence S, Gurling, Hugh, De Bruijn, Huebinger, Ryan M, Guerreiro, Rita, Hüll, Michael, Frosch, Matthew P, O'Donovan, Haines, Bellenguez, Pericak-Vance, Boxer, Adam, Mayhaus, Manuel, Lovestone, Simon, Fitzpatrick, Green, Robert C, Lathrop, Becker, Kunkle, McCormick, Wayne C, Kramer, Joel H, Wilcock, Gordon, Pasquier, Jessen, Frank, Weintraub, Sandra, Gu, Wei, Marson, Daniel C, Evans, Younkin, Amin, Troncoso, Juan C, Van Duijn, Gallacher, John, Campion, Proitsi, Petroula, Grenier-Boley, Saykin, Andrew J, Pichler, Sabrina, Lunetta, Fox, Craig, David, Carrasquillo, Minerva M, Boeve, Bradley F, Clark, David G, Poon, Wayne W, Todd, Stephen, Duara, Ranjan, Atwood, Craig S, Dufouil, Lopez, Oscar L, Olichney, John M, Warner, Nick, Wichmann, H.-Erich, Boland, Holmans, Bowen, James D, Singleton, Andrew B, Harrell, Lindy E, Peskind, Elaine, Bennett, Geschwind, Daniel H, Uphill, James, Thornton-Wells, Tricia A, Harold, Foroud, Zelenika, Crane, Trojanowski, John Q, Fisher, Elizabeth, Growdon, John H, Johnston, Janet A, Sims, Jakobsdóttir, Medway, Christopher, van den Bussche, Hendrik, Van Der Lee, Kornhuber, Johannes, Barber, Chapman, Jade, Jones, Ikram, Kölsch, Heike, Morgan, Wiltfang, Jens, Martin, Ramirez, Drichel, Dmitriy, Potter, Huntington, Hyman, Bradley T, Fievet, Smith, Valladares, Pierce, Aimee, Koutroumani, Maria, Deloukas, Panagiotis, Williams, Hamilton-Nelson, Jarvik, Gail P, Schneider, Lon S, Morgan, Angharad, Sonnen, Joshua A, Bass, Nicholas J, Yu, Chang-En, Beach, Thomas G, Jicha, Gregory A, Hakonarson, Hakon, Montine, Kaye, Jeffrey A, Wishnek, Sarah, Cribbs, David H, Pastor, Rosen, Howard J, Hoffmann, Per, Smith, A. David, Van Deerlin, Vivianna M, Hannequin, Carney, Regina M, Beecham, Goate, Spina, Salvatore, Mack, Wendy J, Mesulam, Marsel, Riemenschneider, Matthias, Reisch, Joan S, Berr, Ertekin-Taner, Nilufer, Deramecourt, Hollingworth, Paul, Avramidou, Despoina, Morris, John C, Wu, Chuang-Kuo, Passmore, Quinn, Joseph F, Feulner, Thomas, Carroll, Steven L, Rogaeva, Ekaterina, Cantwell, Bis, Dickson, Dennis W, Myers, Amanda J, Vardarajan, Badri N, Carasquillo, McGuinness, Bernadette, Kowall, Neil W, Rubinsztein, David C, Mayeux, Carlsson, Cynthia M, Livingston, Gill, Lieberman, Andrew P, Fallon, Kenneth B, Lambert, and Lah, James J

Subjects
3. Good health
Abstract

APOE ε4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics of Alzheimer’s Project (IGAP) Consortium in APOE ε4+ (10,352 cases and 9,207 controls) and APOE ε4− (7,184 cases and 26,968 controls) subgroups as well as in the total sample testing for interaction between a SNP and APOE ε4 status. Suggestive associations (P

48. Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease

Author

Jones, Lesley, Holmans, Peter A., Hamshere, Marian L., Harold, Denise, Moskvina, Valentina, Ivanov, Dobril, Pocklington, Andrew, Abraham, Richard, Hollingworth, Paul, Sims, Rebecca, Gerrish, Amy, Pahwa, Jaspreet Singh, Jones, Nicola, 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., Mead, Simon, Fox, Nick, Rossor, Martin, Collinge, John, Maier, Wolfgang, Jessen, Frank, Schürmann, Britta, Heun, Reinhard, Kölsch, Heike, van den Bussche, Hendrik, Heuser, Isabella, Peters, Oliver, 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, Panos, 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, Heinz-Erich, Rüther, Eckhard, Carrasquillo, Minerva M., Pankratz, V. Shane, Younkin, Steven G., Hardy, John, O'Donovan, Michael C., Owen, Michael J., and Williams, Julie

Subjects
3. Good health
Abstract

Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified the first strongly supported LOAD susceptibility genes since the discovery of the involvement of APOE in the early 1990s. We have now exploited these GWAS datasets to uncover key LOAD pathophysiological processes. We applied a recently developed tool for mining GWAS data for biologically meaningful information to a LOAD GWAS dataset. The principal findings were then tested in an independent GWAS dataset. We found a significant overrepresentation of association signals in pathways related to cholesterol metabolism and the immune response in both of the two largest genome-wide association studies for LOAD. Processes related to cholesterol metabolism and the innate immune response have previously been implicated by pathological and epidemiological studies of Alzheimer's disease, but it has been unclear whether those findings reflected primary aetiological events or consequences of the disease process. Our independent evidence from two large studies now demonstrates that these processes are aetiologically relevant, and suggests that they may be suitable targets for novel and existing therapeutic approaches.

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