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1. Combinations of SNP genotypes from the Wellcome Trust Case Control Study of bipolar patients

Author

Mellerup, Erling Thyge, Jørgensen, Martin Balslev, Dam, Henrik, Møller, Gert Lykke, Mellerup, Erling Thyge, Jørgensen, Martin Balslev, Dam, Henrik, and Møller, Gert Lykke

Abstract

Objectives: Combinations of genetic variants are the basis for polygenic disorders. We examined combinations of SNP genotypes taken from the 446 729 SNPs in The Wellcome Trust Case Control Study of bipolar patients. Methods: Parallel computing by graphics processing units, cloud computing, and data mining tools were used to scan The Wellcome Trust data set for combinations. Results: Two clusters of combinations were significantly associated with bipolar disorder. One cluster contained 68 combinations, each of which included five SNP genotypes. Of the 1998 patients, 305 had combinations from this cluster in their genome, but none of the 1500 controls had any of these combinations in their genome. The other cluster contained six combinations, each of which included five SNP genotypes. Of the 1998 patients, 515 had combinations from the cluster in their genome, but none of the 1500 controls had any of these combinations in their genome. Conclusion: Clusters of combinations of genetic variants can be considered general risk factors for polygenic disorders, whereas accumulation of combinations from the clusters in the genome of a patient can be considered a personal risk factor.

Published
2018

2. Combinations of Genetic Variants Occurring Exclusively in Patients

Author

Mellerup, Erling Thyge, Møller, Gert Lykke, Mellerup, Erling Thyge, and Møller, Gert Lykke

Abstract

The main objective of the study was to find genetic variants that in combination are significantly associated with bipolar disorder. In previous studies of bipolar disorder, combinations of three and four single nucleotide polymorphisms (SNP) genotypes taken from 803 SNPs were analyzed, and five clusters of combinations were found to be significantly associated with bipolar disorder. In the present study, combinations of ten SNP genotypes taken from the same 803 SNPs were analyzed, and one cluster of combinations was found to be significantly associated with bipolar disorder. Combinations from the new cluster and from the five previous clusters were identified in the genomes of 266 or 44% of the 607 patients in the study whereas none of the 1355 control participants had any of these combinations in their genome.The SNP genotypes in the smaller combinations were the normal homozygote, heterozygote or variant homozygote. In the combinations containing 10 SNP genotypes almost all the genotypes were the normal homozygote. Such a finding may indicate that accumulation in the genome of combinations containing few SNP genotypes may be a risk factor for bipolar disorder when those combinations contain relatively many rare SNP genotypes, whereas combinations need to contain many SNP genotypes to be a risk factor when most of the SNP genotypes are the normal homozygote.

Published
2017

3. Combinations of Genetic Variants Occurring Exclusively in Patients

Author

Mellerup, Erling Thyge, Møller, Gert Lykke, Mellerup, Erling Thyge, and Møller, Gert Lykke

Abstract

The main objective of the study was to find genetic variants that in combination are significantly associated with bipolar disorder. In previous studies of bipolar disorder, combinations of three and four single nucleotide polymorphisms (SNP) genotypes taken from 803 SNPs were analyzed, and five clusters of combinations were found to be significantly associated with bipolar disorder. In the present study, combinations of ten SNP genotypes taken from the same 803 SNPs were analyzed, and one cluster of combinations was found to be significantly associated with bipolar disorder. Combinations from the new cluster and from the five previous clusters were identified in the genomes of 266 or 44% of the 607 patients in the study whereas none of the 1355 control participants had any of these combinations in their genome.The SNP genotypes in the smaller combinations were the normal homozygote, heterozygote or variant homozygote. In the combinations containing 10 SNP genotypes almost all the genotypes were the normal homozygote. Such a finding may indicate that accumulation in the genome of combinations containing few SNP genotypes may be a risk factor for bipolar disorder when those combinations contain relatively many rare SNP genotypes, whereas combinations need to contain many SNP genotypes to be a risk factor when most of the SNP genotypes are the normal homozygote.

Published
2017

4. Combinations of genetic data in a study of oral cancer

Author

Mellerup, Erling Thyge, Møller, Gert Lykke, Mondal, Pinaki, Roychoudhury, Susanta, Mellerup, Erling Thyge, Møller, Gert Lykke, Mondal, Pinaki, and Roychoudhury, Susanta

Abstract

In the single locus strategy a number of genetic variants are analyzed, in order to find variants that are distributed significantly different between controls and patients. A supplementary strategy is to analyze combinations of genetic variants. A combination that is the genetic basis for a polygenic disorder will not occur in in control persons genetically unrelated to patients, so the strategy is to analyze combinations of genetic variants present exclusively in patients. In a previous study of oral cancer and leukoplakia 325 SNPs were analyzed. This study has been supplemented with an analysis of combinations of two SNP genotypes from among the 325 SNPs. Two clusters of combinations containing 95 patient specific combinations were significantly associated with oral cancer or leukoplakia. Of 373 patients with oral cancer 205 patients had a number of these 95 combinations in their genome, whereas none of 535 control persons had any of these combinations in their genome.

Published
2015

5. Association of the leucine-7 to proline-7 variation in the signal sequence of neuropeptide Y with major depression

Author

Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, Bolwig, Tom Gert, Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, and Bolwig, Tom Gert

Abstract

Objective: There is clear evidence of a genetic component in major depression, and several studies indicate that neuropeptide Y (NPY) could play an important role in the pathophysiology of the disease. A well-known polymorphism encoding the substitution of leucine to proline in the signal peptide sequence of NPY (Leu7Pro variation) was previously found to protect against depression. Our study aimed at replicating this association in a large Danish population with major depression. Method: Leu7Pro was studied in a sample of depressed patients and ethnically matched controls, as well as psychiatric disease controls with schizophrenia. Possible functional consequences of Leu7Pro were explored in vitro. Results: In contrast to previous studies, Pro7 appeared to be a risk allele for depression, being significantly more frequent in the depression sample (5.5%, n = 593; p = 0.009; odds ratio, OR: 1.46) as compared to ethnically matched controls (3.8%, n = 2912), while schizophrenia patients (4.1%, n = 503) did not differ. In vitro, the Pro7 substitution appeared to be associated with reduced levels of NPY without affecting its mRNA level. Conclusion: The Leu7Pro variation may increase the risk of major depression, possibly by affecting the biosynthesis of NPY. Pernille

Published
2012

6. Association of the leucine-7 to proline-7 variation in the signal sequence of neuropeptide Y with major depression

Author

Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, Bolwig, Tom Gert, Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, and Bolwig, Tom Gert

Abstract

Objective: There is clear evidence of a genetic component in major depression, and several studies indicate that neuropeptide Y (NPY) could play an important role in the pathophysiology of the disease. A well-known polymorphism encoding the substitution of leucine to proline in the signal peptide sequence of NPY (Leu7Pro variation) was previously found to protect against depression. Our study aimed at replicating this association in a large Danish population with major depression. Method: Leu7Pro was studied in a sample of depressed patients and ethnically matched controls, as well as psychiatric disease controls with schizophrenia. Possible functional consequences of Leu7Pro were explored in vitro. Results: In contrast to previous studies, Pro7 appeared to be a risk allele for depression, being significantly more frequent in the depression sample (5.5%, n = 593; p = 0.009; odds ratio, OR: 1.46) as compared to ethnically matched controls (3.8%, n = 2912), while schizophrenia patients (4.1%, n = 503) did not differ. In vitro, the Pro7 substitution appeared to be associated with reduced levels of NPY without affecting its mRNA level. Conclusion: The Leu7Pro variation may increase the risk of major depression, possibly by affecting the biosynthesis of NPY. Pernille

Published
2012

7. Association of the leucine-7 to proline-7 variation in the signal sequence of neuropeptide Y with major depression

Author

Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, Bolwig, Tom Gert, Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, and Bolwig, Tom Gert

Abstract

Objective: There is clear evidence of a genetic component in major depression, and several studies indicate that neuropeptide Y (NPY) could play an important role in the pathophysiology of the disease. A well-known polymorphism encoding the substitution of leucine to proline in the signal peptide sequence of NPY (Leu7Pro variation) was previously found to protect against depression. Our study aimed at replicating this association in a large Danish population with major depression. Method: Leu7Pro was studied in a sample of depressed patients and ethnically matched controls, as well as psychiatric disease controls with schizophrenia. Possible functional consequences of Leu7Pro were explored in vitro. Results: In contrast to previous studies, Pro7 appeared to be a risk allele for depression, being significantly more frequent in the depression sample (5.5%, n = 593; p = 0.009; odds ratio, OR: 1.46) as compared to ethnically matched controls (3.8%, n = 2912), while schizophrenia patients (4.1%, n = 503) did not differ. In vitro, the Pro7 substitution appeared to be associated with reduced levels of NPY without affecting its mRNA level. Conclusion: The Leu7Pro variation may increase the risk of major depression, possibly by affecting the biosynthesis of NPY. Pernille

Published
2012

8. Association of the leucine-7 to proline-7 variation in the signal sequence of neuropeptide Y with major depression

Author

Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, Bolwig, Tom Gert, Koefoed, Pernille, Woldbye, David Paul Drucker, Hansen, Thomas v.O, Eplov, Lene F, Christiansen, Søren Hofman Oliveira, Mors, Ole, Kessing, Lars Vedel, Werge, Thomas, Kaipio, Katja, Pesonen, Ullamani, Fahmy, Thomas, Mellerup, Erling Thyge, Jakobsen, Klaus D, Hansen, Elsebeth S, Knudsen, Gitte Moos, Bukh, Jens D, Bock, Camilla, Lindberg, Camilla, Kristensen, Ann S, Dam, Henrik, Nordentoft, Merete, Als, Thomas D, Wang, August G., Gether, Ulrik, Rehfeld, Jens Frederik, and Bolwig, Tom Gert

Abstract

Objective: There is clear evidence of a genetic component in major depression, and several studies indicate that neuropeptide Y (NPY) could play an important role in the pathophysiology of the disease. A well-known polymorphism encoding the substitution of leucine to proline in the signal peptide sequence of NPY (Leu7Pro variation) was previously found to protect against depression. Our study aimed at replicating this association in a large Danish population with major depression. Method: Leu7Pro was studied in a sample of depressed patients and ethnically matched controls, as well as psychiatric disease controls with schizophrenia. Possible functional consequences of Leu7Pro were explored in vitro. Results: In contrast to previous studies, Pro7 appeared to be a risk allele for depression, being significantly more frequent in the depression sample (5.5%, n = 593; p = 0.009; odds ratio, OR: 1.46) as compared to ethnically matched controls (3.8%, n = 2912), while schizophrenia patients (4.1%, n = 503) did not differ. In vitro, the Pro7 substitution appeared to be associated with reduced levels of NPY without affecting its mRNA level. Conclusion: The Leu7Pro variation may increase the risk of major depression, possibly by affecting the biosynthesis of NPY. Pernille

Published
2012

9. Hjernens belønnings- og strafsystem

Author

Mellerup, Erling Thyge, Wortwein, G., Jensen, T.W., Skov, M., Mellerup, Erling Thyge, Wortwein, G., Jensen, T.W., and Skov, M.

Published
2007

10. Hjernens belønnings- og strafsystem

Author

Mellerup, Erling Thyge, Wortwein, G., Jensen, T.W., Skov, M., Mellerup, Erling Thyge, Wortwein, G., Jensen, T.W., and Skov, M.

Published
2007

18. Associative an nonassociative learning after chronic imipramine in rats

Author

Mogensen, Jesper, Svendsen, Gitte, Tølbøll Lauritsen, Klara, Ermens, Petra, Hasman, Andreas, Elvertorp, Soheyla, Plenge, Per Krener, Mellerup, Erling Thyge, Wörtwein, Gitta, Mogensen, Jesper, Svendsen, Gitte, Tølbøll Lauritsen, Klara, Ermens, Petra, Hasman, Andreas, Elvertorp, Soheyla, Plenge, Per Krener, Mellerup, Erling Thyge, and Wörtwein, Gitta

Published
2003

19. Platelet serotonin transporter in stroke patients

Author

Rasmussen, A., Christensen, J., Clemmensen, P.M., Dalsgaard, N.J., Dam, Henrik O., Hindberg, I., Lunde, M., Plenge, Per Krener, Mellerup, Erling Thyge, Rasmussen, A., Christensen, J., Clemmensen, P.M., Dalsgaard, N.J., Dam, Henrik O., Hindberg, I., Lunde, M., Plenge, Per Krener, and Mellerup, Erling Thyge

Published
2003

21. Platelet serotonin transporter in stroke patients

Author

Rasmussen, A., Christensen, J., Clemmensen, P.M., Dalsgaard, N.J., Dam, Henrik O., Hindberg, I., Lunde, M., Plenge, Per Krener, Mellerup, Erling Thyge, Rasmussen, A., Christensen, J., Clemmensen, P.M., Dalsgaard, N.J., Dam, Henrik O., Hindberg, I., Lunde, M., Plenge, Per Krener, and Mellerup, Erling Thyge

Published
2003

23. Associative an nonassociative learning after chronic imipramine in rats

Author

Mogensen, Jesper, Svendsen, Gitte, Tølbøll Lauritsen, Klara, Ermens, Petra, Hasman, Andreas, Elvertorp, Soheyla, Plenge, Per Krener, Mellerup, Erling Thyge, Wörtwein, Gitta, Mogensen, Jesper, Svendsen, Gitte, Tølbøll Lauritsen, Klara, Ermens, Petra, Hasman, Andreas, Elvertorp, Soheyla, Plenge, Per Krener, Mellerup, Erling Thyge, and Wörtwein, Gitta

Published
2003

32. Platelet serotonin transporters and the transporter gene in control subjects, unipolar patients and bipolar patients

Author

Mellerup, Erling Thyge, Bennike, Bente Guldhammer, Bolwig, Tom G., Dam, Henrik O., Hasholt, Lis, Jørgensen, Martin Balslev, Plenge, Per Krener, Sørensen, Sven Asger, Mellerup, Erling Thyge, Bennike, Bente Guldhammer, Bolwig, Tom G., Dam, Henrik O., Hasholt, Lis, Jørgensen, Martin Balslev, Plenge, Per Krener, and Sørensen, Sven Asger

Abstract

depression, platelet, serotonin transporter, serotonin transporter gene

Published
2001

33. Platelet serotonin transporters and the transporter gene in control subjects, unipolar patients and bipolar patients

Author

Mellerup, Erling Thyge, Bennike, Bente Guldhammer, Bolwig, Tom G., Dam, Henrik O., Hasholt, Lis, Jørgensen, Martin Balslev, Plenge, Per Krener, Sørensen, Sven Asger, Mellerup, Erling Thyge, Bennike, Bente Guldhammer, Bolwig, Tom G., Dam, Henrik O., Hasholt, Lis, Jørgensen, Martin Balslev, Plenge, Per Krener, and Sørensen, Sven Asger

Abstract

depression, platelet, serotonin transporter, serotonin transporter gene

Published
2001

34. Biologisk psykiatri

Author

Mellerup, Erling Thyge and Mellerup, Erling Thyge

Published
1999

35. Serotonintransporteren

Author

Mellerup, Erling Thyge, Plenge, Per Krener, Mellerup, Erling Thyge, and Plenge, Per Krener

Published
1999

36. Kvantitativ bestemmelse af receptorer

Author

Plenge, Per Krener, Bennike, Bente Guldhammer, Mellerup, Erling Thyge, Plenge, Per Krener, Bennike, Bente Guldhammer, and Mellerup, Erling Thyge

Published
1999

39. Kvantitativ bestemmelse af receptorer

Author

Plenge, Per Krener, Bennike, Bente Guldhammer, Mellerup, Erling Thyge, Plenge, Per Krener, Bennike, Bente Guldhammer, and Mellerup, Erling Thyge

Published
1999

40. Serotonintransporteren

Author

Mellerup, Erling Thyge, Plenge, Per Krener, Mellerup, Erling Thyge, and Plenge, Per Krener

Published
1999

43. Biologisk psykiatri

Author

Mellerup, Erling Thyge and Mellerup, Erling Thyge

Published
1999

45. Biologisk psykiatri

Author

Mellerup, Erling Thyge and Mellerup, Erling Thyge

Published
1999

46. Serotonintransporteren

Author

Mellerup, Erling Thyge, Plenge, Per Krener, Mellerup, Erling Thyge, and Plenge, Per Krener

Published
1999

48. Kvantitativ bestemmelse af receptorer

Author

Plenge, Per Krener, Bennike, Bente Guldhammer, Mellerup, Erling Thyge, Plenge, Per Krener, Bennike, Bente Guldhammer, and Mellerup, Erling Thyge

Published
1999

50. Prevalence of winter depression in Denmark

Author

Dam, Henrik O., Jakobsen, Klaus, Mellerup, Erling Thyge, Dam, Henrik O., Jakobsen, Klaus, and Mellerup, Erling Thyge

Abstract

psykiatri, seasonal affective disorder, winter depression, SAD, Denmark

Published
1998

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