Prevalence of Huntington's disease gene CAG trinucleotide repeat alleles in patients with bipolar disorder
Objectives Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat...
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| Published in | Bipolar disorders Vol. 17; no. 4; pp. 403 - 408 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Denmark
Blackwell Publishing Ltd
01.06.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1398-5647 1399-5618 1399-5618 |
| DOI | 10.1111/bdi.12289 |
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| Abstract | Objectives
Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat alleles observed among individuals diagnosed with major depressive disorder raises the possibility that another mood disorder, bipolar disorder, could likewise be associated with Huntington's disease.
Methods
We assessed the distribution of HTT CAG repeat alleles in a cohort of individuals with bipolar disorder. HTT CAG allele sizes from 2,229 Caucasian individuals diagnosed with DSM‐IV bipolar disorder were compared to allele sizes in 1,828 control individuals from multiple cohorts.
Results
We found that HTT CAG repeat alleles > 35 units were observed in only one of 4,458 chromosomes from individuals with bipolar disorder, compared to three of 3,656 chromosomes from control subjects.
Conclusions
These findings do not support an association between bipolar disorder and Huntington's disease. |
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| AbstractList | Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat alleles observed among individuals diagnosed with major depressive disorder raises the possibility that another mood disorder, bipolar disorder, could likewise be associated with Huntington's disease.
We assessed the distribution of HTT CAG repeat alleles in a cohort of individuals with bipolar disorder. HTT CAG allele sizes from 2,229 Caucasian individuals diagnosed with DSM-IV bipolar disorder were compared to allele sizes in 1,828 control individuals from multiple cohorts.
We found that HTT CAG repeat alleles > 35 units were observed in only one of 4,458 chromosomes from individuals with bipolar disorder, compared to three of 3,656 chromosomes from control subjects.
These findings do not support an association between bipolar disorder and Huntington's disease. Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat alleles observed among individuals diagnosed with major depressive disorder raises the possibility that another mood disorder, bipolar disorder, could likewise be associated with Huntington's disease.OBJECTIVESHuntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat alleles observed among individuals diagnosed with major depressive disorder raises the possibility that another mood disorder, bipolar disorder, could likewise be associated with Huntington's disease.We assessed the distribution of HTT CAG repeat alleles in a cohort of individuals with bipolar disorder. HTT CAG allele sizes from 2,229 Caucasian individuals diagnosed with DSM-IV bipolar disorder were compared to allele sizes in 1,828 control individuals from multiple cohorts.METHODSWe assessed the distribution of HTT CAG repeat alleles in a cohort of individuals with bipolar disorder. HTT CAG allele sizes from 2,229 Caucasian individuals diagnosed with DSM-IV bipolar disorder were compared to allele sizes in 1,828 control individuals from multiple cohorts.We found that HTT CAG repeat alleles > 35 units were observed in only one of 4,458 chromosomes from individuals with bipolar disorder, compared to three of 3,656 chromosomes from control subjects.RESULTSWe found that HTT CAG repeat alleles > 35 units were observed in only one of 4,458 chromosomes from individuals with bipolar disorder, compared to three of 3,656 chromosomes from control subjects.These findings do not support an association between bipolar disorder and Huntington's disease.CONCLUSIONSThese findings do not support an association between bipolar disorder and Huntington's disease. Objectives Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG trinucleotide repeat alleles of 36 or more units. A greater than expected prevalence of incompletely penetrant HTT CAG repeat alleles observed among individuals diagnosed with major depressive disorder raises the possibility that another mood disorder, bipolar disorder, could likewise be associated with Huntington's disease. Methods We assessed the distribution of HTT CAG repeat alleles in a cohort of individuals with bipolar disorder. HTT CAG allele sizes from 2,229 Caucasian individuals diagnosed with DSM‐IV bipolar disorder were compared to allele sizes in 1,828 control individuals from multiple cohorts. Results We found that HTT CAG repeat alleles > 35 units were observed in only one of 4,458 chromosomes from individuals with bipolar disorder, compared to three of 3,656 chromosomes from control subjects. Conclusions These findings do not support an association between bipolar disorder and Huntington's disease. |
| Author | Mysore, Jayalakshmi S Gillis, Tammy MacDonald, Marcy E Ramos, Eliana Marisa Lee, Jong-Min Alonso, Isabel Smoller, Jordan W Sklar, Pamela Gusella, James F Perlis, Roy H |
| AuthorAffiliation | c Division of Psychiatric Genomics, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA b UnIGENe, IBMC – Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal a Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA |
| AuthorAffiliation_xml | – name: c Division of Psychiatric Genomics, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA – name: a Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA – name: b UnIGENe, IBMC – Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal |
| Author_xml | – sequence: 1 givenname: Eliana Marisa surname: Ramos fullname: Ramos, Eliana Marisa organization: Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA – sequence: 2 givenname: Tammy surname: Gillis fullname: Gillis, Tammy organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA – sequence: 3 givenname: Jayalakshmi S surname: Mysore fullname: Mysore, Jayalakshmi S organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA – sequence: 4 givenname: Jong-Min surname: Lee fullname: Lee, Jong-Min organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA – sequence: 5 givenname: Isabel surname: Alonso fullname: Alonso, Isabel organization: UnIGENe, IBMC - Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal – sequence: 6 givenname: James F surname: Gusella fullname: Gusella, James F organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA – sequence: 7 givenname: Jordan W surname: Smoller fullname: Smoller, Jordan W organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA – sequence: 8 givenname: Pamela surname: Sklar fullname: Sklar, Pamela organization: Division of Psychiatric Genomics, Department of Psychiatry, Mount Sinai School of Medicine, NY, New York, USA – sequence: 9 givenname: Marcy E surname: MacDonald fullname: MacDonald, Marcy E organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA – sequence: 10 givenname: Roy H surname: Perlis fullname: Perlis, Roy H email: Corresponding author:Roy H. Perlis, M.D.Center for Human Genetic ResearchMassachusetts General HospitalSimches Research Building185 Cambridge StreetBoston, MA 02114USAFax: 617-724-3028, rperlis@mgh.harvard.edu organization: Center for Human Genetic Research, Massachusetts General Hospital, MA, Boston, USA |
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| Cites_doi | 10.1093/hmg/ddp524 10.1176/appi.ajp.2009.09070973 10.1212/WNL.0b013e318249f683 10.1006/mcpr.1993.1034 10.1002/mpr.1359 10.1038/sj.mp.4002151 10.1038/ng0894-525 10.2190/HU6W-3K7Q-NAEL-XU6K 10.1093/hmg/3.12.2103 10.1093/bioinformatics/19.1.149 10.3109/17482968.2011.653573 10.31887/DCNS.2007.9.2/arosenblatt 10.1038/ejhg.2010.229 10.1016/0092-8674(93)90585-E 10.1136/jnnp.2006.103309 10.1016/j.ajhg.2009.11.002 |
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| Keywords | bipolar disorder neurodegenerative disease depression trinucleotide repeat Huntington's disease polyglutamine expansion |
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| References | Warby SC, Visscher H, Collins JA et al. HTT haplotypes contribute to differences in Huntington disease prevalence between Europe and East Asia. Eur J Hum Genet 2011; 19: 561-566. Rubinsztein DC, Amos W, Leggo J et al. Mutational bias provides a model for the evolution of Huntington's disease and predicts a general increase in disease prevalence. Nat Genet 1994; 7: 525-530. MacDonald ME, Ambrose CM, Duyao MP et al. (The Huntington's Disease Collaborative Research Group). A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. Cell 1993; 72: 971-983. Folstein SE, Folstein MF. Psychiatric features of Huntington's disease: recent approaches and findings. Psychiatr Dev 1983; 1: 193-205. Rosenblatt A. Neuropsychiatry of Huntington's disease. Dialogues Clin Neurosci 2007; 9: 191-197. Seong IS, Woda JM, Song JJ et al. Huntingtin facilitates polycomb repressive complex 2. Hum Mol Genet 2010; 19: 573-583. Falush D. Haplotype background, repeat length evolution, and Huntington's disease. Am J Hum Genet 2009; 85: 939-942. Perlis RH, Smoller JW, Mysore J et al. Prevalence of incompletely penetrant Huntington's disease alleles among individuals with major depressive disorder. Am J Psychiatry 2010; 167: 574-579. Purcell S, Cherny SS, Sham PC. Genetic Power Calculator: design of linkage and association genetic mapping studies of complex traits. Bioinformatics 2003; 19: 149-150. Mendez MF. Huntington's disease: update and review of neuropsychiatric aspects. Int J Psychiatry Med 1994; 24: 189-208. Sklar P, Smoller JW, Fan J et al. Whole-genome association study of bipolar disorder. Mol Psychiatry 2008; 13: 558-569. Ramos EM, Keagle P, Gillis T et al. Prevalence of Huntington's disease gene CAG repeat alleles in sporadic amyotrophic lateral sclerosis patients. Amyotroph Lateral Scler 2012; 13: 265-269. Squitieri F, Andrew SE, Goldberg YP et al. DNA haplotype analysis of Huntington disease reveals clues to the origins and mechanisms of CAG expansion and reasons for geographic variations of prevalence. Hum Mol Genet 1994; 3: 2103-2114. Kessler RC, Petukhova M, Sampson NA, Zaslavsky AM, Wittchen HU. Twelve-month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States. Int J Methods Psychiatr Res 2012; 21: 169-184. Julien CL, Thompson JC, Wild S et al. Psychiatric disorders in preclinical Huntington's disease. J Neurol Neurosurg Psychiatry 2007; 78: 939-943. Lee JM, Ramos EM, Lee JH et al. CAG repeat expansion in Huntington disease determines age at onset in a fully dominant fashion. Neurology 2012; 78: 690-695. Warner JP, Barron LH, Brock DJ. A new polymerase chain reaction (PCR) assay for the trinucleotide repeat that is unstable and expanded on Huntington's disease chromosomes. Mol Cell Probes 1993; 7: 235-239. 1993; 7 2009; 85 1993; 72 2010; 19 1983; 1 2010; 167 2007; 9 1994; 24 2008; 13 2003; 19 2012; 13 2012; 78 2011; 19 1994; 3 2007; 78 2012; 21 1994; 7 e_1_2_7_6_1 e_1_2_7_4_1 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_8_1 e_1_2_7_7_1 e_1_2_7_18_1 e_1_2_7_17_1 e_1_2_7_16_1 e_1_2_7_2_1 e_1_2_7_15_1 e_1_2_7_14_1 e_1_2_7_13_1 e_1_2_7_12_1 e_1_2_7_11_1 e_1_2_7_10_1 Folstein SE (e_1_2_7_5_1) 1983; 1 |
| References_xml | – reference: Lee JM, Ramos EM, Lee JH et al. CAG repeat expansion in Huntington disease determines age at onset in a fully dominant fashion. Neurology 2012; 78: 690-695. – reference: Warby SC, Visscher H, Collins JA et al. HTT haplotypes contribute to differences in Huntington disease prevalence between Europe and East Asia. Eur J Hum Genet 2011; 19: 561-566. – reference: Folstein SE, Folstein MF. Psychiatric features of Huntington's disease: recent approaches and findings. Psychiatr Dev 1983; 1: 193-205. – reference: Ramos EM, Keagle P, Gillis T et al. Prevalence of Huntington's disease gene CAG repeat alleles in sporadic amyotrophic lateral sclerosis patients. Amyotroph Lateral Scler 2012; 13: 265-269. – reference: Purcell S, Cherny SS, Sham PC. Genetic Power Calculator: design of linkage and association genetic mapping studies of complex traits. Bioinformatics 2003; 19: 149-150. – reference: Warner JP, Barron LH, Brock DJ. A new polymerase chain reaction (PCR) assay for the trinucleotide repeat that is unstable and expanded on Huntington's disease chromosomes. Mol Cell Probes 1993; 7: 235-239. – reference: Sklar P, Smoller JW, Fan J et al. Whole-genome association study of bipolar disorder. Mol Psychiatry 2008; 13: 558-569. – reference: Falush D. Haplotype background, repeat length evolution, and Huntington's disease. Am J Hum Genet 2009; 85: 939-942. – reference: Perlis RH, Smoller JW, Mysore J et al. Prevalence of incompletely penetrant Huntington's disease alleles among individuals with major depressive disorder. Am J Psychiatry 2010; 167: 574-579. – reference: Seong IS, Woda JM, Song JJ et al. Huntingtin facilitates polycomb repressive complex 2. Hum Mol Genet 2010; 19: 573-583. – reference: Kessler RC, Petukhova M, Sampson NA, Zaslavsky AM, Wittchen HU. Twelve-month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States. Int J Methods Psychiatr Res 2012; 21: 169-184. – reference: Julien CL, Thompson JC, Wild S et al. Psychiatric disorders in preclinical Huntington's disease. J Neurol Neurosurg Psychiatry 2007; 78: 939-943. – reference: MacDonald ME, Ambrose CM, Duyao MP et al. (The Huntington's Disease Collaborative Research Group). A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. Cell 1993; 72: 971-983. – reference: Mendez MF. Huntington's disease: update and review of neuropsychiatric aspects. Int J Psychiatry Med 1994; 24: 189-208. – reference: Rosenblatt A. Neuropsychiatry of Huntington's disease. Dialogues Clin Neurosci 2007; 9: 191-197. – reference: Squitieri F, Andrew SE, Goldberg YP et al. DNA haplotype analysis of Huntington disease reveals clues to the origins and mechanisms of CAG expansion and reasons for geographic variations of prevalence. Hum Mol Genet 1994; 3: 2103-2114. – reference: Rubinsztein DC, Amos W, Leggo J et al. Mutational bias provides a model for the evolution of Huntington's disease and predicts a general increase in disease prevalence. Nat Genet 1994; 7: 525-530. – volume: 19 start-page: 561 year: 2011 end-page: 566 article-title: HTT haplotypes contribute to differences in Huntington disease prevalence between Europe and East Asia publication-title: Eur J Hum Genet – volume: 72 start-page: 971 year: 1993 end-page: 983 article-title: (The Huntington's Disease Collaborative Research Group). A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes publication-title: Cell – volume: 9 start-page: 191 year: 2007 end-page: 197 article-title: Neuropsychiatry of Huntington's disease publication-title: Dialogues Clin Neurosci – volume: 78 start-page: 939 year: 2007 end-page: 943 article-title: Psychiatric disorders in preclinical Huntington's disease publication-title: J Neurol Neurosurg Psychiatry – volume: 7 start-page: 525 year: 1994 end-page: 530 article-title: Mutational bias provides a model for the evolution of Huntington's disease and predicts a general increase in disease prevalence publication-title: Nat Genet – volume: 21 start-page: 169 year: 2012 end-page: 184 article-title: Twelve‐month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States publication-title: Int J Methods Psychiatr Res – volume: 167 start-page: 574 year: 2010 end-page: 579 article-title: Prevalence of incompletely penetrant Huntington's disease alleles among individuals with major depressive disorder publication-title: Am J Psychiatry – volume: 78 start-page: 690 year: 2012 end-page: 695 article-title: CAG repeat expansion in Huntington disease determines age at onset in a fully dominant fashion publication-title: Neurology – volume: 85 start-page: 939 year: 2009 end-page: 942 article-title: Haplotype background, repeat length evolution, and Huntington's disease publication-title: Am J Hum Genet – volume: 1 start-page: 193 year: 1983 end-page: 205 article-title: Psychiatric features of Huntington's disease: recent approaches and findings publication-title: Psychiatr Dev – volume: 3 start-page: 2103 year: 1994 end-page: 2114 article-title: DNA haplotype analysis of Huntington disease reveals clues to the origins and mechanisms of CAG expansion and reasons for geographic variations of prevalence publication-title: Hum Mol Genet – volume: 19 start-page: 149 year: 2003 end-page: 150 article-title: Genetic Power Calculator: design of linkage and association genetic mapping studies of complex traits publication-title: Bioinformatics – volume: 24 start-page: 189 year: 1994 end-page: 208 article-title: Huntington's disease: update and review of neuropsychiatric aspects publication-title: Int J Psychiatry Med – volume: 13 start-page: 265 year: 2012 end-page: 269 article-title: Prevalence of Huntington's disease gene CAG repeat alleles in sporadic amyotrophic lateral sclerosis patients publication-title: Amyotroph Lateral Scler – volume: 7 start-page: 235 year: 1993 end-page: 239 article-title: A new polymerase chain reaction (PCR) assay for the trinucleotide repeat that is unstable and expanded on Huntington's disease chromosomes publication-title: Mol Cell Probes – volume: 19 start-page: 573 year: 2010 end-page: 583 article-title: Huntingtin facilitates polycomb repressive complex 2 publication-title: Hum Mol Genet – volume: 13 start-page: 558 year: 2008 end-page: 569 article-title: Whole‐genome association study of bipolar disorder publication-title: Mol Psychiatry – ident: e_1_2_7_13_1 doi: 10.1093/hmg/ddp524 – volume: 1 start-page: 193 year: 1983 ident: e_1_2_7_5_1 article-title: Psychiatric features of Huntington's disease: recent approaches and findings publication-title: Psychiatr Dev – ident: e_1_2_7_7_1 doi: 10.1176/appi.ajp.2009.09070973 – ident: e_1_2_7_10_1 doi: 10.1212/WNL.0b013e318249f683 – ident: e_1_2_7_11_1 doi: 10.1006/mcpr.1993.1034 – ident: e_1_2_7_18_1 doi: 10.1002/mpr.1359 – ident: e_1_2_7_8_1 doi: 10.1038/sj.mp.4002151 – ident: e_1_2_7_17_1 doi: 10.1038/ng0894-525 – ident: e_1_2_7_4_1 doi: 10.2190/HU6W-3K7Q-NAEL-XU6K – ident: e_1_2_7_15_1 doi: 10.1093/hmg/3.12.2103 – ident: e_1_2_7_12_1 doi: 10.1093/bioinformatics/19.1.149 – ident: e_1_2_7_9_1 doi: 10.3109/17482968.2011.653573 – ident: e_1_2_7_3_1 doi: 10.31887/DCNS.2007.9.2/arosenblatt – ident: e_1_2_7_14_1 doi: 10.1038/ejhg.2010.229 – ident: e_1_2_7_2_1 doi: 10.1016/0092-8674(93)90585-E – ident: e_1_2_7_6_1 doi: 10.1136/jnnp.2006.103309 – ident: e_1_2_7_16_1 doi: 10.1016/j.ajhg.2009.11.002 |
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| Snippet | Objectives
Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene... Huntington's disease is a neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms that are caused by huntingtin gene (HTT) CAG... |
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| SubjectTerms | Adult Alleles Amyotrophic Lateral Sclerosis - genetics bipolar disorder Bipolar Disorder - genetics depression Depressive Disorder, Major - genetics Female Genotype Humans Huntingtin Protein Huntington Disease - diagnosis Huntington Disease - genetics Huntington's disease Male Middle Aged Nerve Tissue Proteins - genetics neurodegenerative disease Penetrance polyglutamine expansion Prevalence Statistics as Topic trinucleotide repeat Trinucleotide Repeats - genetics |
| Title | Prevalence of Huntington's disease gene CAG trinucleotide repeat alleles in patients with bipolar disorder |
| URI | https://api.istex.fr/ark:/67375/WNG-VC5HJ177-G/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fbdi.12289 https://www.ncbi.nlm.nih.gov/pubmed/25726852 https://www.proquest.com/docview/1686415714 https://pubmed.ncbi.nlm.nih.gov/PMC9980711 |
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