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Article ; Online: The retinoid-related orphan receptor alpha (RORA) gene and fear-related psychopathology.

Miller, Mark W / Wolf, Erika J / Logue, Mark W / Baldwin, Clinton T

2013 Volume 151, Issue 2, Page(s) 702–708

Abstract: Background: This study followed on findings from a recent genome-wide association study of PTSD that implicated the retinoid-related orphan receptor alpha (RORA) gene (Logue et al., 2012) by examining its relationship to broader array of disorders.: ... ...

Abstract	Background: This study followed on findings from a recent genome-wide association study of PTSD that implicated the retinoid-related orphan receptor alpha (RORA) gene (Logue et al., 2012) by examining its relationship to broader array of disorders. Methods: Using data from the same cohort (N=540), we analyzed patterns of association between 606 single nucleotide polymorphisms (SNPs) spanning the RORA gene and comorbidity factors termed fear, distress (i.e., internalizing factors) and externalizing. Results: Results showed that rs17303244 was associated with the fear component of internalizing (i.e., defined by symptoms of panic, agoraphobia, specific phobia, and obsessive-compulsive disorder) at a level of significance that withstood correction for gene-wide multiple testing. Limitations: The primary limitations were the modest size of the cohort and the absence of a replication sample. Conclusions: Results add to a growing literature implicating the RORA gene in a wide range of neuropsychiatric disorders and offer new insight into possible molecular mechanisms of the effects of traumatic stress on the brain and the role of genetic factors in those processes.
MeSH term(s)	Adult ; Aged ; Anxiety Disorders/epidemiology ; Anxiety Disorders/genetics ; Female ; Genome-Wide Association Study ; Genotype ; Humans ; Male ; Mental Disorders/epidemiology ; Mental Disorders/genetics ; Middle Aged ; Nuclear Receptor Subfamily 1, Group F, Member 1/genetics ; Polymorphism, Single Nucleotide ; Stress, Psychological/epidemiology ; Stress, Psychological/genetics ; Young Adult
Chemical Substances	Nuclear Receptor Subfamily 1, Group F, Member 1 ; RORA protein, human
Language	English
Publishing date	2013-08-17
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	135449-8
ISSN	1573-2517 ; 0165-0327
ISSN (online)	1573-2517
ISSN	0165-0327
DOI	10.1016/j.jad.2013.07.022
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Article ; Online: The genetics of hemoglobin A2 regulation in sickle cell anemia.

Griffin, Paula J / Sebastiani, Paola / Edward, Heather / Baldwin, Clinton T / Gladwin, Mark T / Gordeuk, Victor R / Chui, David H K / Steinberg, Martin H

American journal of hematology

2014 Volume 89, Issue 11, Page(s) 1019–1023

Abstract: Hemoglobin A2 , a tetramer of α- and δ-globin chains, comprises less than 3% of total hemoglobin in normal adults. In northern Europeans, single nucleotide polymorphisms (SNPs) in the HBS1L-MYB locus on chromosome 6q and the HBB cluster on chromosome 11p ...

Abstract	Hemoglobin A2 , a tetramer of α- and δ-globin chains, comprises less than 3% of total hemoglobin in normal adults. In northern Europeans, single nucleotide polymorphisms (SNPs) in the HBS1L-MYB locus on chromosome 6q and the HBB cluster on chromosome 11p were associated with HbA2 levels. We examined the genetic basis of HbA2 variability in sickle cell anemia using genome-wide association studies. HbA2 levels were associated with SNPs in the HBS1L-MYB interval and SNPs in BCL11A. These effects are mediated by the association of these loci with γ-globin gene expression and fetal hemoglobin (HbF) levels. The association of polymorphisms downstream of the β-globin gene (HBB) cluster on chromosome 11 with HbA2 was not mediated by HbF. In sickle cell anemia, levels of HbA2 appear to be modulated by trans-acting genes that affect HBG expression and perhaps also elements within the β-globin gene cluster. HbA2 is expressed pancellularly and can inhibit HbS polymerization. It remains to be seen if genetic regulators of HbA2 can be exploited for therapeutic purposes.
MeSH term(s)	African Americans/genetics ; Age Factors ; Anemia, Sickle Cell/metabolism ; Asian Continental Ancestry Group/genetics ; Carrier Proteins/genetics ; Chromosomes, Human, Pair 11/genetics ; Chromosomes, Human, Pair 6/genetics ; Cohort Studies ; Europe/ethnology ; European Continental Ancestry Group/genetics ; Female ; Fetal Hemoglobin/genetics ; GTP-Binding Proteins/genetics ; Gene Expression Regulation/genetics ; Genes, myb ; Genome-Wide Association Study ; Genotype ; HSP70 Heat-Shock Proteins/genetics ; Hemoglobin A2/biosynthesis ; Hemoglobin A2/genetics ; Hemoglobin, Sickle/genetics ; Hemoglobin, Sickle/metabolism ; Humans ; Male ; Nuclear Proteins/genetics ; Peptide Elongation Factors/genetics ; Phenotype ; Polymorphism, Single Nucleotide ; Repressor Proteins ; Trans-Activators/genetics ; alpha-Thalassemia/genetics ; beta-Globins/genetics ; delta-Globins/genetics ; gamma-Globins/genetics
Chemical Substances	BCL11A protein, human ; Carrier Proteins ; HSP70 Heat-Shock Proteins ; Hemoglobin, Sickle ; Nuclear Proteins ; Peptide Elongation Factors ; Repressor Proteins ; Trans-Activators ; beta-Globins ; delta-Globins ; gamma-Globins ; Hemoglobin A2 (9034-53-1) ; Fetal Hemoglobin (9034-63-3) ; GTP-Binding Proteins (EC 3.6.1.-) ; HBS1L protein, human (EC 3.6.1.-)
Language	English
Publishing date	2014-08-04
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.23811
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Article ; Online: Genetic variation of the transthyretin gene in wild-type transthyretin amyloidosis (ATTRwt).

Sikora, Jacquelyn L / Logue, Mark W / Chan, Gloria G / Spencer, Brian H / Prokaeva, Tatiana B / Baldwin, Clinton T / Seldin, David C / Connors, Lawreen H

Human genetics

2014 Volume 134, Issue 1, Page(s) 111–121

Abstract: Wild-type transthyretin amyloidosis (ATTRwt), typically diagnosed as congestive heart failure in elderly Caucasian men, features myocardial amyloid deposits of wild-type plasma protein transthyretin (TTR). ATTRwt is sporadic, its pathogenesis is poorly ... ...

Abstract	Wild-type transthyretin amyloidosis (ATTRwt), typically diagnosed as congestive heart failure in elderly Caucasian men, features myocardial amyloid deposits of wild-type plasma protein transthyretin (TTR). ATTRwt is sporadic, its pathogenesis is poorly understood, and currently there are no biomarkers for diagnosis or prognosis. Genetic studies of variant-associated transthyretin amyloidosis have suggested that non-coding TTR gene variants modulate disease. We hypothesized that cis-acting regulatory elements in the TTR gene non-coding regions may modify expression, affecting ATTRwt onset and progression. We studied an ATTRwt cohort consisting of 108 Caucasian males ranging in age from 59 to 87 years with cardiomyopathy due to wild-type TTR deposition; results were compared to 118 anonymous controls matched by age, sex, and race. Four predicted non-coding regulatory regions and all exons in the TTR gene were sequenced using the Sanger method. Eleven common variants were identified; three variants were significantly associated with ATTRwt (p < 0.05), though only one, rs72922940, remained near significance (p corrected = 0.083) after multiple testing correction. Exon analyses demonstrated the occurrence of the p.G26S (G6S) polymorphism in 7 % of ATTRwt subjects and 12 % of controls; this variant was predicted to be a protective factor (p = 0.051). Four variants were significantly associated with age at onset and survival. In this first genetic study of a large, well-characterized cohort of ATTRwt, non-coding and coding variants associated with disease, age at onset, and survival were identified. Further investigation is warranted to determine the prevalence of these variants in ATTRwt, their regulatory function, and potential role in assessing disease risk.
MeSH term(s)	Aged ; Aged, 80 and over ; Amyloid Neuropathies, Familial/genetics ; Case-Control Studies ; Cohort Studies ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Prealbumin/genetics ; Prognosis
Chemical Substances	Prealbumin
Language	English
Publishing date	2014-11-04
Publishing country	Germany
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	223009-4
ISSN	1432-1203 ; 0340-6717
ISSN (online)	1432-1203
ISSN	0340-6717
DOI	10.1007/s00439-014-1499-0
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Article ; Online: A genome-wide association study of clinical symptoms of dissociation in a trauma-exposed sample.

Wolf, Erika J / Rasmusson, Ann M / Mitchell, Karen S / Logue, Mark W / Baldwin, Clinton T / Miller, Mark W

Depression and anxiety

2014 Volume 31, Issue 4, Page(s) 352–360

Abstract: Background: Recent work suggests that a subset of individuals with posttraumatic stress disorder (PTSD) exhibit marked dissociative symptoms, as defined by derealization and depersonalization. A dissociative subtype of PTSD was added to the diagnostic ... ...

Abstract	Background: Recent work suggests that a subset of individuals with posttraumatic stress disorder (PTSD) exhibit marked dissociative symptoms, as defined by derealization and depersonalization. A dissociative subtype of PTSD was added to the diagnostic criteria listed in the Diagnostic and Statistical Manual of Mental Disorders, Version 5 (DSM-5) to capture this presentation of PTSD. This study examined genetic polymorphisms for association with the symptoms that define the dissociative subtype of PTSD using a genome-wide approach. Methods: The sample comprised 484 White, non-Hispanic, trauma-exposed veterans and their partners who were assessed for lifetime PTSD and dissociation using a structured clinical interview. The prevalence of PTSD was 60.5%. Single-nucleotide polymorphisms (SNPs) from across the genome were obtained from a 2.5 million SNP array. Results: Ten SNPs evidenced suggestive association with dissociation (P < 10(-5)). No SNPs met genome-wide significance criteria (P < 5 × 10(-8)). The peak SNP was rs263232 (β = 1.4, P = 6.12 × 10(-7)), located in the adenylyl cyclase 8 (ADCY8) gene; a second SNP in the suggestive range was rs71534169 (β = 1.63, P = 3.79 × 10(-6)), located in the dipeptidyl-peptidase 6 (DPP6) gene. Conclusions: ADCY8 is integral for long-term potentiation and synaptic plasticity and is implicated in fear-related learning and memory and long-term memory consolidation. DPP6 is critical for synaptic integration and excitation. These genes may exert effects on basic sensory integration and cognitive processes that underlie dissociative phenomena.
MeSH term(s)	Adenylyl Cyclases/genetics ; Adult ; Aged ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases/genetics ; Dissociative Disorders/genetics ; Dissociative Disorders/psychology ; Female ; Genome-Wide Association Study/methods ; Genome-Wide Association Study/statistics & numerical data ; Humans ; Male ; Middle Aged ; Nerve Tissue Proteins/genetics ; Polymorphism, Single Nucleotide/genetics ; Potassium Channels/genetics ; Severity of Illness Index ; Stress Disorders, Post-Traumatic/genetics ; Stress Disorders, Post-Traumatic/psychology ; Veterans/psychology ; Veterans/statistics & numerical data ; Young Adult
Chemical Substances	Nerve Tissue Proteins ; Potassium Channels ; DPP6 protein, human (EC 3.4.-) ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases (EC 3.4.14.-) ; Adenylyl Cyclases (EC 4.6.1.1) ; adenylyl cyclase 8 (EC 4.6.1.1)
Language	English
Publishing date	2014-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1378635-0
ISSN	1520-6394 ; 1091-4269
ISSN (online)	1520-6394
ISSN	1091-4269
DOI	10.1002/da.22260
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Article ; Online: Clustering by genetic ancestry using genome-wide SNP data.

Solovieff, Nadia / Hartley, Stephen W / Baldwin, Clinton T / Perls, Thomas T / Steinberg, Martin H / Sebastiani, Paola

BMC genetics

2010 Volume 11, Page(s) 108

Abstract: Background: Population stratification can cause spurious associations in a genome-wide association study (GWAS), and occurs when differences in allele frequencies of single nucleotide polymorphisms (SNPs) are due to ancestral differences between cases ... ...

Abstract	Background: Population stratification can cause spurious associations in a genome-wide association study (GWAS), and occurs when differences in allele frequencies of single nucleotide polymorphisms (SNPs) are due to ancestral differences between cases and controls rather than the trait of interest. Principal components analysis (PCA) is the established approach to detect population substructure using genome-wide data and to adjust the genetic association for stratification by including the top principal components in the analysis. An alternative solution is genetic matching of cases and controls that requires, however, well defined population strata for appropriate selection of cases and controls. Results: We developed a novel algorithm to cluster individuals into groups with similar ancestral backgrounds based on the principal components computed by PCA. We demonstrate the effectiveness of our algorithm in real and simulated data, and show that matching cases and controls using the clusters assigned by the algorithm substantially reduces population stratification bias. Through simulation we show that the power of our method is higher than adjustment for PCs in certain situations. Conclusions: In addition to reducing population stratification bias and improving power, matching creates a clean dataset free of population stratification which can then be used to build prediction models without including variables to adjust for ancestry. The cluster assignments also allow for the estimation of genetic heterogeneity by examining cluster specific effects.
MeSH term(s)	African Continental Ancestry Group/genetics ; Algorithms ; Case-Control Studies ; Cluster Analysis ; Computer Simulation ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genome-Wide Association Study/methods ; Human Genome Project ; Humans ; Polymorphism, Single Nucleotide ; Principal Component Analysis
Language	English
Publishing date	2010-12-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1471-2156
ISSN (online)	1471-2156
DOI	10.1186/1471-2156-11-108
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Article ; Online: Corticotropin releasing hormone receptor 2 (CRHR-2) gene is associated with decreased risk and severity of posttraumatic stress disorder in women.

Wolf, Erika J / Mitchell, Karen S / Logue, Mark W / Baldwin, Clinton T / Reardon, Annemarie F / Humphries, Donald E / Miller, Mark W

Depression and anxiety

2013 Volume 30, Issue 12, Page(s) 1161–1169

Abstract: Background: The corticotropin releasing hormone (CRH) system has been implicated in a variety of anxiety and mood-based symptoms and disorders. CRH receptor-2 (CRHR-2) plays a role in attenuating biological responses to stressful life events and trauma, ...

Abstract	Background: The corticotropin releasing hormone (CRH) system has been implicated in a variety of anxiety and mood-based symptoms and disorders. CRH receptor-2 (CRHR-2) plays a role in attenuating biological responses to stressful life events and trauma, making the CRHR-2 gene a strong candidate to study in relationship to PTSD. Methods: The sample was 491 trauma-exposed white non-Hispanic veterans and their cohabitating intimate partners assessed via structured interview for lifetime DSM-IV PTSD; just over 60% met criteria for the disorder. Thirty-one single nucleotide polymorphisms (SNPs) in and near CRHR-2, obtained from an array of 2.5 million markers, were tested for association with PTSD diagnosis and symptom severity in the whole sample and in men and women separately. Results: Ten SNPs showed nominally significant evidence of association with PTSD in the full sample and two SNPs (rs8192496 and rs2190242) were significant after permutation-based multiple testing correction (uncorrected ps = .0004 and .0005, odds ratios = .60 and .58, respectively). Analyses stratified by sex revealed that the effect was specific to women, who comprised 35% of the sample (uncorrected ps = .0003 and .0002, odds ratios = .41 and .35, respectively). Two additional SNPs (rs2267715 and rs2284218) also showed significant association with PTSD in women (both uncorrected ps = .001, both odds ratios = .48). Conclusions: Results suggest that CRHR-2 variants may affect risk for PTSD in women by attenuating the stress response and reducing symptoms of the disorder.
MeSH term(s)	Adult ; Aged ; European Continental Ancestry Group/genetics ; European Continental Ancestry Group/psychology ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Receptors, Corticotropin-Releasing Hormone/genetics ; Severity of Illness Index ; Sex Factors ; Spouses/psychology ; Stress Disorders, Post-Traumatic/genetics ; Stress Disorders, Post-Traumatic/psychology ; Veterans/psychology ; Young Adult
Chemical Substances	CRF receptor type 2 ; Receptors, Corticotropin-Releasing Hormone
Language	English
Publishing date	2013-10-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1378635-0
ISSN	1520-6394 ; 1091-4269
ISSN (online)	1520-6394
ISSN	1091-4269
DOI	10.1002/da.22176
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Article ; Online: Clustering by genetic ancestry using genome-wide SNP data

Steinberg Martin H / Perls Thomas T / Baldwin Clinton T / Hartley Stephen W / Solovieff Nadia / Sebastiani Paola

BMC Genetics, Vol 11, Iss 1, p

2010 Volume 108

Abstract: Abstract Background Population stratification can cause spurious associations in a genome-wide association study (GWAS), and occurs when differences in allele frequencies of single nucleotide polymorphisms (SNPs) are due to ancestral differences between ... ...

Abstract	Abstract Background Population stratification can cause spurious associations in a genome-wide association study (GWAS), and occurs when differences in allele frequencies of single nucleotide polymorphisms (SNPs) are due to ancestral differences between cases and controls rather than the trait of interest. Principal components analysis (PCA) is the established approach to detect population substructure using genome-wide data and to adjust the genetic association for stratification by including the top principal components in the analysis. An alternative solution is genetic matching of cases and controls that requires, however, well defined population strata for appropriate selection of cases and controls. Results We developed a novel algorithm to cluster individuals into groups with similar ancestral backgrounds based on the principal components computed by PCA. We demonstrate the effectiveness of our algorithm in real and simulated data, and show that matching cases and controls using the clusters assigned by the algorithm substantially reduces population stratification bias. Through simulation we show that the power of our method is higher than adjustment for PCs in certain situations. Conclusions In addition to reducing population stratification bias and improving power, matching creates a clean dataset free of population stratification which can then be used to build prediction models without including variables to adjust for ancestry. The cluster assignments also allow for the estimation of genetic heterogeneity by examining cluster specific effects.
Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	310
Language	English
Publishing date	2010-12-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article ; Online: Fetal hemoglobin in sickle cell anemia.

Akinsheye, Idowu / Alsultan, Abdulrahman / Solovieff, Nadia / Ngo, Duyen / Baldwin, Clinton T / Sebastiani, Paola / Chui, David H K / Steinberg, Martin H

Blood

2011 Volume 118, Issue 1, Page(s) 19–27

Abstract: Fetal hemoglobin (HbF) is the major genetic modulator of the hematologic and clinical features of sickle cell disease, an effect mediated by its exclusion from the sickle hemoglobin polymer. Fetal hemoglobin genes are genetically regulated, and the level ...

Abstract	Fetal hemoglobin (HbF) is the major genetic modulator of the hematologic and clinical features of sickle cell disease, an effect mediated by its exclusion from the sickle hemoglobin polymer. Fetal hemoglobin genes are genetically regulated, and the level of HbF and its distribution among sickle erythrocytes is highly variable. Some patients with sickle cell disease have exceptionally high levels of HbF that are associated with the Senegal and Saudi-Indian haplotype of the HBB-like gene cluster; some patients with different haplotypes can have similarly high HbF. In these patients, high HbF is associated with generally milder but not asymptomatic disease. Studying these persons might provide additional insights into HbF gene regulation. HbF appears to benefit some complications of disease more than others. This might be related to the premature destruction of erythrocytes that do not contain HbF, even though the total HbF concentration is high. Recent insights into HbF regulation have spurred new efforts to induce high HbF levels in sickle cell disease beyond those achievable with the current limited repertory of HbF inducers.
MeSH term(s)	Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/genetics ; Anemia, Sickle Cell/pathology ; Erythrocytes/metabolism ; Erythrocytes/pathology ; Fetal Hemoglobin/genetics ; Fetal Hemoglobin/metabolism ; Haplotypes ; Humans ; Severity of Illness Index
Chemical Substances	Fetal Hemoglobin (9034-63-3)
Language	English
Publishing date	2011-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2011-03-325258
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Article ; Online: The dopamine D3 receptor gene and posttraumatic stress disorder.

Wolf, Erika J / Mitchell, Karen S / Logue, Mark W / Baldwin, Clinton T / Reardon, Annemarie F / Aiello, Alison / Galea, Sandro / Koenen, Karestan C / Uddin, Monica / Wildman, Derek / Miller, Mark W

Journal of traumatic stress

2014 Volume 27, Issue 4, Page(s) 379–387

Abstract: The dopamine D3 receptor (DRD3) gene has been implicated in schizophrenia, autism, and substance use-disorders and is related to emotion reactivity, executive functioning, and stress-responding, processes impaired in posttraumatic stress disorder (PTSD). ...

Abstract	The dopamine D3 receptor (DRD3) gene has been implicated in schizophrenia, autism, and substance use-disorders and is related to emotion reactivity, executive functioning, and stress-responding, processes impaired in posttraumatic stress disorder (PTSD). The aim of this candidate gene study was to evaluate DRD3 polymorphisms for association with PTSD. The discovery sample was trauma-exposed White, non-Hispanic U.S. veterans and their trauma-exposed intimate partners (N = 491); 60.3% met criteria for lifetime PTSD. The replication sample was 601 trauma-exposed African American participants living in Detroit, Michigan; 23.6% met criteria for lifetime PTSD. Genotyping was based on high-density bead chips. In the discovery sample, 4 single nucleotide polymorphisms (SNPs), rs2134655, rs201252087, rs4646996, and rs9868039, showed evidence of association with PTSD and withstood correction for multiple testing. The minor alleles were associated with reduced risk for PTSD (OR range = 0.59 to 0.69). In the replication sample, rs2251177, located 149 base pairs away from the most significant SNP in the discovery sample, was nominally associated with PTSD in men (OR = 0.32). Although the precise role of the D3 receptor in PTSD is not yet known, its role in executive functioning and emotional reactivity, and the sensitivity of the dopamine system to environmental stressors could potentially explain this association.
MeSH term(s)	Adolescent ; Adult ; Black or African American/genetics ; Aged ; Aged, 80 and over ; Alleles ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Receptors, Dopamine D3/genetics ; Sex Factors ; Spouses/psychology ; Stress Disorders, Post-Traumatic/genetics ; United States ; Veterans/psychology ; White People/genetics ; Young Adult
Chemical Substances	Receptors, Dopamine D3
Language	English
Publishing date	2014-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639478-4
ISSN	1573-6598 ; 0894-9867
ISSN (online)	1573-6598
ISSN	0894-9867
DOI	10.1002/jts.21937
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Article ; Online: Serum paraoxonase activity is associated with variants in the PON gene cluster and risk of Alzheimer disease.

Erlich, Porat M / Lunetta, Kathryn L / Cupples, L Adrienne / Abraham, Carmela R / Green, Robert C / Baldwin, Clinton T / Farrer, Lindsay A

Neurobiology of aging

2010 Volume 33, Issue 5, Page(s) 1015.e7–23

Abstract: Previous studies have shown association of single nucleotide polymorphisms (SNPs) in 3 contiguous genes (PON1, PON2, and PON3) encoding paraoxonase with risk of Alzheimer disease (AD). We evaluated the association of serum paraoxonase activity measured ... ...

Abstract	Previous studies have shown association of single nucleotide polymorphisms (SNPs) in 3 contiguous genes (PON1, PON2, and PON3) encoding paraoxonase with risk of Alzheimer disease (AD). We evaluated the association of serum paraoxonase activity measured by phenyl acetate (PA) and thiobutyl butyrolactone (TBBL) with risk of AD and with 26 SNPs spanning the PON gene cluster in 266 AD cases and 306 sibling controls from the MIRAGE study. The odds of AD (adjusted for age, gender, and ethnicity) increased 20% for each standard deviation decrease in PA or TBBL activity. There were association signals with activity in all 3 genes. Haplotypes including SNPs spanning the PON genes were generally more significant than haplotypes comprising SNPs from 1 gene. Significant interactions were observed between SNP pairs located across the PON cluster with either serum activity measure as the outcome, and between several PON SNPs and PA activity with AD status as the outcome. Our results suggest that low serum paraoxonase activity is a risk factor for AD. Furthermore, multiple variants in PON influence serum paraoxonase activity and their effects may be synergistic.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/enzymology ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Aryldialkylphosphatase/blood ; Aryldialkylphosphatase/deficiency ; Aryldialkylphosphatase/genetics ; Aryldialkylphosphatase/physiology ; Drug Synergism ; Female ; Genetic Predisposition to Disease/epidemiology ; Genetic Predisposition to Disease/genetics ; Genetic Variation ; Humans ; Male ; Multigene Family/genetics ; Polymorphism, Single Nucleotide/genetics ; Risk Factors
Chemical Substances	Aryldialkylphosphatase (EC 3.1.8.1) ; PON1 protein, human (EC 3.1.8.1) ; PON2 protein, human (EC 3.1.8.1) ; PON3 protein, human (EC 3.1.8.1)
Language	English
Publishing date	2010-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2010.08.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

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