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Article: Intercontinental epidemiology of Alzheimer disease: a global approach to bad gene hunting.

Farrer, L A

2000 Volume 285, Issue 6, Page(s) 796–798

MeSH term(s)	African Continental Ancestry Group/genetics ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Asian Continental Ancestry Group/genetics ; European Continental Ancestry Group/genetics ; Global Health ; Humans ; Risk Factors
Language	English
Publishing date	2000-12-20
Publishing country	United States
Document type	Comment ; Editorial ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2958-0
ISSN	1538-3598 ; 0098-7484 ; 0254-9077 ; 0002-9955
ISSN (online)	1538-3598
ISSN	0098-7484 ; 0254-9077 ; 0002-9955
DOI	10.1001/jama.285.6.796
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Article: Familial risk for Alzheimer disease in ethnic minorities: nondiscriminating genes.

Farrer, L A

Archives of neurology

2000 Volume 57, Issue 1, Page(s) 28–29

MeSH term(s)	Alzheimer Disease/ethnology ; Alzheimer Disease/genetics ; Family Health ; Humans ; Minority Groups/statistics & numerical data ; Risk Factors ; United States/epidemiology
Language	English
Publishing date	2000-01
Publishing country	United States
Document type	Comment ; Editorial ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80049-1
ISSN	1538-3687 ; 0003-9942
ISSN (online)	1538-3687
ISSN	0003-9942
DOI	10.1001/archneur.57.1.28
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Article ; Online: A protocadherin gene cluster regulatory variant is associated with nicotine withdrawal and the urge to smoke.

Jensen, K P / Smith, A H / Herman, A I / Farrer, L A / Kranzler, H R / Sofuoglu, M / Gelernter, J

Molecular psychiatry

2016 Volume 22, Issue 2, Page(s) 242–249

Abstract: Nicotine withdrawal symptoms contribute to relapse in smokers, thereby prolonging the harm caused by smoking. To investigate the molecular basis for this phenomenon, we conducted a genome-wide association study of DSM-IV nicotine withdrawal in a sample ... ...

Abstract	Nicotine withdrawal symptoms contribute to relapse in smokers, thereby prolonging the harm caused by smoking. To investigate the molecular basis for this phenomenon, we conducted a genome-wide association study of DSM-IV nicotine withdrawal in a sample of African American (AA) and European American (EA) smokers. A combined AA and EA meta-analysis (n=8021) identified three highly correlated single nucleotide polymorphisms (SNPs) in the protocadherin (PCDH)-α, -β and -γ gene cluster on chromosome 5 that were associated with nicotine withdrawal (P<5 × 10
MeSH term(s)	Adult ; African Americans/genetics ; Cadherins/genetics ; Cadherins/metabolism ; Diagnostic and Statistical Manual of Mental Disorders ; European Continental Ancestry Group/genetics ; Female ; Gene Expression Regulation ; Genome-Wide Association Study ; Humans ; Male ; Multigene Family/genetics ; Nicotine/metabolism ; Polymorphism, Single Nucleotide/genetics ; Recurrence ; Smoking/genetics ; Smoking Cessation ; Substance Withdrawal Syndrome/genetics ; Tobacco Use Disorder/genetics
Chemical Substances	Cadherins ; PCDH1 protein, human ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2016-04-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/mp.2016.43
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Article: Gene localization by linkage analysis.

Farrer, L A

Otolaryngologic clinics of North America

1992 Volume 25, Issue 5, Page(s) 907–922

Abstract: Traditional genetic approaches have led to the identification of defects underlying an impressive array of diseases. Genetic terminology, Mendel's laws, chromosomes and linkage, statistical methods for linkage analysis, genetic markers, multilocus ... ...

Abstract	Traditional genetic approaches have led to the identification of defects underlying an impressive array of diseases. Genetic terminology, Mendel's laws, chromosomes and linkage, statistical methods for linkage analysis, genetic markers, multilocus mapping, strategies in linkage studies, linkage heterogeneity, and the future of linkage analysis are discussed in this article. The molecular basis for most disorders, however, cannot be gleaned because there is no identifiable primary metabolic disorder.
MeSH term(s)	Chromosome Mapping ; Genes ; Genetic Linkage/genetics ; Genetic Markers ; Humans
Chemical Substances	Genetic Markers
Language	English
Publishing date	1992-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	417489-6
ISSN	1557-8259 ; 0030-6665
ISSN (online)	1557-8259
ISSN	0030-6665
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Zs.B 183: Show issues

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Article ; Online: The α-endomannosidase gene (MANEA) is associated with panic disorder and social anxiety disorder.

Jensen, K P / Stein, M B / Kranzler, H R / Yang, B Z / Farrer, L A / Gelernter, J

Translational psychiatry

2014 Volume 4, Page(s) e353

Abstract: Unbiased genome-wide approaches can provide novel insights into the biological pathways that are important for human behavior and psychiatric disorder risk. The association of α-endomannosidase gene (MANEA) variants and cocaine-induced paranoia (CIP) was ...

Abstract	Unbiased genome-wide approaches can provide novel insights into the biological pathways that are important for human behavior and psychiatric disorder risk. The association of α-endomannosidase gene (MANEA) variants and cocaine-induced paranoia (CIP) was initially described in a study that used a whole-genome approach. Behavioral effects have been reported for other mannosidase genes, but MANEA function in humans and the clinical potential of the previous findings remain unclear. We hypothesized that MANEA would be associated with psychiatric phenotypes unrelated to cocaine use. We used a multi-stage association study approach starting with four psychiatric disorders to show an association between a MANEA single-nucleotide polymorphism (SNP; rs1133503) and anxiety disorders. In the first study of 2073 European American (EA) and 2459 African American subjects mostly with comorbid drug or alcohol dependence, we observed an association in EAs of rs1133503 with panic disorder (PD) (191 PD cases, odds ratio (OR)=1.7 (95% confidence interval (CI): 1.22-2.41), P=0.002). We replicated this finding in an independent sample of 142 PD cases (OR =1.53 (95% CI: 1.00-2.31), P=0.043) and extended it in an independent sample of 131 generalized social anxiety disorder cases (OR=2.15 (95% CI: 1.27-3.64), P=0.004). MANEA alleles and genotypes were also associated with gene expression differences in whole blood cells. Using publically available data, we observed a consistent effect on expression in brain tissue. We conclude that pathways involving α-endomannosidase warrant further investigation in relation to anxiety disorders.
MeSH term(s)	Adult ; African Americans/genetics ; African Americans/statistics & numerical data ; Blood Cells/metabolism ; Brain/metabolism ; Comorbidity ; European Continental Ancestry Group/genetics ; European Continental Ancestry Group/statistics & numerical data ; Female ; Gene Expression/genetics ; Genome-Wide Association Study ; Humans ; Male ; Mannosidases/genetics ; Mannosidases/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Middle Aged ; Panic Disorder/epidemiology ; Panic Disorder/genetics ; Phobic Disorders/epidemiology ; Phobic Disorders/genetics ; Polymorphism, Single Nucleotide/genetics ; Substance-Related Disorders/epidemiology ; Substance-Related Disorders/genetics ; United States/epidemiology ; Young Adult
Chemical Substances	Membrane Proteins ; MANEA protein, human (EC 3.2.1.-) ; Mannosidases (EC 3.2.1.-)
Language	English
Publishing date	2014-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/tp.2013.122
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Article ; Online: Genome-wide association study of therapeutic opioid dosing identifies a novel locus upstream of OPRM1.

Smith, A H / Jensen, K P / Li, J / Nunez, Y / Farrer, L A / Hakonarson, H / Cook-Sather, S D / Kranzler, H R / Gelernter, J

Molecular psychiatry

2017 Volume 22, Issue 3, Page(s) 346–352

Abstract: Opioids are very effective analgesics, but they are also highly addictive. Methadone is used to treat opioid dependence (OD), acting as a selective agonist at the μ-opioid receptor encoded by the gene OPRM1. Determining the optimal methadone maintenance ... ...

Abstract	Opioids are very effective analgesics, but they are also highly addictive. Methadone is used to treat opioid dependence (OD), acting as a selective agonist at the μ-opioid receptor encoded by the gene OPRM1. Determining the optimal methadone maintenance dose is time consuming; currently, no biomarkers are available to guide treatment. In methadone-treated OD subjects drawn from a case and control sample, we conducted a genome-wide association study of usual daily methadone dose. In African-American (AA) OD subjects (n=383), we identified a genome-wide significant association between therapeutic methadone dose (mean=68.0 mg, s.d.=30.1 mg) and rs73568641 (P=2.8 × 10
MeSH term(s)	Adult ; African Americans/genetics ; Alleles ; Analgesics, Opioid/administration & dosage ; Analgesics, Opioid/pharmacology ; Analgesics, Opioid/therapeutic use ; Dose-Response Relationship, Drug ; European Continental Ancestry Group/genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study/methods ; Genotype ; Humans ; Male ; Methadone/therapeutic use ; Middle Aged ; Morphine/therapeutic use ; Opioid-Related Disorders/genetics ; Pain/drug therapy ; Pain/genetics ; Polymorphism, Single Nucleotide/genetics ; Receptors, Opioid, mu/genetics ; United States
Chemical Substances	Analgesics, Opioid ; OPRM1 protein, human ; Receptors, Opioid, mu ; Morphine (76I7G6D29C) ; Methadone (UC6VBE7V1Z)
Language	English
Publishing date	2017-01-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/mp.2016.257
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Zs.A 4812: Show issues

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Article: Suicide and attempted suicide in Huntington disease: implications for preclinical testing of persons at risk.

Farrer, L A

American journal of medical genetics

1986 Volume 24, Issue 2, Page(s) 305–311

Abstract: Suicide behavior in Huntington disease (HD) was assessed by examining the proportion of deaths attributed to suicide among 452 deceased individuals with HD and the number and pattern of attempted suicides among a total population of 831 HD patients from ... ...

Abstract	Suicide behavior in Huntington disease (HD) was assessed by examining the proportion of deaths attributed to suicide among 452 deceased individuals with HD and the number and pattern of attempted suicides among a total population of 831 HD patients from the National Huntington Disease Research Roster. It was found that 5.7% of deaths among affected persons resulted from suicide and 27.6% of patients attempted suicide at least once. Comparison of this group with the general population indicated that the proportion of deaths due to suicide among persons with HD is almost four times greater than the corresponding proportion for the U.S. Caucasian population. Age at onset of HD was not significantly different between HD suicide and non-suicide patients, although suicide occurred more frequently in the early to middle stages of the illness. The "success" rate among HD suicide attempters did not differ from the general population rates in several western European countries. The relatively high suicide and attempted suicide rates in HD indicate that thorough psychological testing of at-risk persons and extensive patient support systems must be integral components of a program to identify HD gene carriers using a genetic marker.
MeSH term(s)	Humans ; Huntington Disease/complications ; Huntington Disease/mortality ; Risk ; Suicide/complications ; Suicide, Attempted
Language	English
Publishing date	1986-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	133387-2
ISSN	0148-7299
ISSN	0148-7299
DOI	10.1002/ajmg.1320240211
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Zs.A 1376: Show issues

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Article: Managing data for genetic linkage analysis.

Farrer, L A

American journal of human genetics

1986 Volume 39, Issue 1, Page(s) 146–147

MeSH term(s)	Computers ; Genetic Linkage ; Humans ; Software
Language	English
Publishing date	1986-07
Publishing country	United States
Document type	Letter
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
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Zs.A 107: Show issues

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Article: Diabetes mellitus in Huntington disease.

Farrer, L A

Clinical genetics

1985 Volume 27, Issue 1, Page(s) 62–67

Abstract: There have been conflicting reports that individuals with Huntington disease (HD) are prone to abnormalities of carbohydrate metabolism. In this study information about the incidence and control of diabetes mellitus in 620 probands (278 living, 332 ... ...

Abstract	There have been conflicting reports that individuals with Huntington disease (HD) are prone to abnormalities of carbohydrate metabolism. In this study information about the incidence and control of diabetes mellitus in 620 probands (278 living, 332 deceased) with HD and in their first and second degree relatives was obtained by questionnaire method from participants of the National HD Research Roster. Among the probands, 65 individuals (10.5%) were identified by the informant or verified by examination of Roster family records as diabetic. The prevalence of diabetes, particularly among those les than 50 years of age, is significantly greater than corresponding figures among the general U.S. Caucasian population (Scott 1977, Krolewski & Warram 1985). Incidence rates were not calculated because of ascertainment and other biases in the data. Results from the analysis of family data indicate that HD affected relatives of an HD proband with diabetes are 7 times as likely to have diabetes over the proband's non-HD relatives. A non-diabetic HD proband is equally likely to have an HD or non-HD relative with diabetes.
MeSH term(s)	Adult ; Aged ; Diabetes Complications ; Diabetes Mellitus/genetics ; Humans ; Huntington Disease/complications ; Huntington Disease/genetics ; Middle Aged
Language	English
Publishing date	1985-01
Publishing country	Denmark
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	221209-2
ISSN	1399-0004 ; 0009-9163
ISSN (online)	1399-0004
ISSN	0009-9163
DOI	10.1111/j.1399-0004.1985.tb00185.x
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Zs.A 413: Show issues

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Article: Exome Sequencing of Extended Families with Alzheimer's Disease Identifies Novel Genes Implicated in Cell Immunity and Neuronal Function.

Cukier, H N / Kunkle, B K / Hamilton, K L / Rolati, S / Kohli, M A / Whitehead, P L / Jaworski, J / Vance, J M / Cuccaro, M L / Carney, R M / Gilbert, J R / Farrer, L A / Martin, E R / Beecham, G W / Haines, J L / Pericak-Vance, M A

Journal of Alzheimer's disease & Parkinsonism

2017 Volume 7, Issue 4

Abstract: Objective: Alzheimer's disease (AD) is a neurodegenerative disorder for which more than 20 genetic loci have been implicated to date. However, studies demonstrate not all genetic factors have been identified. Therefore, in this study we seek to identify ...

Abstract	Objective: Alzheimer's disease (AD) is a neurodegenerative disorder for which more than 20 genetic loci have been implicated to date. However, studies demonstrate not all genetic factors have been identified. Therefore, in this study we seek to identify additional rare variants and novel genes potentially contributing to AD. Methods: Whole exome sequencing was performed on 23 multi-generational families with an average of eight affected subjects. Exome sequencing was filtered for rare, nonsynonymous and loss-of-function variants. Alterations predicted to have a functional consequence and located within either a previously reported AD gene, a linkage peak (LOD>2), or clustering in the same gene across multiple families, were prioritized. Results: Rare variants were found in known AD risk genes including Conclusion: Utilizing large families with a heavy burden of disease allowed for the identification of rare variants co-segregating with disease. Variants were identified in both known AD risk genes and in novel genes.
Language	English
Publishing date	2017-07-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2711981-6
ISSN	2161-0460
ISSN	2161-0460
DOI	10.4172/2161-0460.1000355
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