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Article ; Online: The Impact of COVID-19 on the All of Us Research Program.

Hedden, Sarra L / McClain, James / Mandich, Allison / Baskir, Rubin / Caulder, Mark S / Denny, Joshua C / Hamlet, Michelle R J / Prabhu Das, Irene / McNeil Ford, Nicole / Lopez-Class, Maria / Elmi, Ahmed / Wallace, Roshedah / Linkie, Amantha / Garriock, Holly A

American journal of epidemiology

2022 Volume 192, Issue 1, Page(s) 11–24

Abstract: The All of Us Research Program, a health and genetics epidemiologic data collection program, has been substantially affected by the coronavirus disease 2019 (COVID-19) pandemic. Although the program is highly digital in nature, certain aspects of the ... ...

Abstract	The All of Us Research Program, a health and genetics epidemiologic data collection program, has been substantially affected by the coronavirus disease 2019 (COVID-19) pandemic. Although the program is highly digital in nature, certain aspects of the data collection require in-person interaction between staff and participants. Before the pandemic, the program was enrolling approximately 12,500 participants per month at more than 400 clinical sites. In March 2020, because of the pandemic, all in-person activity at program sites and by engagement partners was paused to develop processes and procedures for in-person activities that incorporated strict safety protocols. In addition, the program adopted new data collection methodologies to reduce the need for in-person activities. Through February 2022, a total of 224 clinical sites had reactivated in-person activity, and all enrollment and engagement partners have adopted new data collection methods that can be used remotely. As the COVID-19 pandemic persists, the program continues to require safety procedures for in-person activity and continues to generate and pilot methodologies that reduce risk and make it easier for participants to provide information.
MeSH term(s)	Humans ; COVID-19/epidemiology ; Pandemics/prevention & control ; Population Health ; Data Collection
Language	English
Publishing date	2022-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2937-3
ISSN	1476-6256 ; 0002-9262
ISSN (online)	1476-6256
ISSN	0002-9262
DOI	10.1093/aje/kwac169
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Article ; Online: Genetic studies of drug response and side effects in the STAR*D study, part 1.

Garriock, Holly A / Hamilton, Steven P

The Journal of clinical psychiatry

2009 Volume 70, Issue 8, Page(s) 1186–1187

MeSH term(s)	Antidepressive Agents/adverse effects ; Antidepressive Agents/therapeutic use ; Depressive Disorder, Major/drug therapy ; Depressive Disorder, Major/genetics ; Genetic Markers ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Humans ; Pharmacogenetics ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Randomized Controlled Trials as Topic/statistics & numerical data ; Serotonin Plasma Membrane Transport Proteins/genetics ; Treatment Outcome
Chemical Substances	Antidepressive Agents ; Genetic Markers ; SLC6A4 protein, human ; Serotonin Plasma Membrane Transport Proteins
Language	English
Publishing date	2009-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	716287-x
ISSN	1555-2101 ; 0160-6689
ISSN (online)	1555-2101
ISSN	0160-6689
DOI	10.4088/JCP.09ac05519
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Article ; Online: Genetic studies of drug response and side effects in the STAR*D study, part 2.

Garriock, Holly A / Hamilton, Steven P

The Journal of clinical psychiatry

2009 Volume 70, Issue 9, Page(s) 1323–1325

MeSH term(s)	Antidepressive Agents/adverse effects ; Antidepressive Agents/therapeutic use ; Citalopram/adverse effects ; Citalopram/therapeutic use ; Depressive Disorder, Major/drug therapy ; Depressive Disorder, Major/genetics ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study ; Genotype ; Humans ; Pharmacogenetics ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Randomized Controlled Trials as Topic/statistics & numerical data ; Serotonin Plasma Membrane Transport Proteins/genetics ; Sexual Dysfunctions, Psychological/chemically induced ; Suicide/psychology ; Treatment Outcome
Chemical Substances	Antidepressive Agents ; Genetic Markers ; SLC6A4 protein, human ; Serotonin Plasma Membrane Transport Proteins ; Citalopram (0DHU5B8D6V)
Language	English
Publishing date	2009-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	716287-x
ISSN	1555-2101 ; 0160-6689
ISSN (online)	1555-2101
ISSN	0160-6689
DOI	10.4088/JCP.09ac05522
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Article ; Online: Design and Implementation of the All of Us Research Program COVID-19 Participant Experience (COPE) Survey.

Schulkey, Claire E / Litwin, Tamara R / Ellsworth, Genevieve / Sansbury, Heather / Ahmedani, Brian K / Choi, Karmel W / Cronin, Robert M / Kloth, Yasmin / Ashbeck, Alan W / Sutherland, Scott / Mapes, Brandy M / Begale, Mark / Bhat, Geeta / King, Paula / Marginean, Kayla / Wolfe, Keri Ann / Kouame, Aymone / Raquel, Carmina / Ratsimbazafy, Francis /

Bornemeier, Zach / Neumeier, Kyle / Baskir, Rubin / Gebo, Kelly A / Denny, Joshua / Smoller, Jordan W / Garriock, Holly A

American journal of epidemiology

2023 Volume 192, Issue 6, Page(s) 972–986

Abstract: In response to the rapidly evolving coronavirus disease 2019 (COVID-19) pandemic, the All of Us Research Program longitudinal cohort study developed the COVID-19 Participant Experience (COPE) survey to better understand the pandemic experiences and ... ...

Abstract	In response to the rapidly evolving coronavirus disease 2019 (COVID-19) pandemic, the All of Us Research Program longitudinal cohort study developed the COVID-19 Participant Experience (COPE) survey to better understand the pandemic experiences and health impacts of COVID-19 on diverse populations within the United States. Six survey versions were deployed between May 2020 and March 2021, covering mental health, loneliness, activity, substance use, and discrimination, as well as COVID-19 symptoms, testing, treatment, and vaccination. A total of 104,910 All of Us Research Program participants, of whom over 73% were from communities traditionally underrepresented in biomedical research, completed 275,201 surveys; 9,693 completed all 6 surveys. Response rates varied widely among demographic groups and were lower among participants from certain racial and ethnic minority populations, participants with low income or educational attainment, and participants with a Spanish language preference. Survey modifications improved participant response rates between the first and last surveys (13.9% to 16.1%, P < 0.001). This paper describes a data set with longitudinal COVID-19 survey data in a large, diverse population that will enable researchers to address important questions related to the pandemic, a data set that is of additional scientific value when combined with the program's other data sources.
MeSH term(s)	Humans ; United States/epidemiology ; COVID-19/epidemiology ; Ethnicity ; SARS-CoV-2 ; Longitudinal Studies ; Minority Groups ; Population Health
Language	English
Publishing date	2023-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2937-3
ISSN	1476-6256 ; 0002-9262
ISSN (online)	1476-6256
ISSN	0002-9262
DOI	10.1093/aje/kwad035
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Article: Association Study of Genotype by Depressive Response during Tryptophan Depletion in Subjects Recovered from Major Depression.

Moreno, Francisco A / Erickson, Robert P / Garriock, Holly A / Gelernter, Joel / Mintz, Jim / Oas-Terpstra, Jennifer / Davies, Marilyn A / Delgado, Pedro L

Molecular neuropsychiatry

2015 Volume 1, Issue 3, Page(s) 165–174

Abstract: Purpose: The brief and reversible mood response to acute tryptophan (TRP) depletion (ATD) is being studied as a trait marker in subjects considered at risk for major depression (MD).: Procedures: ATD was administered to 64 subjects (54 European- ... ...

Abstract	Purpose: The brief and reversible mood response to acute tryptophan (TRP) depletion (ATD) is being studied as a trait marker in subjects considered at risk for major depression (MD). Procedures: ATD was administered to 64 subjects (54 European-Americans, and10 from other races) with personal and family history of MD. They were in remission and had been medication-free for at least three months. Subjects received an active and sham condition in a random assignment, double-blind crossover design. They were genotyped for serotonin-related candidate genes, and mood response was quantified with the Hamilton Depression Rating Scale (HDRS). Data were analyzed using Poisson regression with repeated measures and latent trajectory models. Results: Compared to the sham control, active ATD caused modest depressive changes showing significant main effects of test condition (χ Conclusions and message: ATD may help the identification of biological subtypes of MD. These data are consistent with imaging reports implicating 5-HT2A receptor function in ATD phenotypes.
Language	English
Publishing date	2015-09-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2806946-8
ISSN	2296-9179 ; 2296-9209
ISSN (online)	2296-9179
ISSN	2296-9209
DOI	10.1159/000439114
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Article: Association Study of Genotype by Depressive Response during Acute Tryptophan Depletion in Subjects Recovered from Major Depression

Moreno, Francisco A. / Erickson, Robert P. / Garriock, Holly A. / Gelernter, Joel / Mintz, Jim / Oas-Terpstra, Jennifer / Davies, Marilyn A. / Delgado, Pedro L.

Molecular Neuropsychiatry

2015 Volume 1, Issue 3, Page(s) 165–174

Abstract: Purpose: To study the brief and reversible mood response to acute tryptophan depletion (ATD) as a trait marker in subjects considered at risk for major depressive disorder (MDD). Procedures: ATD was administered to 64 subjects (54 European-Americans and ... ...

Institution	Departments of Psychiatry Pediatrics and Physiology, College of Medicine, The University of Arizona Health Sciences Center, Tucson, Ariz Division of Translational Research, National Institute of Mental Health, Bethesda, Md Department of Psychiatry, Yale University School of Medicine, VA Connecticut Health Care Center, New Haven, Conn Department of Psychiatry, University of Texas Health Sciences Center San Antonio, San Antonio, Tex Health and Community Systems, University of Pittsburgh School of Nursing, Pittsburgh, Pa., and Department of Psychiatry, University of Arkansas for Medical Sciences, Little Rock, Ark., USA
Abstract	Purpose: To study the brief and reversible mood response to acute tryptophan depletion (ATD) as a trait marker in subjects considered at risk for major depressive disorder (MDD). Procedures: ATD was administered to 64 subjects (54 European-Americans and 10 from other races) with a personal and family history of MDD. They were in remission and had been medication-free for at least 3 months. Subjects were randomly assignment to an active or sham condition in a double-blind crossover design. They were genotyped for serotonin-related candidate genes, and mood response was quantified with the Hamilton Depression Rating Scale (HDRS). Data were analyzed using Poisson regression with repeated measures and latent trajectory models. Results: Compared to the sham controls, active ATD caused modest depressive changes showing significant main effects of test condition (χ2 = 5.14, d.f. = 1, p = 0.023) and time (χ2 = 12.22, d.f. = 3, p = 0.007), but no significant interaction of time and test condition. Latent trajectory analysis revealed two groups, identified as depletion responders and non-responders. Those with the HTR2A rs6313 CC genotype had significantly higher HDRS scores during ATD (χ2 = 11.72, d.f. = 1, p = 0.0006). Conclusions: ATD may help identifying the biological subtypes of MDD. These data are consistent with imaging reports implicating 5-HT2A receptor function in ATD phenotypes.
Keywords	STin2 ; <italic>HTR1A</italic> ; <italic>HTR2A</italic> ; TPH2 ; <italic>SLC6A4</italic> ; 5-HTTLPR ; Serotonin candidate genes ; Neurotransmitter depletion ; Depression endophenotype
Language	English
Publishing date	2015-09-24
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Original Paper
ZDB-ID	2806946-8
ISSN	2296-9179 ; 2296-9209
ISSN (online)	2296-9179
ISSN	2296-9209
DOI	10.1159/000439114
Database	Karger publisher's database

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Article ; Online: A genome-wide association study of a sustained pattern of antidepressant response.

Hunter, Aimee M / Leuchter, Andrew F / Power, Robert A / Muthén, Bengt / McGrath, Patrick J / Lewis, Cathryn M / Cook, Ian A / Garriock, Holly A / McGuffin, Peter / Uher, Rudolf / Hamilton, Steven P

Journal of psychiatric research

2013 Volume 47, Issue 9, Page(s) 1157–1165

Abstract: Genome-wide association studies (GWAS) have failed to replicate common genetic variants associated with antidepressant response, as defined using a single endpoint. Genetic influences may be discernible by examining individual variation between sustained ...

Abstract	Genome-wide association studies (GWAS) have failed to replicate common genetic variants associated with antidepressant response, as defined using a single endpoint. Genetic influences may be discernible by examining individual variation between sustained versus unsustained patterns of response, which may distinguish medication effects from non-specific, or placebo responses to active medication. We conducted a GWAS among 1116 subjects with Major Depressive Disorder from the Sequenced Treatment Alternatives to Relieve Depression (STARD) trial who were characterized using Growth Mixture Modeling as showing a sustained versus unsustained pattern of clinical response over 12 weeks of treatment with citalopram. Replication analyses examined 585 subjects from the Genome-based Therapeutic Drugs for Depression (GENDEP) trial. The strongest association with sustained as opposed to unsustained response in STARD involved a single nucleotide polymorphism (SNP; rs10492002) within the acyl-CoA synthetase short-chain family member 3 gene (ACSS3, p-value=4.5×10(-6), odds ratio=0.61). No SNPs met our threshold for genome-wide significance. SNP data were available in GENDEP for 18 of the top 25 SNPs in STAR*D. The most replicable association was with SNP rs7816924 (p=0.008, OR=1.58); no SNP met the replication p-value threshold of 0.003. Joint analysis of these 18 SNPs resulted in the strongest signal coming from rs7816924 (p=2.11×10(-7)), which resides in chondroitin sulfate N-acetylgalactosaminyltransferase 1 gene (CSGALNACT1). An exploratory genetic pathway analysis revealed evidence for an involvement of the KEGG pathway of long-term potentiation (FDR=.02). Results suggest novel genetic associations to sustained response.
MeSH term(s)	Antidepressive Agents/therapeutic use ; Clinical Trials as Topic ; Confidence Intervals ; Depressive Disorder, Major/drug therapy ; Depressive Disorder, Major/genetics ; Genome-Wide Association Study ; Genotype ; Humans ; Odds Ratio ; Pharmacogenetics ; Polymorphism, Single Nucleotide/genetics
Chemical Substances	Antidepressive Agents
Language	English
Publishing date	2013-05-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3148-3
ISSN	1879-1379 ; 0022-3956
ISSN (online)	1879-1379
ISSN	0022-3956
DOI	10.1016/j.jpsychires.2013.05.002
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Article ; Online: Association of mu-opioid receptor variants and response to citalopram treatment in major depressive disorder.

Garriock, Holly A / Tanowitz, Michael / Kraft, Jeffrey B / Dang, Vu C / Peters, Eric J / Jenkins, Greg D / Reinalda, Megan S / McGrath, Patrick J / von Zastrow, Mark / Slager, Susan L / Hamilton, Steven P

The American journal of psychiatry

2010 Volume 167, Issue 5, Page(s) 565–573

Abstract: Objective: Because previous preclinical and clinical studies have implicated the endogenous opioid system in major depression and in the neurochemical action of antidepressants, the authors examined how DNA variation in the mu-opioid receptor gene may ... ...

Abstract	Objective: Because previous preclinical and clinical studies have implicated the endogenous opioid system in major depression and in the neurochemical action of antidepressants, the authors examined how DNA variation in the mu-opioid receptor gene may influence population variation in response to citalopram treatment. Method: A total of 1,953 individuals from the Sequenced Treatment Alternatives to Relieve Depression (STARD) study were treated with citalopram and genotyped for 53 single nucleotide polymorphisms (SNPs) in a 100-kb region of the OPRM1 gene. The sample consisted of Non-Hispanic Caucasians, Hispanic Caucasians, and African Americans. Population stratification was corrected using 119 ancestry informative markers and principal components analysis. Markers were tested for association with phenotypes for general and specific citalopram response as well as remission. Results:* Association between one SNP and specific citalopram response was observed. After Bonferroni correction, the strongest finding was the association between the rs540825 SNP and specific response. The rs540825 polymorphism is a nonsynonymous SNP in the final exon of the mu-opioid receptor-1X isoform of the OPRM1 gene, resulting in a histidine to glutamine change in the intracellular domain of the receptor. When Hispanic and Non-Hispanic Caucasians were analyzed separately, similar results in the population-corrected analyses were detected. Conclusions: These results suggest that rates of response to antidepressants and consequent remission from major depressive disorder are influenced by variation in the mu-opioid receptor gene as a result of either an effect on placebo response or true pharmacologic response.
MeSH term(s)	Antidepressive Agents, Second-Generation/therapeutic use ; Citalopram/therapeutic use ; Depressive Disorder, Major/drug therapy ; Depressive Disorder, Major/genetics ; European Continental Ancestry Group/genetics ; Genetic Association Studies ; Genotype ; Haplotypes/genetics ; Hispanic Americans/genetics ; Humans ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Psychiatric Status Rating Scales ; Receptors, Opioid, mu/genetics ; Treatment Outcome
Chemical Substances	Antidepressive Agents, Second-Generation ; OPRM1 protein, human ; Receptors, Opioid, mu ; Citalopram (0DHU5B8D6V)
Language	English
Publishing date	2010-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	280045-7
ISSN	1535-7228 ; 0002-953X
ISSN (online)	1535-7228
ISSN	0002-953X
DOI	10.1176/appi.ajp.2009.08081167
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Article ; Online: Number of risk genotypes is a risk factor for major depressive disorder

Schwartz Thomas / Burke William J / Burke Michael / Carpenter Linda L / Kling Mitchel A / Delgado Pedro / Garriock Holly A / Marangell Lauren B / Husain Mustafa / Erickson Robert P / Moreno Francisco A

Behavioral and Brain Functions, Vol 2, Iss 1, p

a case control study

2006 Volume 24

Abstract: Abstract Background The objective of the study was to determine the genetic basis of Major Depressive Disorder, and the capacity to respond to antidepressant treatment. An association study of 21 candidate polymorphisms relevant to monoamine function and ...

Abstract	Abstract Background The objective of the study was to determine the genetic basis of Major Depressive Disorder, and the capacity to respond to antidepressant treatment. An association study of 21 candidate polymorphisms relevant to monoamine function and the mechanism of antidepressant response was conducted in 3 phenotypically distinct samples: a group with chronic or recurrent depression unable to respond to antidepressants (non-responders) (n = 58), a group capable of symptomatic improvement with or without treatment (responders) (n = 39), and volunteer controls (n = 85). The responders and non-responders constituted a larger group of depressed subjects. Methods A candidate gene approach was employed to asses the genetics basis of Major Depressive Disorder. The genotypic frequencies of selected polymorphisms were compared between the controls and depressed subjects. To asses the genetics basis of the capacity to respond to antidepressant treatment, the responders were compared to the non-responders. Candidate genes were chosen based on functional studies and proximity to whole genome linkage findings in the literature. Risk genotypes were identified by previous functional studies and association studies. Results A statistically significant difference in genotype frequency for the SLC6A4 intron 2 VNTR was detected between the subjects with a history of depression and controls (p = 0.004). Surprisingly, a statistically significant difference was detected between responders and non-responders for the DRD4 exon III VNTR genotype frequencies (p = 0.009). Furthermore, a difference between the controls and depressed subjects as well as between the controls and non-responders was detected for the number and distribution of risk genotypes in each group. Conclusion An association between several monoamine-related genes and Major Depressive Disorder is supported. The data suggest that the two depressive phenotypes are genetically different, inferring that the genetic basis for the capacity to respond to standard antidepressant treatment, and the genetic susceptibility to Major Depressive Disorder may be independent. In addition, a proof of concept is provided demonstrating that the number of risk genotypes may be an indication of susceptibility of major depressive disorder and the severity of the disorder.
Keywords	Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Neurology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	150
Language	English
Publishing date	2006-07-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A genomewide association study of citalopram response in major depressive disorder.

Garriock, Holly A / Kraft, Jeffrey B / Shyn, Stanley I / Peters, Eric J / Yokoyama, Jennifer S / Jenkins, Gregory D / Reinalda, Megan S / Slager, Susan L / McGrath, Patrick J / Hamilton, Steven P

Biological psychiatry

2009 Volume 67, Issue 2, Page(s) 133–138

Abstract: Background: Antidepressant response is likely influenced by genetic constitution, but the actual genes involved have yet to be determined. We have carried out a genomewide association study to determine whether common DNA variation influences ... ...

Abstract	Background: Antidepressant response is likely influenced by genetic constitution, but the actual genes involved have yet to be determined. We have carried out a genomewide association study to determine whether common DNA variation influences antidepressant response. Methods: Our sample is derived from Level 1 participants in the Sequenced Treatment Alternatives to Relieve Depression (STARD) study, all treated with citalopram. Association for the response phenotype included 883 responders and 608 nonresponders. For the remission phenotype, 743 subjects that achieved remission were compared with 608 nonresponders. We used a subset of single nucleotide polymorphisms (SNPs; n = 430,198) from the Affymetrix 500K and 5.0 Human SNP Arrays, and association analysis was carried out after correcting for population stratification. Results:* We identified three SNPs associated with response with p values less than 1 x 10(-5) near the UBE3C gene (rs6966038, p = 4.65 x 10(-7)), another 100 kb away from BMP7 (rs6127921, p = 3.45 x 10(-6)), and a third that is intronic in the RORA gene (rs809736, p = 8.19 x 10(-6)). These same SNPs were also associated with remission. Thirty-nine additional SNPs are of interest with p values < or = .0001 for the response and remission phenotypes. Conclusions: Although the findings reported here do not meet a genomewide threshold for significance, the regions identified from this study provide targets for independent replication and novel pathways to investigate mechanisms of antidepressant response. This study was not placebo controlled, making it possible that we are also observing associations to nonspecific aspects of drug treatment of depression.
MeSH term(s)	Antidepressive Agents, Second-Generation/therapeutic use ; Bone Morphogenetic Protein 7/genetics ; Citalopram/therapeutic use ; Cluster Analysis ; Depressive Disorder, Major/drug therapy ; Depressive Disorder, Major/genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Humans ; Male ; Nuclear Receptor Subfamily 1, Group F, Member 1/genetics ; Odds Ratio ; Pharmacogenetics ; Polymorphism, Single Nucleotide/genetics ; Psychiatric Status Rating Scales ; Sex Factors ; Statistics as Topic ; Treatment Outcome ; Ubiquitin-Conjugating Enzymes/genetics
Chemical Substances	Antidepressive Agents, Second-Generation ; BMP7 protein, human ; Bone Morphogenetic Protein 7 ; Nuclear Receptor Subfamily 1, Group F, Member 1 ; RORA protein, human ; Citalopram (0DHU5B8D6V) ; UBE2N protein, human (EC 2.3.2.23) ; Ubiquitin-Conjugating Enzymes (EC 2.3.2.23)
Language	English
Publishing date	2009-10-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2009.08.029
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