Emmanuel Peprah

Assistant Professor of Global and Environmental Health

Professional overview

Dr. Emmanuel Peprah’s research interests lie at the confluence of understanding what, why, and how some evidence-based interventions work in some populations and not others. The programattic focus of his research is understanding the contextual factors that influence the burden of co-morbidity in people living with HIV/AIDS (PLWH), with a particular focus on cardiovascular disease risk factors and mental health. As the burden of non-communicable diseases (NCDs) continues to increase, there is an opportunity to integrate NCD management into HIV care with implemention strategies that leverage the global infrasturcture designed to improve care delivery for PLWH. Dr. Peprah has built collaborations with multidisciplinary teams of investigators, both nationally and internationally, to address the high burden of comorbidity in PLWH globally.  He is also the founder of the Baakoye Foundation, a nonprofit philanthropic organization dedicated to serving people in sub-Saharan Africa, and co-founder of the Washington Leaders Index (WLI), which aims to empower the next generation of emerging leaders through active, innovative, and inclusive leadership programs. Both nonprofit organizations serve the needs of children and people globally within the domains of education and health.

Before joining GPH, Dr. Peprah was a senior program official at the National Institutes of Health (NIH), where he worked with senior leadership to oversee strategic planning, initiative development, and implementation of research priorities in the areas of translational research, implementation science, and global health. He led and managed HIV/AIDS programs and a $10 million portfolio as part of the National Heart, Lung, and Blood Institute’s Trans-Omics for Precision Medicine Program. He was instrumental in launching the Human, Heredity, and Health in Africa (H3Africa) Initiative, a multimillion trans-NIH program, and served on its executive board. Dr. Peprah has received several awards for strategic planning, management, and implementation of large-scale NIH programs.

Education

BS, Biology, Texas A&M University, Commerce, TX

PhD, Molecular Biology & Biomedical Science, Meharry Medical College, Nashville, TN

Honors and awards

NIH Director’s Award for Leadership H3Africa Stage II Team: For exceptional leadership and dedication in implementing Stage II of the Human Heredity and Health in Africa program (2018)

NHLBI’s Director's for Outstanding Service (2018)

NHLBI’s Director's for Outstanding Service Partnership/Collaboration Award for bringing multiple disciplines together to understand HIV-related co-morbidities and prepare for the challenges presented by the complex conditions of the new HIV era (2018)

NHLBI’s Director's for Outstanding Translational Science Award for demonstrating exemplary leadership and service in advancing translation research (2017)

Federal Service Career Promotion (2016)

NHLBI’s Director's for Outstanding Translational Science Award as part of the Center for Translational Research and Implementation Science (CTRIS) Leadership Team for demonstrating exemplary leadership and service in advancing CTRIS’s translation (2016)

NHLBI’s Director's for Breath of Fresh Air (Innovation) award for exemplary work evaluating NHLBI’s support for multi-project research grants and proposing creative and innovative enhancements to the NHLBI’s program project grants (PPG) (2016)

NHLBI’s Director's for Learning Environment Award for fostering a learning environment through effective administration, knowledge sharing, and thoughtful implementation of the NHLBI R35 Program (2016)

NHLBI’s Director's for Partnership/Collaboration in recognition of outstanding collaborative efforts in developing a conceptual framework for the NHLBI R35 program to provide greater funding stability and flexibility to investigators (2015)

NIH Director's Common Fund Leadership Award for the NIH Common Fund Early Independence Award Program (2013)

NIH Director's Award as a member of the Common Fund Global Health Leadership Team for outstanding service in the coordination of the Common Fund Global Health Initiatives (2012)

Certificate of Appreciation for Invited Presenter, NIH Seminar Series, STEM Careers (2012)

Certificate of Appreciation for Invited Presenter, Washington Mathematics Science Technology Public Charter High School, Washington, DC (2012)

Leadership Award, Postdoctoral Fellows Research Symposium Committee, Emory University, Atlanta, GA (2008)

Areas of research and study

Dissemination and Implementation of Evidence-based Programs

HIV/AIDS

Implementation science

Inter-organizational Networks

Translational science

Publications

Publications

Fragile X Syndrome: The FMR1 CGG Repeat Distribution Among World Populations

Peprah, E. (n.d.).

Publication year

2012

Journal title

Annals of Human Genetics

Volume

76

Issue

2

Page(s)

178-191

10.1111/j.1469-1809.2011.00694.x

Abstract

Abstract

Fragile X syndrome (FXS) is characterized by moderate to severe intellectual disability, which is accompanied by macroorchidism and distinct facial morphology. FXS is caused by the expansion of the CGG trinucleotide repeat in the 5′ untranslated region of the fragile X mental retardation 1 (FMR1) gene. The syndrome has been studied in ethnically diverse populations around the world and has been extensively characterized in several populations. Similar to other trinucleotide expansion disorders, the gene-specific instability of FMR1 is not accompanied by genomic instability. Currently we do not have a comprehensive understanding of the molecular underpinnings of gene-specific instability associated with tandem repeats. Molecular evidence from in vitro experiments and animal models supports several pathways for gene-specific trinucleotide repeat expansion. However, whether the mechanisms reported from other systems contribute to trinucleotide repeat expansion in humans is not clear. To understand how repeat instability in humans could occur, the CGG repeat expansion is explored through molecular analysis and population studies which characterized CGG repeat alleles of FMR1. Finally, the review discusses the relevance of these studies in understanding the mechanism of trinucleotide repeat expansion in FXS.

Examination of FMR1 transcript and protein levels among 74 premutation carriers

Peprah, E., He, W., Allen, E., Oliver, T., Boyne, A., & Sherman, S. L. (n.d.).

Publication year

2010

Journal title

Journal of Human Genetics

Volume

55

Issue

1

Page(s)

66-68

10.1038/jhg.2009.121

Abstract

Abstract

Fragile X-associated disorders are caused by a CGG trinucleotide repeat expansion in the 5′-untranslated region of the FMR1 gene. Expansion of the CGG trinucleotide repeats to >200 copies (that is, a full mutation) induces methylation of the FMR1 gene, with transcriptional silencing being the eventual outcome. Previous data have shown that FMR1 premutation carriers (individuals with 55-199 repeats) have increased FMR1 mRNA levels with decreased protein (fragile X mental retardation protein (FMRP)) levels. However, the point at which this translational inefficiency occurs, given the increased transcription mechanism, has not yet been explored and remains to be elucidated. We examined the repeat length group, FMR1 transcript and FMRP levels in 74 males with a wide range of repeat lengths using analysis of covariance to better characterize this association. Results showed that the mean FMRP level among carriers with 80-89 repeats was significantly higher than the mean levels among lower (54-79) and higher (90-120) premutation carriers, in spite of the increasing transcript level with repeat length. Taken together, these results suggest that the 80-89-repeat group may lead to different properties that increase the efficiency of translation compared with other premutation repeat size groups.

Genetic diversity of the Fragile X syndrome Gene (FMR1) in a large sub-saharan West African population

Peprah, E. K., Allen, E. G., Williams, S. M., Woodard, L. M., & Sherman, S. L. (n.d.).

Publication year

2010

Journal title

Annals of Human Genetics

Volume

74

Issue

4

Page(s)

316-325

10.1111/j.1469-1809.2010.00582.x

Abstract

Abstract

Summary: Fragile X syndrome (OMIM #300624) is caused by the expansion of a CGG trinucleotide repeat found in the 5′ untranslated region of the X-linked FMR1 gene. Although examinations of characteristics associated with repeat instability and expansion of the CGG repeat upon transmission from parent to offspring has occurred in various world populations, none has been conducted in large Sub-Saharan African populations. We have examined the FMR1 CGG repeat structure in a sample of 350 males drawn from the general population of Ghana. We found that Ghanaians and African Americans have similar allele frequency distributions of CGG repeat and its flanking STR markers, DXS548 and FRAXAC1. However, the distribution of the more complex marker, FRAXAC2, is significantly different. The haplotype structure of the FMR1 locus indicated that Ghanaians share several haplotypes with African Americans and Caucasians that are associated with the expanded full mutation. In Ghanaians, the majority of repeat structures contained two AGG interruptions, however, the majority of intermediate alleles (35-49) lacked AGG interruptions. Overall, we demonstrate that allelic diversity of the FMR1 locus among Ghanaians is comparable to African Americans, but includes a minority of CGG array structures not found in other populations.

Characterization of the mitochondrial inner membrane protein translocator Tim17 from Trypanosoma brucei

Singha, U. K., Peprah, E., Williams, S., Walker, R., Saha, L., & Chaudhuri, M. (n.d.).

Publication year

2008

Journal title

Molecular and Biochemical Parasitology

Volume

159

Issue

1

Page(s)

30-43

10.1016/j.molbiopara.2008.01.003

Abstract

Abstract

Mitochondrial protein translocation machinery in the kinetoplastid parasites, like Trypanosoma brucei, has been characterized poorly. In T. brucei genome database, one homolog for a protein translocator of mitochondrial inner membrane (Tim) has been found, which is closely related to Tim17 from other species. The T. brucei Tim17 (TbTim17) has a molecular mass 16.2 kDa and it possesses four characteristic transmembrane domains. The protein is localized in the mitochondrial inner membrane. The level of TbTim17 protein is 6-7-fold higher in the procyclic form that has a fully active mitochondrion, than in the mammalian bloodstream form of T. brucei, where many of the mitochondrial activities are suppressed. Knockdown of TbTim17 expression by RNAi caused a cessation of cell growth in the procyclic form and reduced growth rate in the bloodstream form. Depletion of TbTim17 decreased mitochondrial membrane potential more in the procyclic than bloodstream form. However, TbTim17 knockdown reduced the expression level of several nuclear encoded mitochondrial proteins in both the forms. Furthermore, import of presequence containing nuclear encoded mitochondrial proteins was significantly reduced in TbTim17 depleted mitochondria of the procyclic as well as the bloodstream form, confirming that TbTim17 is critical for mitochondrial protein import in both developmental forms. Together, these show that TbTim17 is the translocator of nuclear encoded mitochondrial proteins and its expression is regulated according to mitochondrial activities in T. brucei.