Allison Elizabeth Ashley-Koch

Allison Elizabeth Ashley-Koch

Professor in Medicine

External Address: 
300 N Duke St., Durham, NC 27701
Internal Office Address: 
Duke Box 104775, Durham, NC 27701


One of my major research foci is in the genetic basis of psychiatric and neurological disorders. I am currently involved in studies to dissect the genetic etiology of attention deficit hyperactivity disorder (ADHD), autism, chiari type I malformations, essential tremor, and neural tube defects. Additional research foci include genetic modifiers of sickle cell disease, and genetic contributions to birth outcomes, particularly among African American women.

Education & Training

  • Ph.D., Emory University 1997

Selected Grants

Eyes of Africa: The Genetics of Blindness awarded by (Investigator). 2017 to 2022

Trauma and Genomics Modulate Brain Structure across Common Psychiatric Disorders awarded by National Institutes of Health (Co Investigator). 2017 to 2021

Transfusion Medicine and Hematology awarded by National Institutes of Health (Preceptor). 1975 to 2021

MVP IPA - Allison Ashley-Koch awarded by (Biostatistician). 2019 to 2021

IPA--Allison Ashley-Koch awarded by (Biostatistician). 2018 to 2020

Transcriptomic, therapeutic and genetic investigations of sickle cell nephropathy awarded by National Institutes of Health (Principal Investigator). 2016 to 2020

Bioinformatics and Computational Biology Training Program awarded by National Institutes of Health (Mentor). 2005 to 2020

Genetics Training Grant awarded by National Institutes of Health (Mentor). 1979 to 2020

High-throughput Metabolite Profiling and Genetic Analyses awarded by (Co Investigator). 2015 to 2020


Markunas, C. A., et al. “Genetics of the Chiari i and II malformations.” The Chiari Malformations, vol. 9781461463696, 2013, pp. 93–101. Scopus, doi:10.1007/978-1-4614-6369-6_7. Full Text

Luciano, Mark G., et al. “Development of Common Data Elements for Use in Chiari Malformation Type I Clinical Research: An NIH/NINDS Project.Neurosurgery, vol. 85, no. 6, Dec. 2019, pp. 854–60. Pubmed, doi:10.1093/neuros/nyy475. Full Text

Hansen, Adam W., et al. “A Genocentric Approach to Discovery of Mendelian Disorders.Am J Hum Genet, vol. 105, no. 5, Nov. 2019, pp. 974–86. Pubmed, doi:10.1016/j.ajhg.2019.09.027. Full Text

Worley, Gordon, et al. “Genetic variation in dopamine neurotransmission and motor development of infants born extremely-low-birthweight.Dev Med Child Neurol, Nov. 2019. Pubmed, doi:10.1111/dmcn.14383. Full Text

Genetics of Glaucoma in People of African Descent (GGLAD) Consortium, Chiea Chuen, et al. “Association of Genetic Variants With Primary Open-Angle Glaucoma Among Individuals With African Ancestry.Jama, vol. 322, no. 17, Nov. 2019, pp. 1682–91. Pubmed, doi:10.1001/jama.2019.16161. Full Text

Nievergelt, Caroline M., et al. “International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci.Nat Commun, vol. 10, no. 1, Oct. 2019, p. 4558. Pubmed, doi:10.1038/s41467-019-12576-w. Full Text

Kousa, Youssef A., et al. “The TFAP2A-IRF6-GRHL3 genetic pathway is conserved in neurulation.Hum Mol Genet, vol. 28, no. 10, May 2019, pp. 1726–37. Pubmed, doi:10.1093/hmg/ddz010. Full Text

Oyedeji, Charity, et al. “A multi-institutional comparison of younger and older adults with sickle cell disease.Am J Hematol, vol. 94, no. 4, Apr. 2019, pp. E115–17. Pubmed, doi:10.1002/ajh.25405. Full Text

Xu, Julia Z., et al. “Clinical and metabolomic risk factors associated with rapid renal function decline in sickle cell disease.Am J Hematol, vol. 93, no. 12, Dec. 2018, pp. 1451–60. Pubmed, doi:10.1002/ajh.25263. Full Text

Kimbrel, Nathan A., et al. “A genome-wide association study of suicide attempts and suicidal ideation in U.S. military veterans.Psychiatry Res, vol. 269, Nov. 2018, pp. 64–69. Pubmed, doi:10.1016/j.psychres.2018.07.017. Full Text

Ilboudo, Yann, et al. “A common functional PIEZO1 deletion allele associates with red blood cell density in sickle cell disease patients.Am J Hematol, vol. 93, no. 11, Nov. 2018, pp. E362–65. Pubmed, doi:10.1002/ajh.25245. Full Text


Kachroo, Priyadarshini, et al. “Whole Genome Sequencing Identifies CRISPLD2 as a Lung Function Gene in Children With Asthma.Chest, vol. 156, no. 6, 2019, pp. 1068–79. Pubmed, doi:10.1016/j.chest.2019.08.2202. Full Text

Bundy, Joseph L., et al. “RNA sequencing of isolated cell populations expressing human APOL1 G2 risk variant reveals molecular correlates of sickle cell nephropathy in zebrafish podocytes.Plos One, vol. 14, no. 6, 2019, p. e0217042. Pubmed, doi:10.1371/journal.pone.0217042. Full Text

Gelineau-Van Waes, J., et al. “Fumonisin B1 (FB1) and Fingolimod (FTY720): Tortilla Toxin and Oral Therapeutic Target Sphingolipid Pathways during Neural Tube Closure.” Birth Defects Research, vol. 110, no. 9, WILEY, 2018, pp. 730–730.

Smith, Alicia, et al. “Meta-Analysis of DNA Methylation and PTSD in the Psychiatric Genomics Consortium PTSD Epigenetics Workgroup.” Neuropsychopharmacology, vol. 42, NATURE PUBLISHING GROUP, 2017, pp. S120–21.

Grotegut, Chad A., et al. “Single nucleotide polymorphisms in the oxytocin receptor and GRK6 are associated with oxytocin dosing requirements and labor outcomes.” American Journal of Obstetrics and Gynecology, vol. 216, no. 1, MOSBY-ELSEVIER, 2017, pp. S19–S19.

Jacob, Seethal A., et al. “Thrombospondin-1 Polymorphisms Are Associated with Chronic Kidney Disease in Sickle Cell Anemia.” Blood, vol. 128, no. 22, American Society of Hematology, 2016, pp. 2491–2491. Crossref, doi:10.1182/blood.v128.22.2491.2491. Full Text

Xu, Julia Z., et al. “Factors Related to the Progression of Sickle Cell Disease Nephropathy.” Blood, vol. 128, no. 22, American Society of Hematology, 2016, pp. 9–9. Crossref, doi:10.1182/blood.v128.22.9.9. Full Text

Anderson, Blair R., et al. “GWAS Meta-Analysis of Glomerular Filtration Rate in Three Cohorts of Sickle Cell Disease Patients and In Vivo Functional Analysis Reveals Potential Nephropathy Candidate Genes.” Blood, vol. 128, no. 22, American Society of Hematology, 2016, pp. 269–269. Crossref, doi:10.1182/blood.v128.22.269.269. Full Text

Morey, Rajendra A., et al. “Genome-Wide Association of Neuroimaging Phenotypes in PTSD at Multiple Sites.” Biological Psychiatry, vol. 79, no. 9, ELSEVIER SCIENCE INC, 2016, pp. 165S-165S.

Smith, Alicia, et al. “Epigenome-Wide Association of PTSD from Heterogeneous Cohorts with a Common Multi-Site Analysis Pipeline.” Biological Psychiatry, vol. 79, no. 9, ELSEVIER SCIENCE INC, 2016, pp. 164S-165S.


Aung, Tin, et al. “Corrigendum: a common variant mapping to CACNA1A is associated with susceptibility to exfoliation syndrome.Nat Genet, vol. 47, no. 6, June 2015, p. 689. Pubmed, doi:10.1038/ng0615-689c. Full Text