Melissa Barker-Haliski

Education:

• BA – University of Oregon
• Ph.D. – University of Utah

Research Interests:

• Epilepsy
• Alzheimer’s disease
• drug development
• preclinical research
• translational research
• neuroscience
• pharmacology

Courses Taught:

• PCEUT 451/551 – Introduction to Drug Discovery
• PCEUT 534 – Principles of Precision Medicine
• PCEUT 540 – Communication for Pharmaceutical Sciences

Biography:

1. Dr. Melissa Barker-Haliski’s research emphasizes developing novel strategies and preclinical approaches to uncover precision medicine therapies for unmet medical needs for people with epilepsy and for seizures related to neurodegenerative disease, including Alzheimer’s disease. Using behavioral models and molecular neuroscience, the lab is particularly interested in therapeutic discovery and neuropharmacological interactions to modify disease trajectory. She served as co-chair of the American Epilepsy Society/International League Against Epilepsy (ILAE) Pharmacology Common Data Elements Working Group (2014–2018) and the Phenotyping Common Data Elements Working Group (2019–2022), helping to standardize preclinical pharmacology research across industry, government, and academia. She is current co-chair of the ILAE Precision Therapy for Epilepsy Task Force. Dr. Barker-Haliski actively engages with industry and government leaders to drive next-generation therapeutic discovery for neurological disease.

Publications:

Smith VL, Gidi BZ, Bragg RM, Cantle JP, Ben-Varon A, Noble B, Prades S, Compton A, Greenfield J, Korecka JA, Gemos A, Yu T, Khurana V, Kordasiewicz HB, Zhao HT, Barker-Haliski M, Child DD, Carroll JB. Atrophin-1 antisense oligonucleotide provides robust protection from pathology in a fully humanized DRPLA model. Mol Ther Nucleic Acids. 2025 Dec 31;37(1):102815. doi: 10.1016/j.omtn.2025.102815. PMID: 41624332; PMCID: PMC12857545.

Robinson-Cooper L, Davidson S, Koutoubi R, Zhang K, Park H, Barker-Haliski M. Loss of presenilin 2 function age-dependently increases susceptibility to kainate-induced acute seizures and blunts hippocampal kainate-type glutamate receptor expression. Exp Neurol. 2026 Mar;397:115586. doi: 10.1016/j.expneurol.2025.115586. Epub 2025 Dec 9. PMID: 41380794; PMCID: PMC12799287.

Knox KM, Davidson S, Lehmann LM, Skinner E, Lo A, Jayadev S, Barker-Haliski M. Alzheimer’s disease-associated genotypes differentially influence chronic evoked seizure outcomes and antiseizure medicine efficacy in aged mice. J Alzheimers Dis. 2025 Jul;106(2):547-561. doi: 10.1177/13872877251343321. Epub 2025 Jul 1. PMID: 40458037; PMCID: PMC12282399.

Erickson I, Davidson S, Choi H, Rho S, Guignet M, Peagler K, Thummel K, Ericsson A, Barker-Haliski M. Intestinal dysbiosis alters acute seizure burden and antiseizure medicine activity in Theiler’s virus model of encephalitis. Epilepsia. 2025 Aug;66(8):3022-3034. doi: 10.1111/epi.18395. Epub 2025 Mar 28. PMID: 40153196.

Del Pozo A, Knox KM, Lehmann LM, Davidson S, Rho SL, Jayadev S, Barker-Haliski M. Chronic evoked seizures in young pre-symptomatic APP/PS1 mice induce serotonin changes and accelerate onset of Alzheimer’s disease-related neuropathology. Prog Neurobiol. 2024 Apr;235:102591. doi: 10.1016/j.pneurobio.2024.102591. Epub 2024 Mar 13. PMID: 38484965; PMCID: PMC11015961.