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Research Interests

• Pain Neurobiology and Genetics
• Biomarkers for persistent pain conditions

Research Synopsis

Chronic pain is one of our nation’s most significant healthcare problems. Although our understanding of pain neurobiology has grown over the last several years, few new therapeutics have been developed. Thus, it is imperative that further research is conducted to better understand chronic pain; its causes, effects, and treatments. Recent studies conducted by our laboratory and others demonstrate that a great deal of individual variability exists in pain sensitivity and likelihood to develop chronic pain conditions. Furthermore, there is significant individual variability in the efficacy, tolerance, and side-effect profiles for conventional analgesics used to treat pain. Variability in experimental pain, the development of chronic pain conditions, and analgesic responsiveness is due to a combination of environmental and genetic factors.

My research objectives are to 1) identify and characterize signalling processes that drive persistent pain conditions, 2) evaluate the potential functionality of common genetic polymorphisms that interact with environmental events to produce persistent pain conditions, and 3) identify biological markers predictive for the development of persistent pain conditions, including the severity and duration of the disorder as well as optimal management strategies for different individuals. Thus, my lab integrates molecular genetics, animal models, and clinical epidemiologic measures to better understand the neurobiological processes underlying persistent pain as well as to identify unique markers for the diagnosis of clinical pain conditions in order to ultimately provide novel targets for the development of effective individualized pain therapeutics.

Publications

Click above for PubMed publications.

• Nackley AG, Shabalina SA, Lambert JE, Conrad MS, Gibson DG, Spiridonov AN, Satterfield K, and Diatchenko L. (2009) Low enzymatic activity haplotypes of the human catechol-O-methyltransferase gene: enrichment for marker SNPs. PLoS ONE 4(4): e5237. Abstract
• Tchivileva IE, Nackley AG, Qian L, Wentworth S, Conrad M, and Diatchenko L. (2009) Characterization of NF-kappaB-mediated inhibition of catechol-O-methyltransferase. Molecular Pain 5: 13. Abstract
• Nackley AG, Tan KS, Fecho K, Flood P, Maixner W, and Diatchenko L. (2007) Catechol-O- methyltransferase inhibition increases pain sensitivity through activation of both β2 and β3 adrenergic receptors. Pain 128(3): 199-208. Abstract
• Tan KS, Nackley AG, Satterfield K, Maixner W, Diatchenko L, and Flood PM. (2007) Β2-adrenergic receptor activation stimulates pro-inflammatory cytokine production in macrophages via PKA- and NF-κB- independent mechanisms. Cellular Signaling 19(2): 251-260. Abstract
• Nackley AG, Shabalina SA, Chivileva, IE, Satterfield KS, Korchynskyy O, Makarov SS, Maixner W, and Diatchenko L. (2006) A common human catechol-O-methyltransferase haplotype modulates protein expression by altering mRNA secondary structure. Science 314(5807): 1930-1933. Abstract

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