1Anesthesia Department and Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, United States
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The diverse etiologies of conditions characterized by chronic pain require molecular assessment. Over recent decades, progress in research has enabled studying of the genetic mechanisms underlying pain and consequently realistic clinical solutions. Genetic linkage has unveiled rare single-gene contributions to pain disorders, whilst advances in genome-wide association studies (GWAS) define multigenic mechanisms in conditions such as back pain and migraine. Advances in DNA sequencing now additionally allow us to efficiently identify mutations underlying congenic pain syndromes and diagnose individuals at risk of developing ongoing pain. In the laboratory, targeted modulation of gene expression with RNA interference, as well as the development of transgenic mouse models, has exponentially expanded our ability to interrogate the molecular cascades behind nociceptive and chronic pain. Furthermore, the recent evolution of CRISPR/Cas9 mediated gene editing has produced a simple yet effective method of altering the genome to alleviate ongoing pain. This genetic revolution will undoubtedly lead to more personalized therapeutics, which with consideration of environmental risk factors should combat clinical pain. We believe these improvements will occur in the next few decades. A video accompanying this abstract is available online as Supplemental Digital Content at http://links.lww.com/PAIN/A804.