GENETIC INTERSECTIONS OF PAIN AND ADDICTION
Genetic Factors in the Transition From Acute Injury to Chronic Impairment
Ze’ev Seltzer, D.M.D.
Chronic pain is a major unsolved medical, economical, and societal problem because it is so common (affecting 1 of ~3–4 adults worldwide) and because current treatments provide only partial relief that is traded off by side-effects. New treatments are needed. We describe how it is now possible to use genetic approaches to identify targets for the development of the next generation of pain killers and to revolutionize pain medicine. The rapid implementation of genetics in pain research can proceed because (1) clinically relevant definitions of pain phenotypes for genetic research are already well characterized; (2) robust statistical and epidemiological tools are “at hand”; (3) immortalization methods of human DNA, as well as the whole-genome amplification of DNA samples extracted from saliva or blood, are available, ensuring us a continuous supply of this resource on demand; and (4) massive genotyping using microarrays on chips is also possible and will soon be more economically feasible, enabling us to undertake dense, genome-wide mapping of genetic variations and gene validation. To facilitate this implementation, the number of genetic pain research teams must rapidly increase, and adequate financial support should be allocated now. When identified, the mechanisms by which these genes cause pain chronicity will be studied. A vast body of knowledge already exists, describing a plethora of neural mechanisms that have evolved to ensure a transition from acute injury to chronic impairment, including the persistence of pain. We review these mechanisms in the context of avenues for genetic research.
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