• Study Suggests New Marker for Chronic Pain Susceptibility
    A study published this month in the Journal of Pain by researchers at the Rutgers School of Dental Medicine finds a relationship between the level of postexercise pain sensitivity and the likelihood of developing chronic pain. The results suggest that exercise could be a valuable component in helping doctors predict susceptibility to pain, particularly following injury or surgery. The phenomenon of pain reduction after exercise is known as "exercise-induced hypoanalgesia" or (EIH). The authors believe that an individual's EIH profile can indicate how efficiently their body modulates pain. Chronic pain conditions such as fibromyalgia, migraine, chronic low back pain, and temporomandibular disorder have been shown to be associated with faulty pain modulation. Read more about the findings here.
  • New Research Seeks to Advance Understanding, Improve Treatments of Substance Abuse

    A press release last week from the National Institutes of Health announced the awarding of some $11 million over 3 years to support research exploring the use of social media to advance the scientific understanding, prevention, and treatment of substance use and addiction. The awards are funded through the Collaborative Research on Addiction at NIH (CRAN), an NIH consortium involving the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute on Drug Abuse (NIDA), and the National Cancer Institute (NCI).

    The announcement notes the potential of interactive platforms such as Facebook and Twitter as tools to help scientists identify prevailing attitudes and myths and to gain insights into patterns of use, risk factors, and behaviors associated with substance use and misuse. By providing a platform for communicating science-based, health-related messages, social media may also enhance screening, prevention, and treatment of substance use and addiction.

    Read the NIH press release, with additional information on the funded projects, here.

  • Molecular Discovery May Advance Disease Prevention and Treatment
    New research published this week in the journal Immunity advances our understanding of the mechanisms underlying the onset of chronic inflammation. The discovery of 2 microRNA molecules that appear to control inflammation may also enable the development of more effective treatments for the subsequent ailments, such as cancer or autoimmune disorder that often occur, especially with aging. Previous studies have shown that chronic inflammation is linked to the development of certain conditions including diabetes, lupus, arthritis, obesity, cancer, neurodegeneration, and cardiovascular disease along with a shortened life span. Certain types of immune cells, called T follicular helper cells, are known to promote the production of antibodies that attack our own tissues and contribute to chronic inflammation. This study found that the microRNAs at issue are produced by and act to control these important cell types. Read more about the research here.    
  • Findings May Illuminate New Targets for Therapeutic Intervention of Neuropathic Pain
    New research published online in the journal Neuron may offer leads to improved understanding of neuropathic pain. The authors identified a novel protein expressed specifically in nociceptors that acts as a key player in analgesic signaling through GABAB receptors. The protein, Gα inhibitory interacting protein (GINIP), could offer a new line of attack to boost GABA transmission by targeting peripheral neurons selectively, possibly avoiding side effects of system-wide GABAB activation. With neuropathic pain, the spinal cord suffers a loss of signaling by GABA, the nervous system’s main inhibitory transmitter. GABA receptors have thus seemed a likely target to dampen neuropathic hyperexcitability, but considerable efforts toward that aim have largely failed, mainly because GABA receptors are found throughout the nervous system. Because GINIP is restricted to nociceptors—the neurons relevant to neuropathic pain—targeting the GABAB-GINIP interaction may facilitate the development of a new therapeutic agent that specifically interferes with GABAB signaling related to pain. Read a news story about the findings here.  
Daniel Carr, MD, FABPM
Pain Research, Education, and Policy Program
Department of Public Health and Community Medicine
Tufts Medical Center
Boston, MA


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