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Olga Pol

head of the Molecular Neuropharmacology Group at the Sant Pau Biomedical Research Institute and the UAB Institute of Neuroscience


In recent years, biotechnology has allowed scientists to include genetics and systems plasticity into research on pain, which has led to a very important breakthrough in research into new treatments. And in this sense, it must be taken into account that knowledge of the mechanisms involved in the development of a certain type of pain, the type of cells affected (neuronal, immunological, glial, etc.), the exact distribution of these cells (central or peripheral nervous system, etc.), which genes are activated or inhibited in the affected cells, which proteins are produced or not produced in the affected cells versus normal cells, is key to designing and developing new therapies.

We must also take into account that the use of biotechnology techniques has been a key step forward in studying the mechanisms involved in the development of different types of pain and the search for possible therapies specific to each one. Thus, using microarrays —which allow for the analysis of thousands of genes in just one test— has made it possible to identify the main genes involved in the development of a specific type of nociceptive response and the genes that are able to inhibit the manifestation of certain types of chronic pain. Additionally, using animals deficient in one or various specific genes (knockout) has allowed us to prove the role of specific genes in the manifestation of the main symptoms of pain. For example, using knockout animals for the HCN2 gene has shown that suppression of this gene in nociceptive neurons eliminates the main symptoms of chronic inflammatory and neuropathic pain, without affecting the sensation of acute pain, which is essential for maintaining the body’s warning system in case of new injuries or infections in the affected area.

Using interfering RNA (siRNA, RNA molecules that interfere with the expression of a specific gene) has allowed us to identify new molecular mechanisms involved in the development of chronic pain from various stimuli and offer new gene therapy treatments. This way, we have seen reduced inflammatory pain in animals treated with a specific siRNA for the gene that codifies for the NR1 subunit gene of the NMDA receptor, indicating that activation of this receptor is part of the hypersensitivity brought on by inflammation and suggesting that treatment with anti-NR1 siRNA has potential for treating chronic inflammatory pain. Additionally, applying gene transfer vectors —which can release short-lived bioactive molecules locally— has allowed us to release inhibitory neurotransmitters and anti-inflammatory cytokines in a specific area of the nervous system, obtaining an analgesic effect without the side effects generated by activating receptors located in other parts of the nervous system and/or other tissues. We, thus, are looking at a significant gene therapy to treat chronic pain.

Genetic and epidemiologic studies have shown that there are various risk factors that can contribute to the differences seen among individuals in terms of sensitivity to pain, and may be responsible for the varying efficacy of the main analgesic compounds used to treat pain in clinical practice. For example, a polymorphism in the SCN9A gene plays a key role in determining varying responses to pain observed in different individuals, while polymorphisms in the COMT and OPRM1 genes are associated with reduced analgesic efficacy of morphine. Thus, identifying the various exact polymorphisms can help predict the onset of chronic pain and establish better personalized therapy.
We can conclude by saying that biotechnology, with the resulting development of ever more powerful tools, is key to the advancement of research into new treatments for chronic pain.

(1) Inflammatory pain is caused by the release of inflammatory mediators from damaged tissue and infiltrated immune cells, which make the nociceptive nerve endings more sensitive, causing hypersensitivity.

(2) Neuropathic pain is caused by nerve damage, resulting from direct trauma to a nerve or derived from a disease that affects nerve function like diabetic neuropathy or postherpetic neuralgia, and is characterized by the presence of allodynia (response to normally innocuous stimuli), hyperalgesia (increased response to noxious stimuli) and spontaneous pain.

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