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This is not a single molecule or receptor but refers to the set of cognitive, emotional, and attentional processes in the brain that regulate the experience and modulation of pain, which can be therapeutically influenced by cognitive behavioral therapy (CBT). CBT for pain aims to modify maladaptive thoughts and behaviors to reduce pain perception and improve function. Neuroimaging studies show that CBT can change activation and connectivity in brain regions involved in pain processing and emotional control—including the dorsolateral prefrontal cortex (DLPFC), ventrolateral and orbitofrontal prefrontal cortices (VLPFC, OFC), posterior cingulate cortex (PCC), the amygdala, the anterior cingulate cortex (ACC), and limbic system structures[1][2][3]. These changes help facilitate “top-down” inhibition of nociceptive signals and reduce central sensitization[4]. This entry should not be considered a conventional drug target, as it does not map to any specific molecular entity, receptor, or gene. Summary: This target name refers to higher-order cognitive and emotional brain processes involved in pain perception and the principles of their modulation through CBT—not to a canonical molecule, receptor, or pharmacological target. It is therefore not suitable as a structured molecular drug target[1][2][4].
CBT acts by modifying cognitive and emotional processes, not by direct molecular action; main mechanisms are top-down modulation, restructuring maladaptive thoughts, altering brain network connectivity, and reducing central sensitization[1][2][3][4]
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