, which indicates that these disorders may share some underlying gene regulatory and neural circuit systems," said Philipp Mews, Ph.D., Instructor of Neuroscience at Icahn Mount Sinai and first author of the paper together with Ashley M. Cunningham, a neuroscience Ph.D. student.
"Importantly, the transcriptional abnormalities—in particular, the neuroinflammatory responses that are suppressed in the nucleus accumbens of people with cocaine use disorder—are directionally opposite of the proinflammatory cascade responses conferred by opioid use disorder. The observation that there are distinct molecular changes conferred by each of the two
could be valuable for the development of targeted, effective treatments specific to cocaine use disorder.", researchers often use animal models to study their effects. However, a key question is whether what they learn from these animal models is similar to what happens in the brains of humans who use cocaine.
"Our research team looked at studies performed in mice that were given the opportunity to self-administer cocaine and compared the resultingto those seen in postmortem brain tissue of people with cocaine use disorder. Our analysis revealed strikingly similar changes in the brain's gene expression profiles in both the mice and humans, validating the use of mouse models to study the pathophysiological basis of cocaine use disorder," said Eric J. Nestler, MD, Ph.D.