5. Summary
Although the contribution of drug-induced neuroinflammatory activity to continuous drug abuse and dependence is not entirely clear, the evidence for its association continues to grow. At present, different drugs generally have dissimilar mechanisms for inducing neuroinflammation, but common mechanisms also exist. For example, the TLR4 receptor pathway is mentioned both in opioids and METH, which may be the focus of future research. However, they all cause similar results – changes in the interleukin family. In addition to the association between drugs and the interleukin family listed in the article, the ingestion of cannabis also has an effect on interleukin 1 beta[85-87] and IL-6[88, 89]. Molecular and pharmacological discoveries of their interactions lead to preclinical behavior, with studies showing that altered manipulation of interleukins modulates the effects of many kinds of drugs abuse. There are still significant opportunities to explore the development and testing of glial-targeted drugs and the treatment of substance use disorders.
Some current drug therapies that directly or indirectly alter the neuronal targets of addictive drugs are effective to a certain extent, and targeting the cytokines produced by glial cells is also an approach to treat complex cases such as neuroadaptive and behavioral changes associated with repeated exposure to common drugs of abuse. As research advances, a better understanding of the connection between glia and the pathophysiology of drug abuse may enhance drug testing and development, allowing for the evaluation of the efficacy of glial modulators as addiction treatments and the potential identification of biomarkers that could aid in diagnosis and effective treatment.