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.