Emerging evidence suggests that collapsin response mediator protein 2 (CRMP2) regulates presynaptic excitatory neurotransmission and contributes to pathological changes during diseases, such as neuropathic pain and substance use disorders.
These effects were robust in sibling comparisons, where sibling differences in EduYears-GPS predicted all three SUDs (P < 0.05, R<sup>2</sup> 0.13-0.20%).
Recently, integrated cognitive behavioral therapy (CBT/Integrated) was shown to be more effective than standard CBT (CBT/SUD) in the treatment of SUD + ADHD.
The objective of this systematic review is to characterize the effects of GLP-1-receptor agonists on SUD-related behavioural effects of drugs, nicotine, and alcohol.
BIS and BAS subscale total scores, inter-domain correlation, factor structure, and difference in the early-onset and late-onset SUD subgroup scores were calculated.
This two years long prospective longitudinal study with all HYFEPA (n = 42) admitted to EQIIP SOL between 2012-2015 reports at multiple time points, clinical (CGI, GAF), functional (SOFAS, work/study, housing autonomy) and substance use disorder (DUS, AUS) outcomes and acute services use (hospitalizations, emergency room visits).
They showed lower traits of the SWAP-200's cluster A and B disorders than SUD and PD patients, who presented more severe levels of personality impairment.
By means of Physical Activity Rating Scale (PARS-3), internal Inhibition Scale and Drug Craving Scale, this study investigated the individuals with substance use disorder under rehabilitation in the women compulsory isolation rehabilitation center in Chongqing, China.
Hypofunction of the serotonin (5-HT) 5-HT<sub>2C</sub> receptor (5-HT<sub>2C</sub>R) has been implicated in a variety of disorders including substance use disorders.
The associations of hazardous cannabis use with these measurements were examined after adjusting for substance use disorder severity, age, antiretroviral therapy regimen, CD4 T-cell count, and interleukin-6.
The genetic models used remained highly efficient in predicting SUD in a large sample of individuals with severe SUD from a psychiatric institution that were not ascertained on the basis of ADHD diagnosis, thus identifying ADGRL3 as a risk gene for SUD.
Since then, much research interest has shifted to other cannabinoid-based strategies, such as peripheral CB1R antagonists/inverse agonists, neutral CB1R antagonists, allosteric CB1R modulators, CB2R agonists, fatty acid amide hydrolase (FAAH) inhibitors, monoacylglycerol lipase (MAGL) inhibitors, fatty acid binding protein (FABP) inhibitors, or nonaddictive phytocannabinoids with CB1R or CB2R-binding profiles, as new therapeutics for SUDs.
Seventeen studies were included, investigating the effect of the GLP-1-receptor agonists exendin-4, fluoro-exendin-4, liraglutide, AC3174 and GLP-1 (7-36) on SUD-related behavioural effects of ethanol, cocaine, amphetamine, and/or nicotine.All studies used rodents as subjects.
Since then, much research interest has shifted to other cannabinoid-based strategies, such as peripheral CB1R antagonists/inverse agonists, neutral CB1R antagonists, allosteric CB1R modulators, CB2R agonists, fatty acid amide hydrolase (FAAH) inhibitors, monoacylglycerol lipase (MAGL) inhibitors, fatty acid binding protein (FABP) inhibitors, or nonaddictive phytocannabinoids with CB1R or CB2R-binding profiles, as new therapeutics for SUDs.