覚醒剤使用障害は、血清可溶性細胞間接着分子-1濃度の増加と脳報酬および内受容処理の変化を示唆する

Stimulant use disorders (STIM): (1) elicit compulsive behaviors that can lead to altered brain structure and function; and (2) trigger inflammatory responses by inducing the release of immune molecules, suggesting potential adverse effects. Our previous findings show that amphetamine use disorder is associated with altered neural processing during reward, interoception, and inhibitory control tasks. To extend these findings, we investigated links between neural processing and inflammation that may contribute to STIM. Participants from the first half of the Tulsa-1000 (T1000) study (n = 500) met criteria for either group: (1) stim+ (n = 49) reported methamphetamines/amphetamines as their current drug of choice and met criteria for past-year STIM; or (2) stim- (n = 90) endorsed no past-year diagnosis other than nicotine use disorder. Immunoassays were used to measure six inflammatory analytes. We examined blood oxygen- level-dependent (BOLD) responses to monetary incentive delay (MID), visceral interoceptive awareness (VIA), and inhibitory control with the stop signal task (SST) performed during functional magnetic resonance imaging. The stim + group exhibited higher serum soluble intercellular adhesion molecule-1 (sICAM-1) concentrations than the stim- group, no significant differences or associations were found with the other inflammatory factors. Within the stim + group, greater sICAM-1 levels were associated with: (1) lower right nucleus accumbens (NAc) BOLD signal during MID reward anticipation; and (2) higher right amygdala BOLD signal during interoceptive attention. No significant sICAM-1 associations emerged for the SST in stim + . Inflammation may play a central role in stimulant use as indicated by increased sICAM-1, which may point to central mechanisms. The association between high inflammation and reduced NAc reward activation or higher interoceptive signals in STIM may reflect an STIM-sICAM-1 feedback loop mechanism.