Biology subjects

Stierand, J.

Publications and source records attributed to Stierand, J..

3 recordsLinked to original sources

bioRxiv2026

Interleukin-6 responses to acute stress are not altered in alcohol use disorder despite elevated baseline inflammation

Acute stress activates the immune system, leading to the release of pro-inflammatory cytokines, such as interleukin-6 (IL-6). Chronic alcohol consumption alters the physiological stress systems and is associated with increased chronic inflammation. However, it remains unclear how IL-6 responds to acute stress in individuals with alcohol use disorder (AUD). Forty patients with AUD during early abstinence and 37 healthy controls (HC) completed two study visits. On one day, an acute stress induction task was performed, and on the other, a non-stressful control task, with the order of tasks being balanced. Plasma IL-6 and C-reactive protein (CRP) were measured as inflammatory markers at baseline and changes in IL-6 were assessed 90 minutes after the experimental manipulation. Patients with AUD showed significantly elevated baseline IL-6 and CRP compared to HC and the levels correlated positively with the amount of consumed alcohol in patients. IL-6 responses to the stress intervention did not differ between groups. Increases in IL-6 were observed on stress and control days and were larger when samples were collected via an indwelling catheter than with a butterfly needle. These findings suggest that IL-6 responses to acute stress do not differ between AUD and HC, despite increased baseline inflammation. Furthermore, the results indicate that blood collection methods can influence IL-6 measurements and highlight the importance of methodological considerations.

immunology↗

bioRxiv2025

No neurobehavioral evidence for reduced motivational potential of social rewards in alcohol use disorder

BackgroundThe mesolimbic dopamine system plays a central role in motivating behavior. In alcohol use disorder (AUD), this system is thought to be dysfunctional, leading to hyperreactivity to alcohol-related cues. In contrast, evidence on how individuals with AUD respond to alcohol-unrelated reward cues is inconclusive, and the motivation for social rewards has not yet been investigated. MethodsTo address this gap, 36 individuals with AUD and 34 healthy controls performed an incentive delay task to assess social reward anticipation with a monetary and a non-reward control condition while undergoing functional magnetic resonance imaging. The ventral striatum was defined as region of interest because of its central role in neuronal circuits for motivation. ResultsNeither behavioral nor neuroimaging data provided any evidence of reduced motivation for social or monetary rewards in AUD. Exploratory whole-brain analyses only revealed stronger activation in the occipital/cuneal cortex in individuals with AUD than in healthy controls across all trials. ConclusionTogether, these results suggest that sensitivity to social reward cues is not fundamentally impaired in AUD. Furthermore, they imply that motivational changes related to the substance do not generally alter the reward potential of alcohol-unrelated domains in AUD, opening perspectives for social-behavioral treatments for this disorder.

neuroscience↗

bioRxiv2024

Neurocomputational Mechanisms Underlying Maladaptive Self-Belief Formation in Depression

Maladaptive self-beliefs are a core symptom of major depressive disorder. These beliefs are perpetuated by a negatively biased integration of self-related feedback. Understanding the neurocomputational mechanisms of biased belief updating may help to counteract maladaptive beliefs and the maintenance of depression. The present study uses a belief-updating task and functional neuroimaging to examine the neurocomputational mechanisms associated with self-related feedback processing in individuals with major depression and matched healthy controls. We hypothesized that increased symptom burden in depression is associated with negatively biased self-belief updating and altered neural tracking of social feedback. Our findings show that depression is related to reduced incorporation of unexpected positive feedback, with higher symptom burden alongside heightened insula reactivity to unexpected negative feedback. The interplay of increased neural responsiveness to negative feedback and the reduced learning from positive feedback provide new insights into cognitive distortions in depression and may explain the persistence of maladaptive self-beliefs and, thus, the maintenance of depression.

neuroscience↗