Aberrant limbic circuit reactivity to negative stimuli might be related to alterations in emotion processing and regulation in alcohol use disorder (AUD). The current study tested for the first time in AUD the hypothesis of aberrant amygdala habituation to repeated aversive stimuli-a robust and reliable neuroimaging marker for emotion processing. We explored the link between deficits in habituation to adverse childhood experience (ACE), a common risk factor for impaired emotion regulation and AUD. AUD individuals (N = 36) and healthy controls (HC; N = 26) participated in an observational case-control functional magnetic resonance imaging (fMRI) study. An established habituation index was used to investigate processing of aversive emotional faces of the amygdala. AUD individuals showed an overall deficit in amygdala habituation (right: t = 4.26, pFWE = 0.004; left: t = 4.79, pFWE ≤ 0.001). Amygdala habituation was significantly related to increased exposure to ACE in HC (t = 3.88, pFWE = 0.012), whereas this association was not observed in AUD individuals (T = 1.80, pFWE = 0.662). Further, a significant association between higher alcohol consumption and reduced amygdala habituation (right: R = -0.356, F = 8.736, p = 0.004; left: R = -0.309, F = 6.332, p = 0.015) was observed. We found novel evidence for neural alterations in emotion processing in AUD individuals, indexed by deficient amygdala habituation to negative emotional content. We replicated a prior report on a link between ACE and amygdala habituation, a well-established environmental risk factor for mental disorders and emotion dysregulation, in our control sample. Additionally, deficient amygdala habituation related to the amount of alcohol consumption in the overall sample might indicate a short-term substance effect.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/adb.13251 | DOI Listing |
Dev Cogn Neurosci
January 2025
Department of Medical Sciences, Experimental Cognitive and Affective Neuroscience Lab, Uppsala University, Uppsala, Sweden. Electronic address:
Past results suggest that fear extinction and the return of extinguished fear are compromised in adolescents. However, findings have been inconclusive as there is a lack of fear extinction and extinction retention studies including children, adolescents and adults. In the present study, 36 children (6-9 years), 40 adolescents (13-17 years) and 44 adults (30-40 years), underwent a two-day fear conditioning task.
View Article and Find Full Text PDFJ Behav Addict
January 2025
1Peking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Beijing, China.
Background And Aims: The inclusion of gaming disorder as a new diagnosis in the 11th revision of the International Statistical Classification of Diseases (ICD-11) has caused ongoing debate. This review aimed to summarise the potential neural mechanisms of gaming disorder and provide additional evidence for this debate.
Methods: We conducted a comprehensive literature review of gaming disorder, focusing on studies that investigated its clinical characteristics and neurobiological mechanisms.
Addict Biol
January 2025
Department of Psychiatry and Behavioral Sciences, University of Minnesota, Minneapolis, Minnesota, USA.
The ventromedial prefrontal cortex (VMPFC), located along the medial aspect of the frontal area, plays a critical role in regulating arousal/emotions. Its intricate connections with subcortical structures, including the striatum and amygdala, highlight the VMPFC's importance in the neurocircuitry of addiction. Due to these features, the VMPFC is considered a promising target for transcranial magnetic stimulation (TMS) in substance use disorders (SUD).
View Article and Find Full Text PDFBrain Behav
January 2025
Rehabilitation Psychology, Health Science Center, Texas Tech University, Lubbock, Texas, USA.
Introduction: This extensive literature review investigates the relationship between post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD), focusing on the neurobiological changes associated with their co-occurrence. Given that these disorders frequently coexist, we analyze mechanisms through which alcohol serves as a coping strategy for PTSD symptoms, particularly highlighting the drinking-to-cope self-medication model, which suggests that alcohol use exacerbates PTSD symptoms and complicates recovery.
Methods: A systematic literature search was conducted across multiple databases, including PubMed and Google Scholar, to identify studies examining the intersection of the biopsychosocial model with PTSD, AUD, and associated neural alterations.
Addict Biol
December 2024
Department of Psychological and Brain Sciences, University of California Santa Barbara, Santa Barbara, California, USA.
The early initiation of binge-drinking and biological sex are critical risk factors for the development of affective disturbances and cognitive decline, as well as neurodegenerative diseases including Alzheimer's disease. Further, a history of excessive alcohol consumption alters normal age-related changes in the pattern of protein expression in the brain, which may relate to an acceleration of cognitive decline. Here, we aimed to disentangle the interrelation between a history of binge-drinking during adolescence, biological sex and normal aging on the manifestation of negative affect, cognitive decline and associated biochemical pathology.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!