Rationale: Addiction is a disorder of motivational learning and memory. Maladaptive motivational memories linking drug-associated stimuli to drug seeking are formed over hundreds of reinforcement trials and accompanied by aberrant neuroadaptation in the mesocorticolimbic reward system. Such memories are resistant to extinction. However, the discovery of retrieval-dependent memory plasticity has opened up the possibility of permanent modification of established (long-term) memories during 'reconsolidation'.
Objectives: Here, we investigate whether reappraisal of maladaptive alcohol cognitions performed after procedures designed to destabilize alcohol memory networks affected subsequent alcohol memory, craving, drinking and attentional bias.
Methods: Forty-seven at-risk drinkers attended two sessions. On the first lab session, participants underwent one of two prediction error-generating procedures in which outcome expectancies were violated while retrieving alcohol memories (omission and value prediction error groups). Participants in a control group retrieved non-alcohol memories. Participants then reappraised personally relevant maladaptive alcohol memories and completed measures of reappraisal recall, alcohol verbal fluency and craving. Seven days later, they repeated these measures along with attentional bias assessment.
Results: Omission prediction error (being unexpectedly prevented from drinking beer), but not a value prediction error (drinking unexpectedly bitter-tasting beer) or control procedure (drinking unexpectedly bitter orange juice), was associated with significant reductions in verbal fluency for positive alcohol-related words. No other statistically robust outcomes were detected.
Conclusions: This study provides partial preliminary support for the idea that a common psychotherapeutic strategy used in the context of putative memory retrieval-destabilization can alter accessibility of alcohol semantic networks. Further research delineating the necessary and sufficient requirements for producing alterations in alcohol memory performance based on memory destabilization is still required.
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http://dx.doi.org/10.1007/s00213-015-4164-y | DOI Listing |
Sci Rep
January 2025
Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, No. 38, Italia Ave., Ghods St, Keshavarz Boulevard, Tehran, Iran.
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View Article and Find Full Text PDFMetab Brain Dis
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School of Natural Product Studies, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, 700 032, India.
Alzheimer's disease is a complex neurodegenerative disease characterized by progressive decline in cognitive function and behaviour. Ginger is the rhizome of the plant Zingiber officinale Roscoe, has been an important ingredient of many Ayurveda formulations to treat neurological disorders. The present study aims to estimate the variation of 6-gingerol content in nine different ginger samples collected from Manipur, India, investigate the neuroprotective potential of the most potent ginger sample against scopolamine-induced cognitively impaired mice, and validate the therapeutic claim by molecular docking analysis.
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January 2025
McLean Hospital, Harvard Medical School, Belmont, MA, USA.
Xenon gas is considered to be a safe anesthetic and imaging agent. Research on its other potentially beneficial effects suggests that xenon may have broad efficacy for treating health disorders. A number of reviews on xenon applications have been published, but none have focused on substance use disorders.
View Article and Find Full Text PDFWorld Psychiatry
February 2025
School of Psychology, University of New South Wales, Sydney, NSW, Australia.
Although trauma-focused cognitive behavior therapy (TF-CBT) is the recommended treatment for post-traumatic stress disorder (PTSD), up to one-half of patients do not respond to this intervention. There is an urgent need to develop new strategies to improve treatment response. Training people to recall specific positive memories may augment treatment gains in TF-CBT.
View Article and Find Full Text PDFASN Neuro
January 2025
Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
People living with HIV (PLWH) experience HIV-associated neurocognitive disorders (HAND), even though combination antiretroviral therapy (cART) suppresses HIV replication. HIV-1 transactivator of transcription (HIV-1 Tat) contributes to the development of HAND through neuroinflammatory and neurotoxic mechanisms. C-C chemokine 5 receptor (CCR5) is important in immune cell targeting and is a co-receptor for HIV viral entry into CD4+ cells.
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