Bidirectional causality between addiction and cognitive deficits

Melugin, Patrick R.; Nolan, Suzanne O.; Siciliano, Cody A.

doi:10.1016/bs.irn.2020.11.001

Cited by 26 publications

(24 citation statements)

References 228 publications

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“…We investigated whether sustained exposure to phencyclidine (PCP) or to methamphetamine (METH) causes neurons to change their neurotransmitter identity. We analyzed the medial prefrontal cortex because of its relevance for drug-induced cognitive deficits ( 3, 5, 6 ) and focused on the prelimbic subregion (PrL). Because changes in transmitter identity are activity-dependent ( 10, 12, 13 ), we first determined whether drug administration alters c-fos expression in the PrL.…”

Section: Resultsmentioning

confidence: 99%

“…Repeated exposure to drugs of abuse alters behavior by causing synaptic plasticity in brain circuits that regulate reward and cognitive processing ( 1-4 ). Drug-induced alterations in prefrontal cortex activity and function have been linked to the appearance of cognitive deficits that persist during abstinence and can contribute to relapse ( 3, 5, 6 ). Exposure to drugs also increases the number of neurons expressing a specific transmitter in subcortical regions, promoting nicotine and alcohol preference ( 7 ), withdrawal symptoms ( 8 ) and drug-seeking ( 9 ).…”

Section: Mainmentioning

confidence: 99%

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Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits

Pratelli

Thaker

et al. 2022

Preprint

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Decreased cognitive ability is a major consequence of exposure to drugs of abuse, but the underlying neuroplastic changes have been elusive. We show that both phencyclidine and methamphetamine cause a population of prelimbic pyramidal neurons to switch from a glutamatergic to a GABAergic phenotype. Overriding the gain of GABA with RNA-interference prevents drug-induced cognitive deficits and locomotor sensitization, connecting the change in neurotransmitter identity with altered behavior. Chemogenetic suppression of drug-induced hyperactivity also prevents the change in transmitter phenotype or reverses it after it has occurred, preventing or rescuing the associated behavioral changes. These findings may provide therapeutic opportunities to mitigate drug-induced cognitive deficits by manipulating electrical activity in the prelimbic cortex.

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Section: Resultsmentioning

confidence: 99%

Section: Mainmentioning

confidence: 99%

Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits

Pratelli

Thaker

et al. 2022

Preprint

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Section: Discussionmentioning

confidence: 99%

“…Impairment of executive function has an important role in the formation, maintenance, cessation, and relapse of SUD (24). Long-term substance abuse can lead to pervasive impairment of executive function, resulting in increased impulsive behavior and decreased self-control, in turn affecting the treatment effects of SUD and leading to an increased likelihood of relapse (25,26). ROC curve analysis showed that inhibition subscale scores had no predictive power, and working memory subscale scores and GEC had a predictive power to iTBS therapeutic efficacy.…”

Section: Mud Patients Exhibited Significant Impairment Of Executive Functionmentioning

confidence: 99%

Predictive Role of Executive Function in the Efficacy of Intermittent Theta Burst Transcranial Magnetic Stimulation Modalities for Treating Methamphetamine Use Disorder—A Randomized Clinical Trial

Wang

Ren

et al. 2021

Front. Psychiatry

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Background: Repetitive transcranial magnetic stimulation (rTMS) has therapeutic effects on craving in methamphetamine (METH) use disorder (MUD). The chronic abuse of METH causes impairments in executive function, and improving executive function reduces relapse and improves treatment outcomes for drug use disorder. The purpose of this study was to determine whether executive function helped predict patients' responses to rTMS treatment.Methods: This study employed intermittent theta burst stimulation (iTBS) rTMS modalities and observed their therapeutic effects on executive function and craving in MUD patients. MUD patients from an isolated Drug Rehabilitation Institute in China were chosen and randomly allocated to the iTBS group and sham-stimulation group. All participants underwent the Behavior Rating Inventory of Executive Function - Adult Version Scale (BRIEF-A) and Visual Analog Scales (VAS) measurements. Sixty-five healthy adults matched to the general condition of MUD patients were also recruited as healthy controls.Findings: Patients with MUD had significantly worse executive function. iTBS groups had better treatment effects on the MUD group than the sham-stimulation group. Further Spearman rank correlation and stepwise multivariate regression analysis revealed that reduction rates of the total score of the BRIEF-A and subscale scores of the inhibition factor and working memory factor in the iTBS group positively correlated with improvements in craving. ROC curve analysis showed that working memory (AUC = 87.4%; 95% CI = 0.220, 0.631) and GEC (AUC = 0.761%; 95% CI = 0.209, 0.659) had predictive power to iTBS therapeutic efficacy. The cutoff values are 13.393 and 59.804, respectively.Conclusions: The iTBS rTMS had a better therapeutic effect on the executive function of patients with MUD, and the improved executive function had the potential to become a predictor for the efficacy of iTBS modality for MUD treatment.Clinical Trial Registration:ClinicalTrials.gov, identifier: ChiCTR2100046954.

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“…However, patients suffering from alcohol-related cognitive impairment (ARCI; Heirene et al, 2018 ) themselves do not lodge subjective complaints, possibly due to the lack of judgment ability under the influence of addiction (Walvoort et al, 2016 ). On the other hand, it has been shown in the clinical literature that cognitive deficits indulge addictive behaviors (Melugin et al, 2021 ). Moreover, cognitive impairment can also contribute to the lack of self-control in maintaining abstinence from longstanding alcohol abuse.…”

Section: Introductionmentioning

confidence: 99%

Altered Global Signal Topography in Alcohol Use Disorders

Duan

Jing

et al. 2022

Front. Aging Neurosci.

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The most common symptom of patients with alcohol use disorders (AUD) is cognitive impairment that negatively affects abstinence. Presently, there is a lack of indicators for early diagnosis of alcohol-related cognitive impairment (ARCI). We aimed to assess the cognitive deficits in AUD patients with the help of a specific imaging marker for ARCI. Data-driven dynamic and static global signal topography (GST) methods were applied to explore the cross-talks between local and global neuronal activities in the AUD brain. Twenty-six ARCI, 54 AUD without cognitive impairment (AUD-NCI), and gender/age-matched 40 healthy control (HC) subjects were recruited for this study. We found that there was no significant difference with respect to voxel-based morphometry (VBM) and static GST between AUD-NCI and ARCI groups. And in dynamic GST measurements, the AUD-NCI patients had the highest coefficient of variation (CV) at the right insula, followed by ARCI and the HC subjects. In precuneus, the order was reversed. There was no significant correlation between the dynamic GST and behavioral scores or alcohol consumption. These results suggested that dynamic GST might have potential implications in understanding AUD pathogenesis and disease management.

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Bidirectional causality between addiction and cognitive deficits

Cited by 26 publications

References 228 publications

Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits

Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits

Predictive Role of Executive Function in the Efficacy of Intermittent Theta Burst Transcranial Magnetic Stimulation Modalities for Treating Methamphetamine Use Disorder—A Randomized Clinical Trial

Altered Global Signal Topography in Alcohol Use Disorders

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