Brain network dysfunctions in addiction: a meta-analysis of resting-state functional connectivity

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Resting-state functional connectivity (rsFC) provides novel insights into variabilities in neural networks associated with the use of addictive drugs or with addictive behavioral repertoire. However, given the broad mix of inconsistent findings across studies, identifying specific consistent patterns of network abnormalities is warranted. Here we aimed at integrating rsFC abnormalities and systematically searching for large-scale functional brain networks in substance use disorder (SUD) and behavioral addictions (BA), through a coordinate-based meta-analysis of seed-based rsFC studies. A total of fifty-two studies are eligible in the meta-analysis, including 1911 SUD and BA patients and 1580 healthy controls. In addition, we performed multilevel kernel density analysis (MKDA) for the brain regions reliably involved in hyperconnectivity and hypoconnectivity in SUD and BA. Data from fifty-two studies showed that SUD was associated with putamen, caudate and middle frontal gyrus hyperconnectivity relative to healthy controls. Eight BA studies showed hyperconnectivity clusters within the putamen and medio-temporal lobe relative to healthy controls. Altered connectivity in salience or emotion-processing areas may be related to dysregulated affective and cognitive control-related networks, such as deficits in regulating elevated sensitivity to drug-related stimuli. These findings confirm that SUD and BA might be characterized by dysfunctions in specific brain networks, particularly those implicated in the core cognitive and affective functions. These findings might provide insight into the development of neural mechanistic biomarkers for SUD and BA.

Related collections

Most cited references 111

Record: found
Abstract: found
Article: not found

Neurobiology of addiction: a neurocircuitry analysis.

George F Koob, Nora D. Volkow (2016)

Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction.

0 comments Cited 852 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Neurocircuitry of addiction.

George F Koob, Nora D. Volkow (2010)

Drug addiction is a chronically relapsing disorder that has been characterized by (1) compulsion to seek and take the drug, (2) loss of control in limiting intake, and (3) emergence of a negative emotional state (eg, dysphoria, anxiety, irritability) reflecting a motivational withdrawal syndrome when access to the drug is prevented. Drug addiction has been conceptualized as a disorder that involves elements of both impulsivity and compulsivity that yield a composite addiction cycle composed of three stages: 'binge/intoxication', 'withdrawal/negative affect', and 'preoccupation/anticipation' (craving). Animal and human imaging studies have revealed discrete circuits that mediate the three stages of the addiction cycle with key elements of the ventral tegmental area and ventral striatum as a focal point for the binge/intoxication stage, a key role for the extended amygdala in the withdrawal/negative affect stage, and a key role in the preoccupation/anticipation stage for a widely distributed network involving the orbitofrontal cortex-dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula involved in craving and the cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices in disrupted inhibitory control. The transition to addiction involves neuroplasticity in all of these structures that may begin with changes in the mesolimbic dopamine system and a cascade of neuroadaptations from the ventral striatum to dorsal striatum and orbitofrontal cortex and eventually dysregulation of the prefrontal cortex, cingulate gyrus, and extended amygdala. The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.

0 comments Cited 672 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Large-Scale Network Dysfunction in Major Depressive Disorder: A Meta-analysis of Resting-State Functional Connectivity.

Roselinde H. Kaiser, Jessica Andrews-Hanna, Tor Wager … (2015)

Major depressive disorder (MDD) has been linked to imbalanced communication among large-scale brain networks, as reflected by abnormal resting-state functional connectivity (rsFC). However, given variable methods and results across studies, identifying consistent patterns of network dysfunction in MDD has been elusive.

0 comments Cited 608 times – based on 0 reviews      Review now

All references

Author and article information

Contributors

Serenella Tolomeo: Serenella_Tolomeo@ihpc.a-star.edu.sg

Rongjun Yu:

ORCID: http://orcid.org/0000-0003-0123-1524

rongjunyu@hkbu.edu.hk

Journal

Journal ID (nlm-ta): Transl Psychiatry

Journal ID (iso-abbrev): Transl Psychiatry

Title: Translational Psychiatry

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2158-3188

Publication date (Electronic): 28 January 2022

Publication date PMC-release: 28 January 2022

Publication date Collection: 2022

Volume: 12

Electronic Location Identifier: 41

Affiliations

[1 ]GRID grid.185448.4, ISNI 0000 0004 0637 0221, Institute of High Performance Computing, , Agency for Science, Technology and Research (A*STAR), ; Singapore, Singapore

[2 ]GRID grid.221309.b, ISNI 0000 0004 1764 5980, Department of Management, , Hong Kong Baptist University, ; Hong Kong, China

[3 ]GRID grid.221309.b, ISNI 0000 0004 1764 5980, Department of Sport, Physical Education and Health, , Hong Kong Baptist University, ; Hong Kong, China

[4 ]GRID grid.221309.b, ISNI 0000 0004 1764 5980, Department of Physics, , Hong Kong Baptist University, ; Hong Kong, China

Author information

Rongjun Yu http://orcid.org/0000-0003-0123-1524

Article

Publisher ID: 1792

DOI: 10.1038/s41398-022-01792-6

PMC ID: 8799706

PubMed ID: 35091540

SO-VID: acdbac9a-79ff-4aae-ad5b-9e2d8f40477c

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.