Neuroplastic and cognitive impairment in substance use disorders: a therapeutic potential of cognitive stimulation

Sampedro-Piquero, Patricia; Guevara‐Miranda, David Ladrón de; Pavón, Francisco Javier; Serrano, Antonia; Suárez, Juan; Fonseca, Fernando Rodrı́guez de; Santín, Luis J.; Castilla‐Ortega, Estela

doi:10.1016/j.neubiorev.2018.11.015

Cited by 57 publications

(56 citation statements)

References 589 publications

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“…16, p=1.5e-04), pointing to a common neurobiological aetiology. This is consistent with research indicating that cognitive deficits such as impaired response inhibition and working memory are important features of both ADHD and substance abuse 20,21 , and that both ADHD and substance abuse can be considered forms of externalizing disorders 22 .…”

Section: Introductionsupporting

confidence: 90%

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Treur

Demontis

Sallis

et al. 2019

Preprint

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BackgroundAttention-deficit hyperactivity disorder (ADHD) has consistently been associated with substance (ab)use, but the nature of this association is not fully understood. In view of preventive efforts, a vital question is whether there are causal effects, from ADHD to substance use and/or from substance use to ADHD.MethodsWe applied bidirectional Mendelian randomization using summary-level data from the largest available genome-wide association studies (GWASs) on ADHD, smoking (initiation, cigarettes/day, cessation, and a compound measure of lifetime smoking), alcohol use (drinks/week and alcohol use disorder), cannabis use (initiation and cannabis use disorder (CUD)) and coffee consumption (cups/day). Genetic variants robustly associated with the ‘exposure’ were selected as instruments and then identified in the ‘outcome’ GWAS. Effect estimates from individual genetic variants were combined with inverse-variance weighted regression and five sensitivity analyses were applied (weighted median, weighted mode, MR-Egger, generalized summary-data-based MR, and Steiger filtering).ResultsWe found strong evidence that liability to ADHD increases likelihood of smoking initiation and also cigarettes per day among smokers, decreases likelihood of smoking cessation, and increases likelihood of cannabis initiation and CUD. In the other direction, there was evidence that liability to smoking initiation and CUD increase ADHD risk. There was no clear evidence of causal effects between liability to ADHD and alcohol or caffeine consumption.ConclusionsWe find evidence for causal effects of liability to ADHD on smoking and cannabis use, and of liability to smoking and cannabis use on ADHD risk, indicating bidirectional pathways. Further work is needed to explore causal mechanisms.

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Section: Introductionsupporting

confidence: 90%

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Treur

Demontis

Sallis

et al. 2019

Preprint

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“…The prefrontal cortex has a key role in behavioral control, by guiding the dorsal striatum to select appropriate actions through the abovementioned cortico-striatal circuit [88] (Section 3) and by inhibiting or updating inappropriate behaviors (reviewed in [15]). Accordingly, the prefrontal cortex is responsible of higher cognitive process such as planning, reasoning, behavioral flexibility, or decision-making (executive functions), and it holds the "working-memory" capacity that allows to manipulate information that is stored in the short-term (reviewed in [15]). The hippocampus is involved in the acquisition, long-term storage, and further processing (extinction, retrieval, updating, etc.)…”

Section: Limbic Regions: the Prefrontal Cortex The Amygdala And Thementioning

confidence: 99%

“…In this way, the prefrontal cortex guides the dorsal striatum and acts as an "ON/OFF switch" for drug-seeking, deciding when this behavior should be allowed or inhibited [105]. Regarding the hippocampus and the amygdala, they interact with the prefrontal cortex and the accumbens for the learning of drug-stimuli associations; and these limbic regions collaborate for the subsequent retrieval, extinction, or reinstatement of the drug-related memories (being the reinstatement, a form of "relapse," that in preclinical models is elicited by drug-associated cues, by stress, or by a low dose of the drug-priming) (reviewed in [15,27,116]). Since the drug-related experiences are rewarding and emotionally arousing, they activate neurobiological pathways involved in the emotional enhancement of associative memory, which may potentiate their acquisition and subsequent long-term maintenance [116,117].…”

Section: Limbic Regions: the Prefrontal Cortex The Amygdala And Thementioning

confidence: 99%

“…It is important to note that the aberrant brain structure and function associated to drug addiction most likely results from a combination of (biological) brain features that exist previous to drug use as vulnerability factors, with the neuroadaptations that are induced by the drug itself ( Figure 1A). Solid evidence has been provided in both ways (reviewed in [15]). On the one hand, individual differences in the form of stable personality traits such as impulsivity, elevated anxiety, risk-taking, and sensation seeking that are assumed to entail a particular biological and brain basis [16,17] may predispose to engage in both drug use and addiction.…”

Section: Introductionmentioning

confidence: 99%

“…On the one hand, individual differences in the form of stable personality traits such as impulsivity, elevated anxiety, risk-taking, and sensation seeking that are assumed to entail a particular biological and brain basis [16,17] may predispose to engage in both drug use and addiction. On the other hand, brain and behavioral abnormalities often correlate with drug use patterns (i.e., the amount of drug consumed and/or the number of years using the drug) and may be completely or partially recovered by protracted drug abstinence [7,8,11,13,15,18], suggesting that they were directly induced by the continuous action of the drug. Notably, preclinical studies in laboratory animals (that allow the exposure to the drug to be controlled by the experimenter) have confirmed both evidences.…”

Section: Introductionmentioning

confidence: 99%

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Aberrant Brain Neuroplasticity and Function in Drug Addiction: A Focus on Learning-Related Brain Regions

Sampedro-Piquero¹,

Santín²,

Castilla‐Ortega³

2019

Behavioral Neuroscience

Self Cite

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This chapter will review the altered brain structure and function associated to drug addiction, with a focus on brain regions involved in learning and motivated behavior. As evidenced by both clinical and preclinical studies, repeated drug exposure affects whole brain neuroplasticity including the mesolimbic system which is a main locus for reward, an action-control center such as the dorsal striatum, and limbic brain regions such as the prefrontal cortex, the hippocampus, and the amygdala that are involved in behavioral control, memory, and mood. In this way, the drug-seeking actions that were initially intentional responses become involuntary habits governed by the dorsal striatum. Drug addiction may also curse with a reduced ability to experience rewards that are unrelated to drugs and emotional dysregulation, while the impairment on limbic regions contributes to generate cognitive symptoms. These entail persistent memories for previous experiences with the drug contrasting with a global cognitive decline that may hamper the acquisition of new, adaptive learnings. Overall, these features promote a desire for the drug, leading to relapse in drug use. Further drug exposure, in turn, aggravates its consequences on the brain and behavior, creating the harmful "addiction cycle."

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Recovery of superior frontal gyrus cortical thickness and resting‐state functional connectivity in abstinent heroin users after 8 months of follow‐up

Yang

Zhang

Tang

et al. 2022

Human Brain Mapping

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Compared with healthy controls, heroin users (HUs) show evidence of structural and functional brain alterations. However, little is known about the possibility of brain recovery after protracted heroin abstinence. The purpose of this study was to investigate whether brain recovery is possible after protracted abstinence in HUs. A total of 108 subjects with heroin addiction completed structural and functional scans, and 61 of those subjects completed 8-month follow-up scans. Resting-state data and 3D-T1 MR images were collected for all participants, first at baseline and again after 8 months. Cognitive function and craving were measured by the Trail Making Test-A (TMT-A) and Visual Analog Scale for Craving, respectively. The cortical thickness and resting-state functional connectivity (RSFC) differences were then analyzed and compared between baseline and follow-up, and correlations were obtained between neuroimaging and behavioral changes. HUs demonstrated improved cognition (shorter TMT-A time) and reduced craving at the follow-up (HU2) relative to baseline (HU1), and the cortical thickness in the bilateral superior frontal gyrus (SFG) was significantly greater at HU2 than at HU1. Additionally, the RSFC of the left SFG with the inferior frontal gyrus (IFG), insula, and nucleus accumbens and that of the right SFG with the IFG, insula and orbitofrontal cortex (OFC) were increased at HU2. The changes in TMT-A time were negatively correlated with the RSFC changes between the left SFG and the bilateral IFG, the bilateral caudate, and the right insula. The changes in

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Neuroplastic and cognitive impairment in substance use disorders: a therapeutic potential of cognitive stimulation

Cited by 57 publications

References 589 publications

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

Aberrant Brain Neuroplasticity and Function in Drug Addiction: A Focus on Learning-Related Brain Regions

Recovery of superior frontal gyrus cortical thickness and resting‐state functional connectivity in abstinent heroin users after 8 months of follow‐up

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