Table 1.

Overview of addiction-related neurocognitive constructs and related brain circuits, tasks, and interventions.

	Positive affect, Response (13), (80), (82), (84)	Positive affect, Anticipation (13), (83), (84)	Negative affect (13), (80), (82),	Learning/habit (13), (83), (84)	Cognitive control (13), (82), (83), (84)	Interoception (83), (86)
Brain circuit	Medial OFC, ventral striatum	Medial OFC, sgACC (subgenual)	Amygdala	Lateral OFC, Dorsal striatum (Caudate, putamen), Hippocampus	DLPFC, dACC (dorsal), IFG	Insula, posterior cingulate
fMRI tasks	Monetary incentive delay (reward receipt) (87), probabilistic reward task (88), activity incentive Delay task (98)	Monetary Incentive delay (reward anticipation) (87), cue-reactivity (90), attentional bias (89)	Cue reactivity (90) during withdrawal, negative or stress cue reactivity	Instrumental reward-gain and loss-avoidance task (89)	Stop Signal (91), Go-no go (92), Stroop (93), PASAT-M (97)	heartbeat counting task (94), visceral interoceptive attention task (95)
Cognitive	Reward receipt, response to reward, reward satiation	Motivation, saliency valuation, reward anticipation, drive expectancy, approach/attentional bias	Acute/sustained threat	Stimulus-response conditioned habits, compulsivity, learning reward/loss contingencies	Loss of cognitive control, disinhibition, performance monitoring, action/response selection, low distress tolerance	"Momentary mapping of the body’s internal landscape" (96) during craving and withdrawal
Behavior	Experience of reward with drug use, response to substance-free reward	Increased: attention/salience of drugs and related stimuli, reward when anticipating drug use.	Experience of withdrawal, stress, anxiety, anhedonia	Drug use as: repetitive, compulsive drive, conditioned response to seek positive affect & avoid/mitigate negative affect, learnt association with people, situations, places	Drug use even when known as harmful and in response to affective distress	Heightened/lowered awareness to drug-related physical & psychological states; increase distance between cue and behavioral response.
Intervention strategies	Decrease reward value of drug (e.g., methadone or nicotine patches), suppression of mPFC with low frequency rTMS or cTBS; increase reward value of drug-free activities (e.g., behavioral activation, physical activity)	Cognitive bias modification, reappraisal training for drug cues, exposure therapy, motivational interviewing, contingency management	Strategies to address negative affect (e.g., behavioral activation and cognitive reappraisal training), medication that counter stress response, rtfMRI neurofeedback on Insula or sgACC	Strategies that weaken conditioned drug behaviors, memory reconsolidation	Strengthen inhibitory/executive control, inhibitory control training (e.g., Go-No-Go), working memory training, goal management training, stimulating DLPFC with anodal tDCS or high frequency rTMS	Mindfulness-based therapies, physical exercise

Columns reflect key neurocognitive constructs for addiction research. Identified constructs also map onto the three domains of the Addiction Neuroclinical Assessment (ANA) (11) framework: Positive affect (response and anticipation), Negative affect, and Cognitive control map directly onto the three domains of ANA (i.e., Incentive salience, Negative affectivity and Executive function). Learning/habit is part of Incentive salience (reward learning); Interoception is at the interface of the three ANA domains. Rows reflect functional neuroimaging methods (e.g., fMRI tasks), cognitive/behavioral assessments, and examples of neuroscience informed intervention strategies aligned with each of the identified constructs.

ACC, anterior cingulate cortex; cTBS, continuous theta burst stimulation; DLPFC, dorsolateral PFC; IFG, Inferior Frontal Gyrus; mPFC, medial PFC; OFC, orbitofrontal cortex; PFC, prefrontal cortex; rtfMRI, real-time functional MRI; rTMS, repeated transcranial magnetic stimulation; tDCS, transcranial direct current stimulation.