Addiction management is complex, and it requires a bio-psycho-social perspective, that ought to consider the multiple etiological and developmental factors. Because of this, a large amount of resources has been allocated to assess the vulnerability to dependence, i.e., to identify the processes underlying the transition from substance use to dependence, as well as its course, in order to determine the key points in its prevention, treatment, and recovery. Consequently, knowledge from neuroscience must be taken into account, which is why different initiatives have emerged with this objective, such as the "Research Domain Criteria" (RDoC), and the "Addiction Neuroclinical Assessment" (ANA). Particularly, neuropsychophysiological measures could be used as markers of cognitive and behavioral attributes or traits in alcohol dependence, and even trace clinical change. In this way, the aim of this narrative review is to provide an overview following ANA clinical framework, to the most robust findings in neuropsychophysiological changes in alcohol dependence, that underlie the main cognitive domains implicated in addiction: incentive salience, negative emotionality and executive functioning. The most consistent results have been found in event-related potential (ERP) analysis, especially in the P3 component, that could show a wide clinical utility, mainly for the executive functions. The review also shows the usefulness of other components, implicated in affective and substance-related processing (P1, N1, or the late positive potential LPP), as well as event-related oscillations, such as theta power, with a possible use as vulnerability or clinical marker in alcohol dependence. Finally, new tools emerging from psychophysiology research, based on functional connectivity or brain graph analysis could help towards a better understanding of altered circuits in alcohol dependence, as well as communication efficiency and effort during mental operations. This review concludes with an examination of these tools as possible markers in the clinical field and discusses methodological differences, the need for more replicability studies and incipient lines of work. It also uses consistent findings in psychophysiology to draw possible treatment targets and cognitive profiles in alcohol dependence.

The cognitive decline in people with substance use disorders is well known and can be found during both the dependence and drug abstinence phases. At the clinical level, cognitive decline impairs the response to addiction treatment and increases dropout rates. It can be irreversible, even after the end of drug abuse consumption. Improving our understanding of the molecular and cellular alterations associated with cognitive decline could be essential to developing specific therapeutic strategies for its treatment. Developing animal models to simulate drug abuse-induced learning and memory alterations is critical to continue exploring this clinical situation. The main aim of this review is to summarize the most recent evidence on cognitive impairment and the associated biological markers in patients addicted to some of the most consumed drugs of abuse and in animal models simulating this clinical situation. The available information suggests the need to develop more studies to further explore the molecular alterations associated with cognitive impairment, with the ultimate goal of developing new potential therapeutic strategies.

Aims: To assess inhibitory processes and the ongoing event-related potential (ERP) activity of offspring of alcoholics (OA) during a Go/No-Go task, with the purpose of characterizing possible psychophysiological endophenotypes for alcohol-dependent vulnerability. Short summary: EEG recordings and ERP measurements of young adults with positive and negative family history of alcoholism where obtained while they performed a Go/No-Go task to assess inhibitory processes. Offspring of alcoholics showed a different ERP pattern compared to the control group and exerted greater effort than the control group. Methods: ERP measurements were obtained by electroencephalogram (EEG) recordings of 65 participants divided into two groups: one group of 30 subjects with positive family history of alcoholism and a control group of 35 subjects with negative family history of alcoholism. They performed a Go/No-Go task, where each individual was required to classify visual stimuli by colour (Go) and inhibit their response to a No-Go signal. Results: OA have higher P3 amplitudes during the Go condition in all of the regions analysed and higher No-Go P3 amplitudes than control subjects in the frontal region. Unlike controls, OA have no differences between the P3 amplitudes across conditions. Conclusions: The absence of differences between the P3 Go and No-Go observed in the OA group can be interpreted as a possible alteration related with inhibition, in a way that they may need to recruit similar resources for inhibitory and classificational processes for both conditions. Therefore, the P3 component may be considered as a useful endophenotype and a vulnerability marker to develop addictive behaviour.