The cerebral and cognitive consequences of alcohol-dependence have been widely explored during the last decades, but the emotional and interpersonal alterations associated with this psychiatric state have only been described recently. In view of the implication of these deficits in relapse after detoxification and of their omnipresence in clinical settings, there is an urgent need to further study these affective and social deficits presented by alcohol-dependent individuals. The present communication aims at offering a summary of the available empirical results on this topic and at underlining the usefulness of a multidisciplinary neuroscience approach to better understand these alterations. The initial studies, focusing on emotion decoding abilities, will first be described as they clearly established that alcohol-dependence is associated with a massive deficit in the identification of the emotional content of faces. The causal link between emotional alterations and alcohol-related problems will also be evoked, with a special focus on recent studies exploring the roots of alcohol-dependence. We will then show how more recent studies have capitalized on these first results to further explore affective and social abilities in alcohol-dependence, leading to the current development of a new research field: the affective and social neurosciences of alcohol-dependence, which combines neuroscience approaches by integrating neuropsychological, electrophysiological and neuroimaging techniques. Finally, we will identify the main fundamental and clinical perspectives in this field, and we will particularly insist on: (1) the need to take the emotional and social impairments into account in the new theoretical models of addictive states and; (2) the urgency to develop neuropsychological programs specifically dedicated to the rehabilitation of these deficits.

Part of the familial factor of alcoholism is associated with the existence of genetic vulnerability. Genetic factors which interact with the pathogenesis of alcoholism are nevertheless complex, partial and for the moment partly unknown at the biological level. Recently, many association studies have been published concerning alcohol-dependence and genes coding for the second dopamine receptor. These associations, which have had positive replications, raise many questions. First of all, should the inheritance of alcoholism be regarded as a definitive fact? Secondly what is inherited? It could be alcoholism in general, a component of this disease (for instance, dependence on, sensitivity to or the seeking-process for alcohol), a specific pattern of drinking, presence of complications linked to alcohol abuse, or more general features, common to many addiction diseases. Thirdly, how could dopamine be linked to alcoholism? Furthermore, how should these positive associations be considered, given that two of these studies were negative, and that all linkage studies were negative. Lastly, are there other clues and ways of finding genetic vulnerability factors for alcohol abuse?

Emotional and interpersonal difficulties have been widely described in alcohol-dependence [1] and are thought to play a crucial role in the development and maintenance of this disease [2]. In particular, impairments in the decoding of emotional facial expression (EFE) have been repeatedly reported and may have serious deleterious effects for the everyday life of alcohol-dependent individuals (ADI), notably by affecting their interpersonal relationships [3]. However, the large majority of earlier studies that assessed emotional decoding abilities among ADI were interested in the processing of prototypical full-blown EFE while in everyday social life, EFE are usually not entirely straightforward but are rather composed of a mix of different emotions [4]. The aim of this study was therefore to determine whether ADI exhibit the categorical perception effect, which is a critical process observed in healthy populations to efficiently decode ambiguous EFE. Nineteen recently detoxified ADI and 19 healthy controls (HC), matched for age and gender, were presented with facial stimuli depicting [4] EFE (happy, angry, sad, and neutral), morphed along continua between each possible pair of emotions. Participants had to indicate the predominant emotion within the randomly presented facial stimuli. For each EFE, a sigmoid function that estimated the percentage of identifications according to the morph steps was adjusted for each participant's data. While there was no significant group difference regarding the response slope (indicating how abruptly the shift in responses happens), the identification threshold (i.e. the function midpoint) was significantly increased in ADI compared to HC, independently of the EFE category. The categorical perception of EFE per se appeared thus preserved in alcohol-dependence, but ADI exhibited a bias in EFE decoding characterized by a global under-identification. To conclude, this study is the first to evidence an EFE processing deficit in ADI by using this kind of emotional continuum paradigm measuring the categorical perception effect.