Cognitive neuropsychological theory of antidepressant action: a modern-day approach to depression and its treatment

Beata R Godlewska, Catherine J Harmer, Beata R Godlewska, Catherine J Harmer

Abstract

Depression is a leading cause of disability worldwide and improving its treatment is a core research priority for future programmes. A change in the view of psychological and biological processes, from seeing them as separate to complementing one another, has introduced new perspectives on pathological mechanisms of depression and treatment mode of action. This review presents a theoretical model that incorporated this novel approach, the cognitive neuropsychological hypothesis of antidepressant action. This model proposes that antidepressant treatments decrease the negative bias in the processing of emotionally salient information early in the course of antidepressant treatment, which leads to the clinically significant mood improvement later in treatment. The paper discusses the role of negative affective biases in the development of depression and response to antidepressant treatments. It also discusses whether the model can be applied to other antidepressant interventions and its potential translational value, including treatment choice, prediction of response and drug development.

Keywords: Antidepressant response; Cognitive neuropsychological model; Emotional processing; Negative bias.

Conflict of interest statement

BRG has received travel expenses from Janssen UK. CJH has received consultancy fees from Lundbeck, P1vital, Pfizer, Sage Pharmaceuticals and Servier.

Figures

Fig. 1
Fig. 1
Schematic presentation of the cognitive neuropsychological model of antidepressant action. ‘Classical’ antidepressant drugs (ADs) (i.e. the ones that take weeks to induce mood change, such as selective serotonin reuptake inhibitors, SSRIs, or selective serotonin reuptake inhibitors, SNRIs, significantly improve mood only after a few weeks of treatment, despite biological changes taking place already in the first few hours after the first dose is applied, and continuing thereafter. The model proposes that for these early biological effects to be translated into clinical improvement, two key processes need to happen. The first one is a positive shift in the processing of emotionally salient information. Such a shift has been shown to occur at behavioural and neural level as early as after a single antidepressant dose. Subsequently, this new more positive bias needs to be ‘enacted’ by interactions with the social environment, which leads to the development of new positive associations in the learning associated processes. This happens in the context of continued downstream biological and neuroadaptive processes, for which repeated administration of ADs is needed. This is a lengthy process and explains the delay in the symptomatic improvement.
Fig. 2
Fig. 2
The hypothetical place of rapid acting ADs within the cognitive neuropsychological model of antidepressant action. Rapid-acting ADs, such as ketamine, were hypothesised to reduce or abolish memory for already existing negative associations. This, contrary to learning new positive ones, is a fast process, resulting in faster but more transient effect on mood. More research is needed to validate this hypothesis.
Fig. 3
Fig. 3
A schematic representation of changes in brain activity over an acute (one dose) or short-term (7–10 days) treatment with an antidepressant medication. Brain regions in which such changes were identified are listed in corresponding colour-coded boxes. Emotions, which processing in these regions has changed over treatment, and studies that showed these changes, are listed. Most of the studies used a variation of emotional faces processing task, the minority—self-referential processing task. Medications were applied orally unless otherwise indicated

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