Emotional cognition and effective interpretation of affective information is an important factor in social interactions and everyday functioning, and difficulties in these areas may contribute to aetiology and maintenance of mental health conditions. In younger people with depression and anxiety, research suggests significant alterations in behavioural and brain activation aspects of emotion processing, with a tendency to appraise neutral stimuli as negative and attend preferentially to negative stimuli. However, in ageing, research suggests that emotion processing becomes subject to a ‘positivity effect’, whereby older people attend more to positive than negative stimuli.

This review examines data from studies of emotion processing in Late-Life Depression and Late-Life Anxiety to attempt to understand the significance of emotion processing variations in these conditions, and their interaction with changes in emotion processing that occur with ageing.

We conducted a systematic review following PRISMA guidelines. Articles that used an emotion-based processing task, examined older persons with depression or an anxiety disorder and included a healthy control group were included.

In Late-Life Depression, there is little consistent behavioural evidence of impaired emotion processing, but there is evidence of altered brain circuitry during these processes. In Late-Life Anxiety and Post-Traumatic Stress disorder, there is evidence of interference with processing of negative or threat-related words.

How these findings fit with the positivity bias of ageing is not clear. Future research is required in larger groups, further examining the interaction between illness and age and the significance of age at disease onset.

The apolipoprotein E ε4 allele (APOE*ε4) is indicated as a risk for Alzheimer's disease and other age-related diseases. The risk attributable to APOE*ε4 for depression is less clear and may be because of confounding of the relationship between dementia and depression.

We examined the risk of APOE* ε4 for incident depression and depressive symptomology over a 12-year period across the adult lifespan.

Participants were from the Personality and Total Health Through Life study, aged 20 to 24 (n = 1420), 40 to 44 (n = 1592) or 60–64 (n = 1768) at baseline, and interviewed every 4 years since 1999. Ethnicities other than White, those without genotyping and those with depression at baseline, or who reported strokes and scores on the Mini-Mental State Examination <27 at any observation, were excluded.

Over the study period, there was no evidence that APOE*ε4+ was a risk factor for depression, including any depression (odds ratio (OR) = 0.94, 95% CI 0.77–1.16, P = 0.573), major depression (OR = 0.96, 95% CI 0.60–1.53, P = 0.860), minor depression (OR = 0.94, 95% CI 0.67–1.30, P = 0.695) or depressive symptomology (incidence rate ratio (IRR) = 1.02, 95% CI 0.97–1.08, P = 0.451). APOE*ε4 was unrelated to incident depression. Findings were consistent for all age cohorts.

Among cognitively intact Australian adults who were free of depression at baseline, there was little evidence that APOE*ε4+ carriers are at increased risk for depression over a 12-year period among those who are cognitively intact.

Cognitive impairment is considered a core feature of major depressive disorder (MDD) and research into psychological treatments aiming to address cognitive impairment are gaining momentum. Compared with the well-established research base of cognitive treatment trials in schizophrenia, including meta-analyses, mood disorder research is much more preliminary.

To focus on identifying the important factors to consider in developing larger-scale psychological treatment trials targeting cognitive impairment in mood disorders. Trial design recommendations have been published for cognitive treatment trials in bipolar disorder.

An in-depth discussion of methodological considerations in the development of cognitive treatment trials for MDD.

Methodological considerations include: screening for, and defining, cognitive impairment; mood state when cognitive intervention begins; medication monitoring during cognitive interventions; use of concomitant therapy; level of therapist involvement; duration and dose of treatment; choice of specific cognitive training exercises; home practice; improving adherence; appropriate comparison therapies in clinical trials; and choice of primary outcomes.

As well as guidance for clinical trial development, this review may be helpful for clinicians wanting to provide cognitive interventions for individuals with MDD.

Subjective cognitive difficulties are common in mental illness and have a negative impact on role functioning. Little is understood about subjective cognition and the longitudinal relationship with depression and anxiety symptoms in young people.

To examine the relationship between changes in levels of depression and anxiety and changes in subjective cognitive functioning over 3 months in help-seeking youth.

This was a cohort study of 656 youth aged 12–25 years attending Australian headspace primary mental health services. Subjective changes in cognitive functioning (rated as better, same, worse) reported after 3 months of treatment was assessed using the Neuropsychological Symptom Self-Report. Multivariate multinomial logistic regression analysis was conducted to evaluate the impact of baseline levels of and changes in depression (nine-item Patient Health Questionnaire; PHQ9) and anxiety symptoms (seven-item Generalised Anxiety Disorder scale; GAD7) on changes in subjective cognitive function at follow-up while controlling for covariates.

With a one-point reduction in PHQ9 at follow-up, there was an estimated 11–18% increase in ratings of better subjective cognitive functioning at follow-up, relative to stable cognitive functioning. A one-point increase in PHQ9 from baseline to follow-up was associated with 7–14% increase in ratings of worse subjective cognitive functioning over 3 months, relative to stable cognitive functioning. A similar attenuated pattern of findings was observed for the GAD7.

A clear association exists between subjective cognitive functioning outcomes and changes in self-reported severity of affective symptoms in young people over the first 3 months of treatment. Understanding the timing and mechanisms of these associations is needed to tailor treatment.

Depression is characterised by negative views of the self. Antidepressant treatment may remediate negative self-schema through increasing processing of positive information about the self. Changes in affective processing during social interactions may increase expression of prosocial behaviours, improving interpersonal communications.

To examine whether acute administration of citalopram is associated with an increase in positive affective learning biases about the self and prosocial behaviour.

Healthy volunteers (n = 41) were randomised to either an acute 20 mg dose of citalopram or matched placebo in a between-subjects double-blind design. Participants completed computer-based cognitive tasks designed to measure referential affective processing, social cognition and expression of prosocial behaviours.

Participants administered citalopram made more cooperative choices than those administered placebo in a prisoner's dilemma task (β = 20%, 95% CI: 2%, 37%). Exploratory analyses indicated that participants administered citalopram showed a positive bias when learning social evaluations about a friend (β = 4.06, 95% CI: 0.88, 7.24), but not about the self or a stranger. Similarly, exploratory analyses found evidence of increased recall of positive words and reduced recall of negative words about others (β = 2.41, 95% CI: 0.89, 3.93), but not the self, in the citalopram group.

Participants administered citalopram showed greater prosocial behaviours, increased positive recall and increased positive learning of social evaluations towards others. The increase in positive affective bias and prosocial behaviours towards others may, at least partially, be a mechanism of antidepressant effect. However, we found no evidence that citalopram influenced self-referential processing.

Cognitive impairment is a core feature of depression and has a negative effect on a person's functioning, in psychosocial and interpersonal areas, and on workforce performance. Cognitive impairment often persists, even with the remittance of mood symptoms. One potential way of improving treatment of cognitive impairment would be to identify variables that predict cognitive change in patients with depression.

To systematically examine findings from studies that investigate baseline variables and how they predict, or correlate with, cognitive change in mood disorders, and to examine methodological issues from these studies.

Studies that directly measured associations between at least one baseline variable and change in cognitive outcome in patients with current major depressive episode were identified using PubMed and Web of Science databases. Narrative review technique was used because of the heterogeneity of patient samples, outcome measures and study procedures. The review was registered on PROSPERO with registration number CRD42020150975.

Twenty-four studies met the inclusion criteria. Evidence from the present review for prediction of cognitive change from baseline variables was limited for demographic factors, with some preliminary evidence for depression, cognitive and biological factors. Identification of patterns across studies was difficult because of methodological variability across studies.

Findings from the present review suggest there may be some baseline variables that are useful in predicting cognitive change in mood disorders. This is an area warranting further research focus.

People with bipolar disorder have moderate cognitive difficulties that tend to be more pronounced during mood episodes but persist after clinical remission and affect recovery. Recent evidence suggests heterogeneity in these difficulties, but the factors underlying cognitive heterogeneity are unclear.

To examine whether distinct cognitive profiles can be identified in a sample of euthymic individuals with bipolar disorder and examine potential differences between subgroups.

Cognitive performance was assessed across four domains (i.e. processing speed, verbal learning/memory, working memory, executive functioning) in 80 participants. We conducted a hierarchical cluster analysis and a discriminant function analysis to identify cognitive profiles and considered differences in cognitive reserve, estimated cognitive decline from premorbid cognitive functioning, and clinical characteristics among subgroups.

Four discrete cognitive profiles were identified: cognitively intact (n = 25; 31.3%); selective deficits in verbal learning and memory (n = 15; 18.8%); intermediate deficits across all cognitive domains (n = 30; 37.5%); and severe deficits across all domains (n = 10; 12.5%). Cognitive decline after illness onset was greater for the intermediate and severe subgroups. Cognitive reserve scores were increasingly lower for subgroups with greater impairments. A smaller proportion of cognitively intact participants were using antipsychotic medications compared with all other subgroups.

Our findings suggest that individuals with cognitively impaired profiles demonstrate more cognitive decline after illness onset. Cognitive reserve may be one of the factors underlying cognitive variability across people with bipolar disorder. Patients in the intermediate and severe subgroups may be in greater need of interventions targeting cognitive difficulties.