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Our memories for past personally experienced autobiographical events play an important role in therapy, irrespective of presenting issue, diagnoses or therapeutic modality. Here, we summarise evidence for how autobiographical memory abilities can influence our mental health and the relevance of this for the treatment of mental health problems. We then guide the reader through principles and strategies for optimising autobiographical memory within treatment. We ground these recommendations within research for stand-alone interventions for improving autobiographical memory and from studies of how to support the formation and retrieval of therapeutic memories. Options are given for clinicians to guide clients in improving retrieval of autobiographical memories within treatment, for improving autobiographical memory for the therapeutic experience itself, and for creating improvements in autobiographical memory that endure post-treatment. We also provide worksheets for clinicians to use within treatment.

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The memories for past autobiographical experiences that we share can influence relationship formation and consolidation with important implications for our mental health. However, little is known about how people's responses to our memories can influence subsequent memory sharing. Previous research examined how operant processes (i.e., punishment with aversive sounds) influence the sharing of memories for specific events from our past. Understanding the (social) mechanisms associated with difficulty sharing specific autobiographical memories is important given the association between these difficulties and a range of psychiatric diagnoses. We investigate the effects of verbal and non-verbal social operants on the willingness to share specific autobiographical memories. Participants shared memories with a confederate who coded their memories as specific or non-specific and responded in either an engaged/attentive, dismissive manner or gave no feedback depending on participants' assigned condition. Participants who were reinforced for sharing specific memories and punished for sharing non-specific memories, were more likely to share specific than non-specific memories compared to those who received no feedback. Reinforcement alone was not sufficient for modifying specificity. The ways that we respond to people when they share memories with us can influence their subsequent willingness to share specific events from their past.

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BACKGROUND: Anxiety disorders are highly prevalent with an early age of onset. Understanding the aetiology of disorder emergence and recovery is important for establishing preventative measures and optimising treatment. Experimental approaches can serve as a useful model for disorder and recovery relevant processes. One such model is fear conditioning. We conducted a remote fear conditioning paradigm in monozygotic and dizygotic twins to determine the degree and extent of overlap between genetic and environmental influences on fear acquisition and extinction. METHODS: In total, 1937 twins aged 22-25 years, including 538 complete pairs from the Twins Early Development Study took part in a fear conditioning experiment delivered remotely via the Fear Learning and Anxiety Response (FLARe) smartphone app. In the fear acquisition phase, participants were exposed to two neutral shape stimuli, one of which was repeatedly paired with a loud aversive noise, while the other was never paired with anything aversive. In the extinction phase, the shapes were repeatedly presented again, this time without the aversive noise. Outcomes were participant ratings of how much they expected the aversive noise to occur when they saw either shape, throughout each phase. RESULTS: Twin analyses indicated a significant contribution of genetic effects to the initial acquisition and consolidation of fear, and the extinction of fear (15, 30 and 15%, respectively) with the remainder of variance due to the non-shared environment. Multivariate analyses revealed that the development of fear and fear extinction show moderate genetic overlap (genetic correlations 0.4-0.5). CONCLUSIONS: Fear acquisition and extinction are heritable, and share some, but not all of the same genetic influences.

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Impairments in retrieving event-level, specific autobiographical memories, termed overgeneral memory (OGM), are recognised as a feature of clinical depression. A previous meta-analytic review assessing how OGM predicts the course of subsequent depressive symptoms showed small effects for correlations and regression analyses when baseline depressive symptoms were controlled for. We aimed to update this study and examine whether their findings replicate given the decade of research that has been published since. A systematic literature review using the same eligibility criteria as the previous meta-analysis led to a doubling of eligible studies (32 v. 15). The results provided more precise estimates of effect sizes, and largely support the finding that OGM predicts the course of depressive symptoms. The effects were generally small, but significantly larger among clinical samples, compared to studies with non-clinical samples. There was some evidence that higher age was associated with stronger effects, and longer follow-up was associated with weaker effects. The findings on other moderating variables that were analysed were mixed. Continued research into this modifiable cognitive process may help to provide an avenue to better understand and treat highly prevalent and impactful depressive disorders.

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BACKGROUND: Characteristic of the cardinal symptom of anhedonia, people with clinical depression report lower levels of anticipatory pleasure. However, the psychological mechanisms underlying these deficits are poorly understood. This is the first study to assess whether, and to what extent, phenomenological characteristics of episodic future thinking for positive future events are associated with anticipatory pleasure among depressed individuals. METHODS: Individuals with a Major Depressive Episode (MDE; N = 117) and without (N = 47) completed ratings scales for depressive symptoms and trait anticipatory and consummatory pleasure. They then provided descriptions of personally-relevant positive future events and rated them for phenomenological characteristics and state anticipatory pleasure. RESULTS: Between-groups analysis showed that those with MDE reported lower trait anticipatory and consummatory pleasure. They also simulated future events with less specificity, less detail/vividness, less use of mental imagery, less use of first-person perspective, less plausibility/perceived likelihood of occurring, and reported less associated state anticipatory pleasure. In regression analyses in the depressed group, lower scores for detail/vividness, mental imagery, and personal significance all uniquely predicted lower state anticipatory pleasure. LIMITATIONS: Cognitive functioning was not assessed, which may help clarify deficits that underpin these findings. History of previous depressive episodes in the comparison group were not assessed, which may mean the observed between-group effects are underestimated. CONCLUSIONS: This study provides further evidence of deficits in episodic future thinking and anticipatory pleasure in depressed individuals. It also establishes links between particular characteristics of episodic future thinking and state anticipatory pleasure, and indicates cognitive targets that may be amenable to intervention in order to reduce anhedonia.

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People can regulate negative emotional states using personal episodic information stored in memory. However, amongst older adults, assistance in retrieving personal memories might be needed. As such, positive personal images might better facilitate the retrieval of positive personal memories, relative to generic positive images. The present study induced older adults (N = 40; Mage = 76.28) into a negative mood state using a validated film clip ("Dead Man Walking"; Robbins et al. in Dead Man Walking [Cinta Cinematográfica]. PolyGram Filmed Entertainment, Working Title Films, Estados Unidos, 1995). Participants were then shown positive personal images (album photos) or positive non-personal images from the International Affective Picture System (IAPS) and between-group differences in their mood state and their ability to retrieve positive autobiographical memories were measured. Although participants' moods decreased after the negative mood induction, their mood then recovered after picture cuing regardless of whether images were personal or non-personal. Furthermore, the positive mood evoked by non-personal, but not personal, images was significantly positively associated with self-reported feelings of reliving of the memories evoked by those images. These results suggest that, when pictures from personal life are not available, the selection of images able to generate positive autobiographical memories with a sense of reliving, is a feasible tool for older adult's emotional regulation.

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Fear conditioning models key processes related to the development, maintenance and treatment of anxiety disorders and is associated with group differences in anxiety. However, laboratory administration of tasks is time and cost intensive, precluding assessment in large samplesnecessary for the analysis of individual differences. This study introduces a newly developed smartphone app that delivers a fear conditioning paradigm remotely using a loud human scream as an aversive stimulus. Three groups of participants (total n = 152) took part in three studies involving a differential fear conditioning experiment to assess the reliability and validity of a smartphone administered fear conditioning paradigm. This comprised of fear acquisition, generalisation, extinction, and renewal phases during which online US-expectancy ratings were collected during every trial with evaluative ratings of negative affect at three time points. We show that smartphone app delivery of a fear conditioning paradigm results in a pattern of fear learning comparable to traditional laboratory delivery and is able to detect individual differences in performance that show comparable associations with anxiety to the prior group differences literature.

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The presence of oxidized species of the dithiol-chelating agents, meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercaptopropane-1-sulfonic acid (DMPS), in human urine was determined by chemical and electrolytic reduction methods. Urine from a human given either DMSA or DMPS was treated with electrolysis, dithiothreitol, or sodium tetrahydridoborate (NaBH4). The SH groups were derivatized with monobromobimane for the determination of unaltered dithiols. Total dithiol (unaltered and oxidized) was determined by reduction followed by derivatization with monobromobimane. The bimane derivatives were identified and quantified by HPLC and fluorescence. Although all three reduction methods gave similar results, electrolytic reduction of oxidized DMSA and chemical reduction with NaBH4 of oxidized DMPS are recommended based upon both day to day reproducibility and recovery of standards. After reduction a 4-fold increase in DMSA and a 20-fold increase in DMPS were found in urine by 12 h after an oral dose of DMSA or DMPS. These new methods for the determination of dithiols and their oxidized forms should lead to a better understanding of the metabolic properties of these increasingly important orally effective chelating agents.

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When the amplitude of pupillary contraction of normal, healthy adults was binocularly recorded as a function of increasing intensity of light-stimulation, a linear relationship was found between the amplitude and log intensity. Schizophrenic patients deviated significantly from this systematic response pattern in two ways. One group of patients (35%) manifested the same pupillomotor threshold as the normals, however, as the intensity of light was systematically increased mean amplitude and rate of pupillary contraction fell below that evidenced by normals. Another group of patients (65%) were distinguished by an abnormal pupillomotor threshold, specifically requiring an increase of one log intensity unit for the elicitation of a recordable pupillary contraction. Moreover, as the light intensity increased, the mean amplitude of contraction was significantly attenuated at all intensities below that of the normals and of the schizophrenics who manifested a normal pupillomotor threshold. In addition, it was found that the average diameter of the dark-adapted pupil was smaller in both groups of patients as compared to the healthy adults, although there was no difference between the patient groups on the variable. As pupillary reactivity to stress in normals is characterized by an increase in the diameter of the dark-adapted pupil representing increased sympathetic outflow and by a reciprocal increase in the diameter of the light-adapted pupil representing increased supranuclear inhibition, the results of the study do not support the assertion that schizophrenics are hyperaroused. It is suggested schizophrenia may be considered a tonic autonomic dysfunctional state of mock-arousal characterized by either abnormally high levels of central supranuclear inhibition or by defective sympathetic outflow, or both.

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