Speaker 4: Trevor Robbins, UK

s | 25 further mechanistic evidence for its beneficial effect on cognitive function. Through continued research efforts vortioxetine showed to be an antidepressant with a distinct clinical and pharmacological profile different from other currently available antidepressants, with a proven beneficial effect on CD in patients with MDD. Speaker 4: Trevor Robbins, UK Title: Translational models for drug discovery in depression Abstract Clinical depression entails cognitive deficits often across a range of domains including impairments, not only of memory but also executive functioning, such as decision-making, sustained attention (‘concentration’) and working memory, although these deficits are frequently age-dependent and correlated with discrete brain pathology. I will review evidence of heterogeneous and homologous patterns of cognitive deficit across a number of human and animal studies focusing especially on decision-making and attention, measured in a variety of ways. In addition, it is evident that depression is also associated with distinctive cognitive or affective biases evident in different settings, such as a tendency to say “no” in tests of memory recognition, to over-respond to faces expressing negative emotion, to overreact to negative feedback and also to respond more quickly to sad rather than happy words. These phenomena indicate the importance in depression of a motivational interface with respect to cognitive function and vice versa. By comparison, preclinical models of depression have frequently been criticised for their emphasis on species-typical maladaptive responses to stress (as in chronic mild stress, learned helplessness and ‘behavioural despair’), that are more predictive of the effects of drugs assumed to have anti-depressant effects than the symptoms of human depression themselves. Recently however, relevant aspects of behaviour such as affective bias and response to negative feedback have been employed successfully in rodents in a manner parallel to what is measured in human depressed patients, using for example tests of generalisation and probabilistic reversal learning. These new tests may complement the rich translational tests we already have available for assessing other aspects of cognition in humans and experimental animals and their neural correlates.Clinical depression entails cognitive deficits often across a range of domains including impairments, not only of memory but also executive functioning, such as decision-making, sustained attention (‘concentration’) and working memory, although these deficits are frequently age-dependent and correlated with discrete brain pathology. I will review evidence of heterogeneous and homologous patterns of cognitive deficit across a number of human and animal studies focusing especially on decision-making and attention, measured in a variety of ways. In addition, it is evident that depression is also associated with distinctive cognitive or affective biases evident in different settings, such as a tendency to say “no” in tests of memory recognition, to over-respond to faces expressing negative emotion, to overreact to negative feedback and also to respond more quickly to sad rather than happy words. These phenomena indicate the importance in depression of a motivational interface with respect to cognitive function and vice versa. By comparison, preclinical models of depression have frequently been criticised for their emphasis on species-typical maladaptive responses to stress (as in chronic mild stress, learned helplessness and ‘behavioural despair’), that are more predictive of the effects of drugs assumed to have anti-depressant effects than the symptoms of human depression themselves. Recently however, relevant aspects of behaviour such as affective bias and response to negative feedback have been employed successfully in rodents in a manner parallel to what is measured in human depressed patients, using for example tests of generalisation and probabilistic reversal learning. These new tests may complement the rich translational tests we already have available for assessing other aspects of cognition in humans and experimental animals and their neural correlates. S16: Cognitive Function in Bipolar Disorder: State of the Art Chair: Lakshmi Yatham, Canada Co-Chair: Shigenobu Kanba, Japan Speaker 1: Eduard Vieta, Spain Title: Cognitive impairment in bipolar disorder: Magnitude, moderators, and prevention strategies Abstract Neurocognition has been the focus of extensive research in schizophrenia and, more recently, in bipolar disorder and in depression (1). Neuropsychological testing may represent a tool able to identify potential neuroimaging markers and endophenotypes and to better understand the underlying neurophysiology (2). However, only lately the highly consistent findings from research began to be applied to clinical practice, and many clinicians are not yet much aware of how neurocognitive deficits affect their patients’ daily life, and, importantly, what can be done to prevent or at least mitigate cognitive impairment. Recent evidence suggests that neurocognitive status may be the most powerful predictor of functional outcome in BD, even more so than clinical features. Cognitive deficits may be related to neurodevelopmental issues, but in bipolar disorder the most accepted model is the “neuroprogression” one, in which recurring episodes and concurrent allostatic load contribute to neuropsychological difficulties and disability. Comorbidities and medication may also contribute to cognitive deficits. Research efforts are now focusing on drugs to ameliorate cognition and psychological interventions, such as functional remediation (3), which may have a positive impact on cognitive and functional outcome. Potential strategies aimed at preventing cognitive impairment and neuroprogression include: Effective pharmacotherapy for relapse prevention, psychoeducation, healthy habits (physical exercise, diet, sleep, no smoking), and cognitive enhancing psychological interventions (i.e.: promotion of cognitive reserve) and pro-cognitive drugs.Neurocognition has been the focus of extensive research in schizophrenia and, more recently, in bipolar disorder and in depression (1). Neuropsychological testing may represent a tool able to identify potential neuroimaging markers and endophenotypes and to better understand the underlying neurophysiology (2). However, only lately the highly consistent findings from research began to be applied to clinical practice, and many clinicians are not yet much aware of how neurocognitive deficits affect their patients’ daily life, and, importantly, what can be done to prevent or at least mitigate cognitive impairment. Recent evidence suggests that neurocognitive status may be the most powerful predictor of functional outcome in BD, even more so than clinical features. Cognitive deficits may be related to neurodevelopmental issues, but in bipolar disorder the most accepted model is the “neuroprogression” one, in which recurring episodes and concurrent allostatic load contribute to neuropsychological difficulties and disability. Comorbidities and medication may also contribute to cognitive deficits. Research efforts are now focusing on drugs to ameliorate cognition and psychological interventions, such as functional remediation (3), which may have a positive impact on cognitive and functional outcome. Potential strategies aimed at preventing cognitive impairment and neuroprogression include: Effective pharmacotherapy for relapse prevention, psychoeducation, healthy habits (physical exercise, diet, sleep, no smoking), and cognitive enhancing psychological interventions (i.e.: promotion of cognitive reserve) and pro-cognitive drugs.