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As some authors suggest, the neurocognitive variability might also reflect an etiological heterogeneity in BD including potential different subtypes associated with different genetic susceptibility factors (Bora, 2016). Evidence shows that BD shares some susceptibility genes with schizophrenia, whereas some other genetic susceptibility factors seem to be specific of each disorder (Lichtenstein et al., 2009; Craddock et al., 2010). Taking all these findings into consideration, the existence of 2 groups has been hypothesized: a group of bipolar patients characterized by normal neurodevelopmental and cognitive functioning, whose cognitive decline is probably influenced by the impact of repetitive affective episodes, and another much smaller group of patients presenting with a pattern of cognitive impairment comparable with that observed in schizophrenia, characterized by a low premorbid cognitive functioning before illness onset. This latter group of patients would share common genetic risk factors with schizophrenia and might be associated with neurodevelopmental abnormalities. Nonetheless, at this point, further genetic and neurobiological research is needed to confirm this hypothesis. Moreover, inconsistent findings between the extant cross-sectional and longitudinal studies highlight the necessity for further research to elucidate the veritable evolution of cognitive dysfunction in bipolar illness and potential selection bias in longitudinal studies, since disturbance progress following repeated episodes is not entirely clear. Most cross-sectional studies find an association between cognitive impairment and number of episodes, whereas the longitudinal ones indicate a stable pattern over time (Budde et al., 2014; Samame et al., 2014). During the last decade, different staging model approaches have been proposed for BD (Berk et al., 2007; Kapczinski et al., 2008). These models assume an underlying pathophysiological process of neuroprogression associated with cognitive decline among other neurobiochemical changes; however, not every patient will proceed through all stages. Therefore, an early identification of which patients will develop a neuroprogressive disorder as well as the link with staging models are some of the challenges in the upcoming years (Rosa et al., 2014; Passos et al., 2016).
It is worth mentioning that neurocognitive impairment needs to be considered a therapeutic clinical target in order to improve both psychosocial functioning and quality of life of patients with BD (Grande et al., 2016). Available evidence underscores that cognitive dysfunction is a critical mediator of adverse psychosocial outcomes in BD and a predictor of unfavorable employment outcomes (Tse et al., 2014; Baune and Malhi, 2015;). It is worthy to note that similarly to cognitive dysfunction, functional deficits persist even after symptomatic remission in a significant subset of patients with BD, thus aggregating additional burden to patients and also possibly increasing illness-related direct and indirect costs. In this sense, BD is ranked among the leading causes of burden of disease worldwide associated with a high level of disability-adjusted life years (Catalá-López, et al., 2013).
Among all the components tested, very few of them have demonstrated positive effects on cognition. Mifepristone, a corticosteroid receptor antagonist, showed preliminary evidence to improve spatial working memory in depressed bipolar patients in 2 studies, the enhancement occurring in the absence of an improvement in depressed mood (Young et al., 2004; Watson et al., 2012). Pramipexole, a dopaminergic agonist, could have a beneficial effect on processing speed and working memory, but it was only observed in those euthymic bipolar I patients in a posthoc analysis of an 8-week, double-blind, placebo-controlled trial (Burdick et al., 2012). Another agent that showed an improvement in a secondary measure of executive function (the trail-making test part B) in euthymic patients was the intranasal insulin. However, this component did not show any therapeutic effect neither on the primary cognition outcomes nor on other secondary cognitive outcomes (memory measures) (McIntyre et al., 2012). Another compound demonstrating a positive effect in some cognitive measures in euthymic or subsyndromal bipolar patients was the extract of Withania somnifera, an herbal medicine with antioxidant and neuroprotective effects (Chengappa et al., 2013). Patients taking this agent showed a better performance mainly in measures related to auditory-verbal working memory. Erythropoietin was another adjunctive treatment that improved some secondary and tertiary cognitive measures related to sustained attention, working memory, executive function, and recognition of facial expression in euthymic patients, but not in verbal memory, which was the primary outcome (Miskowiak et al., 2014). Despite the negative primary outcome on this study, positive effects on secondary outcomes are encouraging, so it warrants the investigation with nonhematopoietic erythropoietin analogs, since its hematopoietic activity limits its clinical use. Galantamine, a cholinesterase inhibitor, has been proved in more studies. Although some of them have reported a potential benefit in verbal memory, even for those patients receiving electroconvulsive therapy, these studies have important caveats and merit further investigation (Matthews et al., 2008; Ghaemi et al., 2009; Iosifescu et al., 2009; Matthews et al., 2013). Results from a large, randomized, double-blind controlled trial showed that N-acetyl cysteine (NAC) as an add-on treatment in patients with BD failed to find benefits in cognitive functioning (Berk et al., 2008, 2012; Dean et al., 2012). Instead, when patients with psychotic BD from this previous study were grouped with other patients with schizophrenia and were analyzed as a whole of patients with psychotic features, those subjects following a treatment with NAC for 6 months enhanced their working memory performance (Rapado-Castro et al., 2016). Therefore, these results warrant an avenue for further exploration with NAC as an agent to treat cognitive dysfunction. Lastly, given the preliminary support for cognitive enhancement of lurasidone in patients with schizophrenia, a randomized, open-label pilot trial has examined the efficacy of this agent as an add-on treatment in comparison with treatment as usual (TAU) in euthymic bipolar I patients (Yatham et al., 2017). There was a greater improvement for the primary outcome (changes in a global cognition score) in the lurasidone group compared with the TAU group. An improvement was also observed in specific cognitive measures related to visual memory and working memory as well as in subjective cognitive complaints. Although the exact mechanisms underlying the cognitive effects of lurasidone are still unclear, its high affinity for 5-HT7 receptors might be an important contributor.
In the last decade, there has been growing interest in implementing mindfulness-based interventions for the treatment of mental disorders, with some studies focusing on BD. Overall, mindfulness appears as a useful intervention for the reduction of anxiety symptoms and, probably, to reduce depression symptoms (Reinares et al., 2014). More recently, some studies have analyzed the impact of mindfulness on cognitive functioning in BD. For example, the study of Stange and colleagues (2011) provides preliminary results that mindfulness may be an adjunct treatment option to medication to improve cognitive functioning in BD. Likewise, the cognitive remediation program proposed by Demant and colleagues (2015) also included some mindfulness exercises to practice at home and at the beginning of each session as a means to enhance the attentional capacity. Nevertheless, further research is needed in this area.
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