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Memory and cognition are critical parts of who we are. Our capacity for recall allows us to use past experience to guide our actions. Our cognitive abilities allow us to monitor events and evaluate plans for action. In aging there are varying degrees of decline in cognitive function which begin in the 30s and are quite common. They are not a disease and are accompanied by the growth of wisdom which can negate the influence of age-related memory changes. Memory losses with aging can be avoided with consideration of the importance of attention for memory. The role of forgetting as a normal activity of the brain is critical. It is necessary to realize that the influences of aging and age-related disease (such as Alzheimer’s) on brain function are not determined only on the processes of aging and disease -- the effect of these processes on our performance abilities depends upon our cognitive, physical, psychological, and social reserves. We all need to enhance these reserve capacities to decrease the influence of the aging process and developing brain disease on our function. This chapter reviews the functions of memory and how losses that accompany aging can best be managed.
The neurodegenerative diseases Alzheimer’s, Parkinson’s, frontotemporal lobar degeneration, Lewy body disease, and amyotrophic lateral sclerosis are all age-related and caused by genes in only 1-10 percent of cases. Dementia describes a syndrome in which there are cognitive difficulties including impaired memory, judgment, planning, language, and other deficits. Alzheimer’s is the commonest cause of dementia. In the brain in neurodegenerative diseases there is abnormal folding of proteins creating thread-like filaments called amyloid. There is also abnormal activation of inflammation with free radicals and harmful cells. There are things we can do regarding diet and other actions that can lower the risk of developing neurodegenerative diseases with aging. High levels of physical and mental activity throughout life along with attention to a healthy plant-based diet can enhance our four reserves and diminish amyloid deposition and overactivity of the immune system. Lifestyle measures can also protect us from the effect of brain pathologies that may develop. There are many causes of memory loss other than Alzheimer’s disease which are completely reversible when properly recognized.
Understanding of the magnificence and uniqueness of the brain is important for realizing the goals of aging. We must respect its central role in our lives and work to see what we must do to enhance its health throughout life. The brain is precisely responsive to activities and its structure is changed by learning. It is also uniquely sensitive to damage and has a limited capacity for repair, compared to other body parts. What we do changes the brain, and the nature of our mental activities modifies the ability of the brain to resist declines with aging and disease. Cognitive involvement in educational, occupational, and recreational tasks throughout life, as well as physical activities, helps to enhance resistance to decline with age and diseases such as Alzheimer’s. This chapter examines how the four reserves (cognitive, physical, psychological, and social) help to maintain brain function with age. Recent research has uncovered the influence of our partner microbes in the gut on learning, memory, and age-related diseases of the brain. These developments beautifully illustrate how there are things we can all do to maintain brain function with age.
Cognitive impairment is a core feature of schizophrenia, associated with poor functional outcomes. The course of cognitive function in the years following illness onset has remained a subject of debate, with a previous analysis finding no worsening, providing support for the neurodevelopmental model of schizophrenia. Since then, many more studies have reported on longitudinal cognitive performance in early psychosis, with some indicating deterioration, which does not align with this view.
This study aims to quantitatively review the literature on the longitudinal trajectory of cognitive deficits in the years following psychosis onset, in comparison with healthy controls. It is the first to also synthesise longitudinal data on social cognition.
Electronic databases (‘PubMed’, ‘PsycInfo’ and ‘Scopus’) were searched (to end September 2021). Meta-analyses of 25 longitudinal studies of cognition in early psychosis were conducted (1480 patients, 789 health controls). Unlike previous analyses, randomised controlled trials and those with multiple cognitive testing periods within the first year were excluded to minimise bias (PROSPERO, ID: CRD42021241525).
Small improvements were observed for global cognition (g = 0.25, 95% CI 0.17–0.33) and individual cognitive domains, but these were comparable with healthy controls and likely an artefact of practice effects.
There is no evidence of continued cognitive decline or improvement in the early years following psychosis onset, with a need for more studies over longer follow-up periods. Practice effects highlight the importance of including control samples in longitudinal and intervention studies. Further data are needed to evaluate the course of social cognition subdomains.
Relative to youth with early-treated phenylketonuria (ETPKU), much less is known regarding the cognitive profile of adults with ETPKU. The present study aimed to address this gap by providing a comprehensive assessment of neuropsychological functioning among adults with ETPKU.
A sample of 40 adults with ETPKU (ages 18 – 36) and a demographically matched group of 32 healthy individuals without PKU participated. Participants completed a comprehensive neuropsychological battery including the NIH Toolbox, Wechsler Abbreviated Scale of Intelligence – Second Edition (WASI-II), Conners’ Continuous Performance Test (CPT-3), select subtests from the Weschler Adult Intelligence Scale – Fourth Edition (WAIS-IV) as well as several self-report measures of cognitive and psychoemotional functioning. Scores from these tests were combined to create cognitive composites reflecting overall task performance in the areas of verbal ability, visuospatial skills, executive functioning, motor skills, and processing speed.
No group differences were observed for full scale IQ or verbal ability. However, individuals with ETPKU demonstrated poorer performance on measures of executive functioning, processing speed, motor skills, and visuospatial skills as compared to the non-PKU group. Within the ETPKU group, recent blood phenylalanine levels (an indicator of metabolic control) were significantly correlated with performance across most cognitive domains and aspects of psychological functioning.
Present findings suggest that the neuropsychological profile of adult ETPKU is characterized by circumscribed impairments in select cognitive domains. In addition, the results underscore the importance of maintaining metabolic control across the lifespan in individuals with ETPKU.
This paper discusses a research agenda for post-Northian institutional economics, which focuses on economic cognitive institutions and minds–institutions interactions. Douglass North introduced the ‘shared mental models’ and ‘shared beliefs’ concepts, which were considered the cutting edge of cognitive science at that time, the so-called first wave of extended mind theory. Subsequently, two more waves arose, but they went unnoticed by institutional economists who mostly continue to use internalist and reductionist approaches to cognition. Post-Northian institutional economics offers a deeper understanding of the relationship between cognition and institutions in the spirit of third-wave extended mind theory. The research agenda emphasizes a focus on socially extended cognition and the conception of cognitive institutions as shared mental processes (Petracca and Gallagher, 2020). I propose an alternative definition of cognitive institutions as interactively and polycentrically co-produced cognitive norms; this approach highlights normativity, co-production, and distributed active agency in extended cognitive processes. I propose two domains in which this third-wave framework can be used: ecological rationality and cognitive–cultural niche construction. This paper encourages a discussion on the prospects of a third-wave enactivist turn in institutional economics.
Cognitive impairment affects older adults’ capacity to live independently and make lifestyle decisions (lifestyle decision-making capacity; LS-DMC). Cognitive screens and clinical interviews are often used to assess people’s need for living-supports prior to conducting comprehensive LS-DMC assessments in busy clinical settings. This study investigated whether the QuickSort – a brief new cognitive screen – provides efficient and accurate information regarding patients’ LS-DMC when initially interviewed.
This is an observational and diagnostic accuracy study of older inpatients (≥60 years) consecutively referred for neuropsychological assessment of LS-DMC (n = 124). The resources required by inpatients with questionable LS-DMC were quantified (length of hospital stay, living-supports). QuickSort scores, patient background information, and two common cognitive screens were used to differentiate between older inpatients (n = 124) who lacked (64%)/did not-lack (36%) LS-DMC.
Hospitalizations averaged 49 days, with 62% of inpatients being readmitted within one year. The QuickSort differentiated between those lacking/not-lacking LS-DMC better than two common cognitive screens and patient information. The likelihood that inpatients lacked LS-DMC increased by a factor of 65.26 for QuickSort scores <2 and reduced by a factor of 0.32 for scores ≥13. Modeling revealed that the post-test likelihood of lacking LS-DMC increased to 99% (scores <2) and reduced to 30% (scores ≥ 13) in settings where many inpatients lack LS-DMC.
Older adult inpatients with questionable LS-DMC have a high risk of extended hospitalization and readmission. The QuickSort provides time-efficient and sensitive information regarding patients’ LS-DMC, making it a viable alternative to longer cognitive screens that are used at the initial interview stage.
Aging is a subject of concern to everyone, but is widely misunderstood. If we view it as inevitable, we miss the fact that not everyone is able to grow to an old age. Realization of this reality helps us to understand that aging presents a wonderful opportunity - an opportunity to make choices about how we live which can enhance the aging process and offer a chance to live to our potential. This book clearly presents the four, multiple reserve, factors (cognitive, physical, psychological and social) which impact our ability to have healthy responses to the stresses of aging. By giving the biological basis for the advice given, you will learn the steps to take in your activities, diet and mental outlook to grasp the opportunity that aging offers. Everyone must know that what we do makes a difference.
Cognitive dispersion across neuropsychological measures within a single testing session is a promising marker predictive of cognitive decline and development of Alzheimer’s disease (AD). However, little is known regarding brain changes underlying cognitive dispersion, and the association of cognitive dispersion with in vivo AD biomarkers and regional cerebral blood flow (CBF) has received limited study. We therefore examined associations among cognitive dispersion, amyloid-beta (Aβ) positivity, and regional CBF among older adults free of dementia.
One hundred and forty-eight Alzheimer’s Disease Neuroimaging Initiative (ADNI) participants underwent neuropsychological testing and neuroimaging. Pulsed arterial spin labeling (ASL) magnetic resonance imaging (MRI) was acquired to quantify CBF. Florbetapir positron emission tomography (PET) imaging determined Aβ positivity.
Adjusting for age, gender, education, and mean cognitive performance, older adults who were Aβ+ showed higher cognitive dispersion relative to those who were Aβ-. Across the entire sample, higher cognitive dispersion was associated with reduced CBF in inferior parietal and temporal regions. Secondary analyses stratified by Aβ status demonstrated that higher cognitive dispersion was associated with reduced CBF among Aβ+ individuals but not among those who were Aβ-.
Cognitive dispersion may be sensitive to early Aβ accumulation and cerebrovascular changes adjusting for demographics and mean neuropsychological performance. Associations between cognitive dispersion and CBF were observed among Aβ+ individuals, suggesting that cognitive dispersion may be a marker of brain changes among individuals on the AD continuum. Future studies should examine whether cognitive dispersion predicts brain changes in diverse samples and among those with greater vascular risk burden.
Cognitive impairments are well-established features of psychotic disorders and are present when individuals are at ultra-high risk for psychosis. However, few interventions target cognitive functioning in this population.
To investigate whether omega-3 polyunsaturated fatty acid (n−3 PUFA) supplementation improves cognitive functioning among individuals at ultra-high risk for psychosis.
Data (N = 225) from an international, multi-site, randomised controlled trial (NEURAPRO) were analysed. Participants were given omega-3 supplementation (eicosapentaenoic acid and docosahexaenoic acid) or placebo over 6 months. Cognitive functioning was assessed with the Brief Assessment of Cognition in Schizophrenia (BACS). Mixed two-way analyses of variance were computed to compare the change in cognitive performance between omega-3 supplementation and placebo over 6 months. An additional biomarker analysis explored whether change in erythrocyte n−3 PUFA levels predicted change in cognitive performance.
The placebo group showed a modest greater improvement over time than the omega-3 supplementation group for motor speed (ηp2 = 0.09) and BACS composite score (ηp2 = 0.21). After repeating the analyses without individuals who transitioned, motor speed was no longer significant (ηp2 = 0.02), but the composite score remained significant (ηp2 = 0.02). Change in erythrocyte n-3 PUFA levels did not predict change in cognitive performance over 6 months.
We found no evidence to support the use of omega-3 supplementation to improve cognitive functioning in ultra-high risk individuals. The biomarker analysis suggests that this finding is unlikely to be attributed to poor adherence or consumption of non-trial n−3 PUFAs.
Tobacco use is common in subjects with schizophrenia (SZ) and has sometimes been associated with better functioning in short-term studies. Only few studies embrace an extensive examination of tobacco influence on clinical, cognitive and therapeutic characteristics in stabilized SZ outpatients. The objective of the present study was to assess the association between cognitive performances and smoking status in SZ subjects.
In total, 1233 SZ participants (73.9% men, mean age 31.5) were included and tested with a comprehensive battery. Tobacco status was self-declared (never-, ex-, or current smokers). Multivariable analyses including principal component analyses (PCA) were used.
In total, 53.7% were smokers with 33.7% of them nicotine-dependent. Multiple factor analysis revealed that current tobacco smoking was associated with impaired general intellectual ability and abstract reasoning (aOR 0.60, 95% IC 0.41–0.88, p = 0.01) and with a lifetime alcohol use disorder (p = 0.026) and a lifetime cannabis use disorder (p < 0.001). Ex- and never-smokers differed for age, mean outcome, cannabis history and medication [ex-smokers being older (p = 0.047), likely to have higher income (p = 0.026), a lifetime cannabis use disorder (p < 0.001) and higher CPZeq doses (p = 0.005)]. Premorbid IQ in the three groups significantly differed with, from higher to lower: ex-smokers, never-smoker, current smokers (all p < 0.001).
This study is the largest to date providing strong evidence that chronic smoking is associated with cognitive impairment in SZ, arguing against the self-medication hypothesis as a contributor to the high prevalence of smoking in SZ. Ex-smokers may also represent a specific subgroup. Longitudinal studies are warranted to determine the developmental impact of tobacco on neurocognition.
The purpose of this exploratory study was to describe associations between NIH Toolbox-Cognition Battery subtests and legacy measures of neurocognitive function in two samples with neurological conditions (stroke and sickle cell disease (SCD)).
This exploratory secondary analysis uses data from two studies that assessed cognition at one time point using the NIH Toolbox-Cognition Battery, the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), and subtests from the Delis-Kaplan Executive Functions System (DKEFS). People with stroke (n = 26) and SCD (n = 64) were included. Associations between the NIH Toolbox-Cognition Battery subtests and corresponding legacy measures were examined using linear correlations, Bland–Altman analysis, and Lin’s Concordance Correlation Coefficient.
Linear correlations and Lin’s Concordance Correlation Coefficient were poor to strong in both samples on NIH Toolbox-CB subtests: Flanker Inhibitory Control and Attention (r = .35 to .48, Lin CCC = .27 to .37), Pattern Comparison Processing Speed (r = .40 to .65, Lin CCC = .37 to .62), Picture Sequence Memory (r = .19 to .55, Lin CCC = .18 to .48), Dimensional Change Card Sort (r = .39 to .77, Lin CCC = .38 to .63), Fluid Cognition Composite (r = .88 to .90, Lin CCC = .60 to .79), and Total Cognition Composite (r = .64 to .83, Lin CCC = .60 to .78). Bland–Altman analyses demonstrated wide limits of agreement across all subtests (–3.17 to 3.78).
The NIH Toolbox-Cognition Battery subtests may behave similarly to legacy measures as an overall assessment of cognition across samples at risk for neurological impairment. Findings should be replicated across additional clinical samples.
Chronic Hepatitis C infection is considered a systemic disease with extrahepatic manifestations, mainly neuropsychiatric symptoms,
which is associated with a chronic low-grade inflammatory state. Hepatitis C virus (HCV) eradication is currently achieved in >98% of cases with oral direct-acting antivirals (DAA).
To study potential clinical neuropsychiatric changes (mood, cognition, sleep, gastrointestinal, sickness, and motion) in HCV-infected patients after HCV eradication with DAA.
Design: Cohort study. Subjects: 37 HCV-infected patients, aged<55 years old, with non-advanced liver disease receiving DAA; free of current mental disorder. 24 healthy controls were included at baseline. Assessment: -Baseline (BL) (socio-demographic and clinical variables, MINI-DSM-IV, and Neurotoxicity Scale (NRS), (mood, cognitive, sleep, gastrointestinal, sickness and motor dimensions). Follow-up: End-of-treatment, 12weeks-after and 48weeks-after DAA: NRS. Analysis: Descriptive and bivariate non-parametrical analysis.
NRS total score and dimensions where different between cases and controls (.000) at baseline. NRS total score (.000) and mood (.000), cognition (.000), sleep (.002), gastrointestinal (.017), and sickness (.003), except motor dimension score (.130) showed significant longitudinal improvement.
HCV-infected patients with mild liver disease presented significantly worse scores for neurotoxicity symptomatology in all dimensions compared to healthy individuals. After HCV eradication with DAA, both at short and long follow-up a significant improvement of the NRS total score and each of the dimensions (except motor) were observed. However, they did not reach the values of healthy individuals, suggesting a not complete neuropsychiatric restoration in the period studied. Grant: ICIII-FIS:PI17/02297.(One way to make Europe) (RMS) and Gilead Fellowship-GLD17/00273 (ZM); and the support of SGR17/1798 (RMS)
Coordination between the thalamus and cortex is necessary for efficient processing of sensory information and appears disrupted in schizophrenia. The significance of this disrupted coordination (i.e. thalamocortical dysconnectivity) to the symptoms and cognitive deficits of schizophrenia is unclear. It is also unknown whether similar dysconnectivity is observed in other forms of psychotic psychopathology and associated with familial risk for psychosis. Here we examine the relevance of thalamocortical connectivity to the clinical symptoms and cognition of patients with psychotic psychopathology, their first-degree biological relatives, and a group of healthy controls.
Patients with a schizophrenia-spectrum diagnosis (N = 100) or bipolar disorder with a history of psychosis (N = 33), their first-degree relatives (N = 73), and a group of healthy controls (N = 43) underwent resting functional MRI in addition to clinical and cognitive assessments as part of the Psychosis Human Connectome Project. A bilateral mediodorsal thalamus seed-based analysis was used to measure thalamocortical connectivity and test for group differences, as well as associations with symptomatology and cognition.
Reduced connectivity from mediodorsal thalamus to insular, orbitofrontal, and cerebellar regions was seen in schizophrenia. Across groups, greater symptomatology was related to less thalamocortical connectivity to the left middle frontal gyrus, anterior cingulate, right insula, and cerebellum. Poorer cognition was related to less thalamocortical connectivity to bilateral insula. Analyses revealed similar patterns of dysconnectivity across patient groups and their relatives.
Reduced thalamo-prefrontal-cerebellar and thalamo-insular connectivity may contribute to clinical symptomatology and cognitive deficits in patients with psychosis as well as individuals with familial risk for psychotic psychopathology.
Improving real-life functioning is the main goal of the most advanced integrated treatment programs in people with schizophrenia. The Italian Network for Research on Psychoses used network analysis in a four-year follow-up study to test whether the pattern of relationships among illness-related variables, personal resources and context-related factors differed between patients who were classified as recovered at follow-up versus those who did not recover. In a large sample (N=618) of clinically-stable, community-dwelling subjects with schizophrenia, the study demonstrated a considerable stability of the network structure. Functional capacity and everyday life skills had a high betweenness and closeness in the network at both baseline and follow-up, while psychopathological variables remained more peripheral. The network structure and connectivity of non-recovered patients were similar to those observed in the whole sample, but very different from those in recovered subjects, in which we found few connections only. These data strongly suggest that tightly coupled symptoms/dysfunctions tend to maintain each other’s activation, contributing to poor outcome in subjects with schizophrenia. The data suggest that early and integrated treatment plans, targeting variables with high centrality, might prevent the emergence of self-reinforcing networks of symptoms and dysfunctions in people with schizophrenia.
Honoraria, advisory board, or consulting fees from Angelini, Astra Zeneca, Bristol-Myers Squibb, Gedeon Richter Bulgaria, Innova-Pharma, Janssen Pharmaceuticals, Lundbeck, Otsuka, Pfizer, and Pierre Fabre, for services not related to this abstract
Executive function organizes and directs behaviour but alterations in this cognitive domain can lead to inaccurate perception, interpretation and response to environmental information, which could be a risk factor for suicide.
To explore executive function performance of depressed recent suicide attempters in comparison to depressed past suicide attempters, depressed non-attempters and healthy controls.
96 participants from the Psychiatry Department of the Araba University Hospital-Santiago were recruited as follows: 20 patients with a recent suicide attempt (<30days) diagnosed with a Major Depressive Disorder (MDD), 33 MDD patients with history of attempted suicide, 23 non-attempter MDD patients and 20 healthy controls. All participants underwent a clinical interview and neuropsychological assessment on executive function with the Wisconsin Sorting Card Test. Backward multiple regressions were performed adjusting for significant confounding variables. For group comparisons ANOVA test and Bonferroni post hoc test were performed with p<0.05 significance level.
Patient groups did not differ regarding severity of depression. All patient groups performed significantly worse than healthy controls on executive function. Adjusted comparisons between patient groups indicated that recent suicide attempters had a poorer performance in this cognitive domain in comparison to both depressed lifetime attempters and depressed non-attempters (B=0.296, p=0.019 and B=0.301, p=0.028 respectively).
Executive function performance is altered in recent suicide attempts. As impaired executive function can be a risk factor for suicide, preventive interventions on suicide should focus on its assessment and rehabilitation.
The three anterior thalamic nuclei and the nucleus reuniens are essential for spatial navigation, yet their exact role in this function remains elusive. Specifically, it remains to be answered whether the thalamus acts a simple relay of spatial and executive signals or whether it critically operates on its inputs to convey processed signals to its cortical targets. The anterior thalamus and nucleus reuniens are at the center stage of anatomical networks that share one common aspect: their association with the hippocampus. Here, I review the large body of literature, starting from the classic Papez circuits, which describe how these thalamic nuclei are interconnected with subcortical, medial cortex, and parahippocampal regions, as well as their neuromodulatory inputs. I then provide an overview of the spatial and other electrophysiological correlates of anterior thalamic and reuniens neurons and of how their firing and oscillatory properties depend on ongoing behavior. Finally, I discuss the clinical and experimental evidence pointing to the role of the thalamus in navigation and, specifically, how spatial and executive signals are processed in thalamocortical loops. I conclude by discussing how the same thalamic circuits may be at play in the processing of episodic memories during sleep.
Cognitive and social cognitive impairments are a central feature of schizophrenia and are known to significantly affect real-life functioning . These impairments include deficits in memory, language function and executive function, as well as in processing speed and attention. In the domains of social cognition, face perception , voice perception, mentalizing and emotion regulation have been described to be affected. All deficits, cognitive and social-cognitive, can persist during symptomatic remission. Social cognition is a partial mediator between neurocognition and functional outcome. Recent research has demonstrated that neurocognition affects functional capacity and that social cognition affects community functioning . The impact of cognition on quality of life (QOL) was shown in a large meta-analytic study, in which a moderate correlation of verbal ability and processing speed with subjective quality of life was found . A network analysis showed that functional capacity and everyday life skills were the most central and highly interconnected nodes in the network. Functional capacity bridged cognition with everyday life skills, the everyday life skills node was linked to disorganization and expressive deficits . Deficits in neurocognition and social cognition play a pivotal role as enduring impairment after clinical remission and as a critical rate-limiting factor in functional recovery.  Green et al. Schizophr Bull. 2000; 26(1): 119-136  Sachs et al. Schizophr Res. 2004; 68(1):27-35  Bechi et al. Psychiatry Res. 2017; 251:118-124  Tolman & Kurtz Schizophr Bull. 2012; 272:419-424  Galderisi et al. JAMA Psychiatry. 2018; 75(4):396-404
Ocular Coherence Tomography (OCT) to measure retinal thickness is the current method to observe neurological impairment in neurodegenerative diseases  and in mental disorders  due to the composition of the retina itself as an anatomic extension of the brain.There can be found some factors to improve the resilience like the years of study.
Our aim is to evaluate cognitive and clinical impairment in Bipolar Disorder and see the correlation to the retinal thinning.
Twenty-seven patients diagnosed with Bipolar Disorder were assessed in the context of the FINEXT programme (3). Selective attention, executive functions and verbal memory were measured among other variables. Using the OCT technique, we measured the thickness of the ppRNFL, the RFNL, GCL and IPL layers in the macula in both eyes through several radial segments. Partial correlations were performed with Bonferroni correction (p≤0.006) adjusted for age and academic status except for the variable years of study which was adjusted for age.
Significant direct correlations were observed between:
- The study-years and the thickness of the retina in the NO and RFNL. -Selective attention and GCL and RFNL layers. -Executive function and the GCL and IPL.
We can observe some preliminar results showing a significant correlation between some layers of the retina, upper segments more frequently, and the outcomes of the neurocognitive assessment. We can see a relationship as well between years of study and the thickness of the Retinal Nerve Fibre Layer in the retina and optic nerve head, the axons of the neurons in the eye.
In bipolar disorder, cognitive deficits persist across mood episodes and euthymia. Despite recent advances, cognitive impairment in bipolar disorder remains poorly understood. The presentation will focus on recent work where different approaches are used to clarify the role of cognitive deficits in bipolar disorder.
First, we have examined the clinical relevance of cognitive impairments and examined if cognitive abilities differ between bipolar disorder subtypes and healthy controls. Second, we examined if cognitive abilities differ between individuals with bipolar disorder with and without attention-deficit hyperactivity disorder. Third, we examined the relationship between cognitive functioning and occupational functioning. Lastly, we examined if long-term changes in cognitive functioning in bipolar disorder patients differ from normal aging.
The St. Göran Bipolar Project is an interdisciplinary, prospective, naturalistic study of bipolar disorder. Patients were recruited and followed-up at two specialized out-patient clinics in Stockholm and Gothenburg, Sweden.
We showed that there is evidence for significant cognitive heterogeneity in bipolar disorder. Comorbid ADHD could not explain this heterogeneity. Moreover, we showed that excutive functioning is a powerful predictor of occupational functioning. The cognitive trajectory over a 6-year period did not differ between bipolar disorder patients and healthy controls.
There is no conclusive cognitive profile characterizing bipolar disorder. However, cognitive functioning is of great importance in understanding occupational functioning in bipolar disorder. Contrary to the assumption that cognitive impairments may be progressive we show that changes in cognitive functioning over time do not differ between patients and healthy controls.