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A scientist's exploration of the working of memory begins with a story by Borges about a man who could not forget. Imagine the astonishment felt by neuroscientist Rodrigo Quian Quiroga when he found a fantastically precise interpretation of his research findings in a story written by the great Argentinian fabulist Jorge Luis Borges fifty years earlier. Quian Quiroga studies the workings of the brain—in particular how memory works—one of the most complex and elusive mysteries of science. He and his fellow neuroscientists have at their disposal sophisticated imaging equipment and access to information not available just twenty years ago. And yet Borges seemed to have imagined the gist of Quian Quiroga's discoveries decades before he made them. The title character of Borges's \"Funes the Memorious\" remembers everything in excruciatingly particular detail but is unable to grasp abstract ideas. Quian Quiroga found neurons in the human brain that respond to abstract concepts but ignore particular details, and, spurred by the way Borges imagined the consequences of remembering every detail but being incapable of abstraction, he began a search for the origins of Funes. Borges's widow, María Kodama, gave him access to her husband's personal library, and Borges's books led Quian Quiroga to reread earlier thinkers in philosophy and psychology. He found that just as Borges had perhaps dreamed the results of Quian Quiroga's discoveries, other thinkers—William James, Gustav Spiller, John Stuart Mill—had perhaps also dreamed a story like \"Funes.\" With Borges and Memory, Quian Quiroga has given us a fascinating and accessible story about the workings of the brain that the great creator of Funes would appreciate.

Posttraumatic-stress disorder (PTSD) patients suffer from cognitive dysfunction and show impairments even in non-trauma-related memory. Research has focused on the relationship between associative-memory and PTSD severity due to patients' tendency to over-generalize from traumatic cues to neutral ones, leading to escalation of traumatic symptoms. In this study we aim to test to what extent inhibitory control impairments are correlated to associative-memory deficits in PTSD. Twenty PTSD and 22 control participants were included. Posttraumatic symptoms were assessed via a board-qualified psychiatrist and the Post-Traumatic Diagnostic Scale. Inhibitory abilities were evaluated using the anti-saccade task and memory performance was probed using a words/pictures item-association paradigm. Generally, PTSD patients performed lower than controls in both tasks. Lower associative-memory performance was observed in posttraumatic patients and was attributed to increased false-alarm rate in this group. In addition, we observed a strong significant positive correlation between associative pictorial memory performance and inhibitory performance, and in accordance, a significant negative correlation between the number of false-alarm responses in the associative pictorial test and inhibitory performance in the PTSD group. These results support the hypothesis that inhibitory control impairments are associated with (pictorial) associative-memory deficits in PTSD.

BackgroundAdolescents with single ventricle heart disease (SVHD) who have undergone the Fontan procedure show cognitive/memory deficits. Mammillary bodies are key brain sites that regulate memory; however, their integrity in SVHD is unclear. We evaluated mammillary body (MB) volumes and their associations with cognitive/memory scores in SVHD and controls.MethodsBrain MRI data were collected from 63 adolescents (25 SVHD; 38 controls) using a 3.0-Tesla MRI scanner. Cognition and memory were assessed using Montreal Cognitive Assessment (MoCA) and Wide Range Assessment of Memory and Learning 2. MB volumes were calculated and compared between groups (ANCOVA, covariates: age, sex, and total brain volume [TBV]). Partial correlations and linear regression were performed to examine associations between volumes and cognitive scores (covariates: age, sex, and TBV).ResultsSVHD group showed significantly lower MoCA and WRAML2 scores over controls. MB volumes were significantly reduced in SVHD over controls. After controlling for age, sex, and TBV, MB volumes correlated with MoCA and delayed memory recall scores in SVHD and controls.ConclusionAdolescents with SVHD show reduced MB volumes associated with cognitive/memory deficits. Potential mechanisms of volume losses may include developmental and/or hypoxic/ischemic-induced processes. Providers should screen for cognitive deficits and explore possible interventions to improve memory.

Little is known about the pathophysiology of memory deficits in patients with major depressive disorder (MDD) treated with modified electroconvulsive therapy (MECT). This study examined the profiles of cytokines, the memory function, and their association in MECT-treated MDD patients. Forty first-episode, drug-free MDD patients and 40 healthy controls were recruited. MECT was started with antidepressant treatment at a stable initial dose. The Wechsler Memory Scale (WMS) and Hamilton Rating Scale for Depression 17 (HRSD-17) were used to assess the cognitive function. MDD patients were divided into the memory impairment group (WMS < 50) and the non-memory impairment group (WMS ≥ 50) based on the total WMS scores after MECT. The levels of NOD-like receptor 3 (NLRP3) inflammasome, interleukin-18 (IL-18) and nuclear factor kappa-B (NF-κB) in the serum were measured. MDD patients showed significantly higher levels of NLRP3 inflammasome, IL-18 and NF-κB than that in the controls prior to MECT, and the levels also significantly increased after MECT. In MDD patients, the serum levels of these inflammatory cytokines were negatively associated with the total WMS scores and likely contributed to the scores independently. The receiver operating characteristic curve showed that the serum levels of these inflammatory cytokines may predict the cognitive impairment risk in MDD patients receiving MECT. Abnormal levels of NLRP3 inflammasome, IL-18 and NF-κB reflecting the disturbed balance of pro-inflammatory and anti-inflammatory mechanisms likely contribute to the MECT-induced cognitive deficits in MDD patients.

Memory decline is a central cognitive symptom in Parkinson’s Disease (PD). While task-fMRI studies link hippocampal activity (AHA) to poorer memory and olfactory performance, this relationship during rest remains understudied. The objectives of this study are to examine differences in resting-state hippocampal networks, explore the occurrence of reduced AHA within these networks, and investigate its impact on memory and olfaction in PD. Thirty-nine PD patients awaiting evaluation for device-aided Parkinson therapy and 46 healthy controls (HC) underwent resting-state fMRI (rs-fMRI). PD patients also completed a memory and olfactory assessment. Co-activation pattern (CAP) analysis was performed on the rs-fMRI data. Our results demonstrated reduced activity in two hippocampal networks in PD: Network 1, incorporating the visual cortex, cerebellum, superior parietal lobule, and precuneus, and Network 5, incorporating parts of the central executive network. PD subgroups with reduced AHA in Network 1 and 5 performed significantly worse on tests of auditory-verbal short-term, long-term and recognition memory, as well as odor identification. In conclusion, within specific resting-state hippocampal networks, reduced AHA in PD is linked to poorer auditory-verbal memory and odor identification.

The neurocognitive trajectory in bipolar disorder (BD) is variable, with controversial findings, and most evidence come from cross-sectional studies. We aimed to examine the course of neurocognitive functioning in a sample of euthymic BD patients in comparison with a control group during a 5-year follow-up. Ninety-nine euthymic bipolar patients and 40 healthy controls were assessed using a comprehensive neurocognitive battery (six neurocognitive domains) at baseline (T1) and then at 5-year follow-up (T2) in a longitudinal study. No evidence of a progression in neurocognitive dysfunction was found either in cognitive composite index or in any of the neurocognitive domains for the whole cohort. However, there was a negative correlation between number of manic episodes and hospitalisations due to manic episodes and change in neurocognitive composite index (NCI) during the follow-up. Moreover, patients with higher number of manic and hypomanic episodes have a greater decrease in NCI, working memory and visual memory. History of psychotic symptoms was not related to the trajectory of neurocognitive impairment. Our results suggest that, although the progression of cognitive decline is not a general rule in BD, BD patients who have a greater number of manic or hypomanic episodes may constitute a subgroup characterised by the progression of neurocognitive impairment. Prevention of manic and hypomanic episodes could have a positive impact on the trajectory of cognitive function.

Autism spectrum disorders (ASD) are lifelong neurodevelopmental disorders. It is not clear whether working memory (WM) deficits are commonly experienced by individuals with ASD. To determine whether individuals with ASD experience significant impairments in WM and whether there are specific domains of working memory that are impaired. We conducted a meta-analysis using four electronic databases EMBASE (OVID), MEDLINE (OVID), PsychINFO (EBSCOHOST), and Web of Science, to examine the literature to investigate whether people with ASD experience impairments related to WM. Meta-analyses were conducted separately for phonological and visuospatial domains of WM. Subgroup analyses investigated age and intelligence quotient as potential moderators. A total of 29 papers containing 34 studies measuring phonological and visuospatial domains of WM met the inclusion criteria. WM scores were significantly lower for individuals with ASD compared to typically developed (TD) controls, in both the visuospatial domain when investigating accuracy (d: -0.73, 95% CI -1.04 to -0.42, p < 0.05) and error rates (d: 0.56, 95% CI 0.25 to 0.88, p<0.05), and the phonological domain when investigating accuracy (d:-0.67, 95% CI -1.10 to -0.24, p>0.05) and error rate (d: 1.45, 95% CI -0.07 to 2.96, p = 0.06). Age and IQ did not explain the differences in WM in ASD. The findings of this meta-analysis indicate that across the lifespan, individuals with ASD demonstrate large impairments in WM across both phonological and visuospatial WM domains when compared to healthy individuals.

Psychotic Experiences (PEs) during adolescence index increased risk for psychotic disorders and schizophrenia in adult life. Working memory (WM) deficits are a core feature of these disorders. Our objective was to examine the relationship between PEs and WM in a general population sample of young people in a case control study. 4744 individuals of age 17-18 from Bristol and surrounding areas (UK) were analyzed in a cross-sectional study nested within the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort study. The dependent variable was PEs, assessed using the semi-structured Psychosis-Like Symptom Interview (PLIKSi). The independent variable was performance on a computerized numerical n-back working memory task. Signal-Detection Theory indices, including standardized hits rate, false alarms rate, discriminability index (d') and response bias (c) from 2-Back and 3-Back tasks were calculated. 3576 and 3527 individuals had complete data for 2-Back and 3-Back respectively. Suspected/definite PEs prevalence was 7.9% (N = 374). Strongest evidence of association was seen between PEs and false alarms on the 2-Back, (odds ratio (OR) = 1.17 [95% confidence intervals (CI) 1.01, 1.35]) and 3-back (OR = 1.35 [1.18, 1.54]) and with c (OR = 1.59 [1.09, 2.34]), and lower d' (OR = 0.76 [0.65, 0.89]), on the 3-Back. Adjustment for several potential confounders, including general IQ, drug exposure and different psycho-social factors, and subsequent multiple imputation of missing data did not materially alter the results. WM is impaired in young people with PEs in the general population. False alarms, rather than poor accuracy, are more closely related to PEs. Such impairment is consistent with different neuropsychological models of psychosis focusing on signal-to-noise discrimination, probabilistic reasoning and impaired reality monitoring as a basis of psychotic symptoms.

Tetris has been proposed as a preventive intervention to reduce intrusive memories of a traumatic event. However, no neuroimaging study has assessed Tetris in patients with existing posttraumatic stress disorder (PTSD) or explored how playing Tetris may affect brain structure. We recruited patients with combat-related PTSD before psychotherapy and randomly assigned them to an experimental Tetris and therapy group (n = 20) or to a therapy-only control group (n = 20). In the control group, participants completed therapy as usual: eye movement desensitization and reprocessing (EMDR) psychotherapy. In the Tetris group, in addition to EMDR, participants also played 60 minutes of Tetris every day from onset to completion of therapy, approximately 6 weeks later. Participants completed structural MRI and psychological questionnaires before and after therapy, and we collected psychological questionnaire data at follow-up, approximately 6 months later. We hypothesized that the Tetris group would show increases in hippocampal volume and reductions in symptoms, both directly after completion of therapy and at follow-up. Following therapy, hippocampal volume increased in the Tetris group, but not the control group. As well, hippocampal increases were correlated with reductions in symptoms of PTSD, depression and anxiety between completion of therapy and follow-up in the Tetris group, but not the control group. Playing Tetris may act as a cognitive interference task and as a brain-training intervention, but it was not possible to distinguish between these 2 potential mechanisms. Tetris may be useful as an adjunct therapeutic intervention for PTSD. Tetris-related increases in hippocampal volume may ensure that therapeutic gains are maintained after completion of therapy.

Previous cross-sectional studies report that cognitive impairment is associated with poor psychosocial functioning in euthymic bipolar patients. There is a lack of long-term studies to determine the course of cognitive impairment and its impact on functional outcome. Method A total of 54 subjects were assessed at baseline and 6 years later; 28 had DSM-IV TR bipolar I or II disorder (recruited, at baseline, from a Lithium Clinic Program) and 26 were healthy matched controls. They were all assessed with a cognitive battery tapping into the main cognitive domains (executive function, attention, processing speed, verbal memory and visual memory) twice over a 6-year follow-up period. All patients were euthymic (Hamilton Rating Scale for Depression score lower than 8 and Young mania rating scale score lower than 6) for at least 3 months before both evaluations. At the end of follow-up, psychosocial functioning was also evaluated by means of the Functioning Assessment Short Test. Repeated-measures multivariate analysis of covariance showed that there were main effects of group in the executive domain, in the inhibition domain, in the processing speed domain, and in the verbal memory domain (p<0.04). Among the clinical factors, only longer illness duration was significantly related to slow processing (p=0.01), whereas strong relationships were observed between impoverished cognition along time and poorer psychosocial functioning (p<0.05). Executive functioning, inhibition, processing speed and verbal memory were impaired in euthymic bipolar out-patients. Although cognitive deficits remained stable on average throughout the follow-up, they had enduring negative effects on psychosocial adaptation of patients.