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Background: Patient-reported outcome (PRO) measures produce scores that do not always have obvious clinical meaning. The PRO-bookmarking procedure is a new and promising way to make PRO measures more meaningful and interpretable. However, the materials and procedures of the task may benefit from adaptations to be more accessible to individuals with cognitive and language disorders. Aims: This study aims to provide an overview of the iterative refinement process used to modify the materials and procedures of the PRO-bookmarking task so that they are more accessible to adults with acquired cognitive and language impairments. Method and Procedures: Our team of health psychologists, neuropsychologists, and speech-language pathologists (SLPs) conducted two focus groups with SLPs and care partners of people with aphasia using the same PRO-bookmarking materials and procedures as previous reports. These PRO-bookmarking materials and procedures were then refined iteratively based on discussion with those who participated in focus groups and among the research team, and three more times in the course of 16 additional focus groups of different stakeholders: people with Parkinson's disease, aphasia, or traumatic brain injury; care partners of people with those conditions; and SLPs who have experience with those, and other adult-acquired conditions. Outcomes and Results: The PRO-bookmarking materials and procedures underwent four iterations to make them clearer, simpler, and more accessible. For example, the materials included more structured text and graphic supports where appropriate and the procedures were clustered into smaller discrete tasks and displayed graphically when possible and appropriate. Conclusions: PRO-bookmarking materials and procedures were made simpler and more structured to increase their accessibility to adults with cognitive and language impairments. In fact, these adaptations made the tasks simpler and clearer for all types of stakeholders., Patient-reported outcome measures (PROMs) quantify health outcomes from the patient's perspective, such as emotional well-being, functional status, symptoms, and social participation (Cella et al., 2015; Mayo et al., 2017). Over [...]

Purpose: This research investigated the nature of cognitive decline in prodromal Alzheimer's disease (AD), particularly in mild cognitive impairment, amnestic type (aMCI). We assessed language in aMCI as compared with healthy aging (HA) and healthy young (HY) with new psycholinguistic assessment of complex sentences, and we tested the degree to which deficits on this language measure relate to performance in other general cognitive domains such as memory. Method: Sixty-one individuals with aMCI were compared with 24 HA and 10 HY adults on a psycholinguistic measure of complex sentence production (relative clauses). In addition, HA, HY, and a subset of the aMCI participants (n = 22) were also tested on a multidomain cognitive screen, the Addenbrooke's Cognitive Examination-Revised (ACE-R), and on a verbal working memory Brown-Peterson (BP) test. General and generalized linear mixed models were used to test psycholinguistic results and to test whether ACE-R and BP performance predicted performance on the psycholinguistic test similarly in the aMCI and HA groups. Results: On the psycholinguistic measure, sentence imitation was significantly deficited in aMCI in comparison with that in HA and HY. Experimental factorial designs revealed that individuals with aMCI had particular difficulty repeating sentences that especially challenged syntax-semantics integration. As expected, the aMCI group also performed significantly below the HY and HA groups on the ACE-R. Neither the ACE-R Memory subtest nor the BP total scores predicted performance on the psycholinguistic task for either the aMCI or the HA group. However, the ACE-R total score significantly predicted psycholinguistic task performance, with increased ACe-R performance predicting increased psycholinguistic task performance only for the HA group, not for the aMCI group. Conclusions: Results suggest a selective deterioration in language in aMCI, specifically a weakening of syntaxsemantics integration in complex sentence processing, and a general independence of this language deficit and memory decline. Results cohere with previous assessments of the nature of difficulty in complex sentence formation in aMCI. We argue that clinical screening for prodromal AD can be strengthened by supplementary testing of language, as well as memory, and extended evaluation of strength of their relation., Early detection of Alzheimer's disease (AD) during its long prodromal period is of paramount importance. Such detection requires strong and focused clinical psychometric profiling of cognitive function, which can complement [...]

BACKGROUND/OBJECTIVES: Mild cognitive impairment (MCI), often considered as an early stage of dementia, is heterogeneous, and not all subjects with MCI progress into clinically diagnosed dementia. Low body weight (and body mass index, BMI) as well as losing weight while in MCI stadium have been proposed as possible risk factors of MCl-to-dementia conversion. SUBJECTS/METHODS: A prospective, 2-year observation of 102 MCI subjects has been conducted. Data on MCI subtype, somatic and neuropsychiatric co-morbidity and demographic characteristics (including age, gender and education), were collected. In addition, baseline and yearly BMI were calculated. RESULTS: Data of 83 out of the originally included 102 subjects were available after 2 years; 27 of those (32.5%) progressed to dementia. In univariate analysis, multiple-deficit MCI subtype (as compared with pure amnestic), higher age, the presence of diabetes and apathy, and lower baseline BMI (and losing weight on 2-year follow-up) were associated with conversion to dementia. Variables retained in the multivariate backward stepwise logistic regression model for conversion after 24 months of observation included lower baseline BMI (odds ratio, OR (95% cofidence interval, Cl): 0.6 (0.4-0.9)), weight loss on 2-year follow- up (OR (95% Cl): 1.3 (1.1-1.5)), male gender (OR (95% Cl): 0.1 (0.01-0.9)) and presence of apathy (OR (95% Cl): 70.7 (5.6-699)). Apathetic subjects had lower BMI and higher weight loss after controlling for potential confounders (age, gender, years of education and baseline ADAScog (Alzheimer's Disease Assessment Scale-cognitive subscale) score). CONCLUSION: MCI subjects presenting with apathy, low initial BMI and losing weight on follow-up have a significantly greater risk of developing dementia. Nutritional and behavioural assessment should be considered as additional tools in evaluating the risk of dementia among MCI subjects. European Journal of Clinical Nutrition (2014) 68, 1216-1219; doi:10.1038/ejcn.2014.167; published online 13 August 2014, INTRODUCTION The relationship between body mass index (BMI), used as a proxy measure of nutritional status, and the risk of cognitive decline and dementia appears to be complex. Both high [...]

Background. There is growing interest in determining the degree of anemia, which is clinically significant. The goal of this study was to determine the association between hemoglobin concentration and cognitive impairment in a large sample of U.S. adults. Methods. We used cross-sectional data from 19,701 adults participating in the REasons for Geographic And Racial Differences in Stroke study. Cognitive impairment was defined as a score of 4 or less on the six-item screener. Hemoglobin was analyzed in 1 g/dL increments relative to the World Health Organization (WHO) threshold l< 13 g/dL for men and < 12 g/dL for women). Results. The mean hemoglobin concentration was 13.7 [+ or -] 1.5 g/dL. The prevalence of cognitive impairment increased from 4.39; among individuals with a hemoglobin >3 g/dL above the WHO threshold to 16.8c/c for those with a hemoglobin [greater than or equal to] 2 g/dL below the WHO threshold. After adjustment for demographics, chronic health conditions, health status, and inflammation, the association between reduced hemoglobin and cognitive impairment was attenuated and no longer significant, including among those with hemoglobin [greater than or equal to] 2 g/dL below the WHO threshold (odds ratio 1.39, 95% confidence interval = 0.94 2.04). A test for linear trend way of borderline significance (p value = .06). For 94% of the sample within 2 g/dL of the WHO threshold, there way no relationship between hemoglobin concentration and the odds of cognitive impairment. The associations did not differ by sex and race. Conclusions. Within a large sample of community-dwelling adults, there v, as no significant association between hemoglobin concentration and cognitive impairment after multivariable adjustment. Key Words: Hemoglobin--Anemia--Cognitive impairment. doi: 10.1093/gerona/glq126

Mild cognitive impairment (MCI) and dementia affect many aspects of emotion processing. Even though the ability to detect threat is a particularly important aspect of emotion processing, no study to date has assessed threat perception in either of these groups. The purpose of the present study was to test whether individuals with MCI (n = 38) and mild dementia (n = 34) have difficulty differentiating between faces and situations normatively judged to be either high or low in threat relative to age-matched controls (n = 34). To achieve this aim, all participants completed 2 danger rating tasks that involved viewing and rating high- and low-danger images. It was also assessed whether threat perception was related to cognitive functioning and emotion recognition. The results indicated that all 3 groups were accurately, and comparably, able to differentiate high from low-danger faces. However, the dementia group had difficulties differentiating high from low-danger situations, which reflected a bias to overattribute the level of threat posed by normatively judged nonthreatening situations. This difficulty was related to more general cognitive decline. Key Words: Dementia--Emotion--Social cognition

Dendritic spine morphogenesis contributes to brain function, cognition, and behavior, and is altered in psychiatric disorders. Kalirin is a brain-specific guanine-nucleotide exchange factor (GEF) for Rac-like GTPases and is a key regulator of spine morphogenesis. Here, we show that KALRN-knockout mice have specific reductions in cortical, but not hippocampal, Rac1 signaling and spine density, and exhibit reduced cortical glutamatergic transmission. These mice exhibit robust deficits in working memory, sociability, and prepulse inhibition, paralleled by locomotor hyperactivity reversible by clozapine in a kalirin-dependent manner. Several of these deficits are delayed and age-dependent. Our study thus links spine morphogenic signaling with age-dependent, delayed, disease-related phenotypes, including cognitive dysfunction. prefrontal cortex | antipsychotic | schizophrenia | Alzheimer's disease | synaptic plasticity

Background. Cognitive impairment is an important contributor to disability. Limited clinical trial evidence exists regarding the impact of physical exercise on cognitive function (CF). We report results of a pilot study to provide estimates of the relative impact of physical activity (PA) on l-year changes in cognitive outcomes and to characterize relationships between changes in mobility disability and changes in cognition in older adults at increased risk for disability. Methods. Sedentary persons (102) at increased risk for disability (aged 70-89 years) were randomized to moderate_intensity PA or health education. Participants were administered the Digit Symbol Substitution Test (DSST), Rey Auditory Verbal Learning Test (RAVLT), modified Stroop test, and Modified Mini-Mental State Examination at baseline and 1 year. Results. Group differences were not significant but improvements in cognitive scores were associated with improvements in physical function. Specifically, the DSST significantly correlated with change in the Short Physical Performance Battery score (r = .38, p = .0002), in chair stand score (r = .26, p = .012), in balance score (r = .21, p = .046), and in 400-m gait speed (r = .15, p = .147). Change recall on the RAVLT and in the Stroop test was also positively correlated with changes in chair stand and balance, respectively. Conclusions. These results provide further support for the benefits of exercise on CF in older adults. An adequately powered clinical trial of PA involving older adults at increased risk for cognitive disability is needed to expand the indications for prescribing exercise for prevention of decline in brain function. Key Words: Exercise--Cognition--Aging--Prevention--LIFE study.

Background: Patients with major depressive disorder (MDD) show impairments in cognitive functions. However, neural mechanisms underlying these disturbances are poorly understood. We investigated whether MDD affects neural mechanisms of involuntary [...]

Oxidative stress has been implicated in cognitive impairment in both old experimental animals and aged humans. This implication has led to the notion that antioxidant defense mechanisms in the brain are not sufficient to prevent age-related increase in oxidative damage and that dietary intake of a variety of antioxidants might be beneficial for preserving brain function. Here we report a dramatic loss of learning and memory function from 8 to 11 months of age in mice, associated with marked increases in several markers of brain oxidative stress. Chronic systemic administration of two synthetic catalytic scavengers of reactive oxygen species, Eukarion experimental compounds EUK-189 and EUK-207, from 8 to 11 months almost completely reversed cognitive deficits and increase in oxidative stress taking place during this time period in brain. In particular, increase in protein oxidation was completely prevented, whereas increase in lipid peroxidation was decreased by [approximately equal to] 50%. In addition, we observed a significant negative correlation between contextual fear learning and levels of protein oxidation in brain. These results further support the role of reactive oxygen species in age-related learning impairment and suggest potential clinical applications for synthetic catalytic scavengers of reactive oxygen species.

The additional arguments and evidence supplied by the commentaries strengthen the hypothesis that underactivity of NMDA receptors produces impaired cognitive coordination in schizophrenia. This encourages the hope that though the distance from molecules to mind is great, it can nevertheless be traversed. We therefore predict that in this decade or the next molecular psychology will be seen to be as fundamental to our understanding of mind as molecular biology is to our understanding of life.

The concept of locally specialized functions dominates research on higher brain function and its disorders. Locally specialized function must be complementedby processes that coordinate those functions, however, and impairment of coordinating processes may be central to some psychotic conditions. Evidence for processes that coordinate activity is provided by neurobiological and psychological studies of contextual disambiguation and dynamic grouping. Mechanisms by which this important class of cognitive functions could be achieved include those long-range connections within and between cortical regions that active synaptic channels via NMDA-receptors, and which control gain through their voltage-dependent mode of operation. An impairment of these mechanisms is central to PCP-psychosis, and the cognitive capabilities that they could provide are impaired in some forms of schizophrenia. We conclude that impaired cognitive coordination due to reduced ion flow through NMDA-channels is involved in schizophrenia, and we suggest that it may also be involved in other disorders. This perspective suggests several ways in which further research could enhance our understanding of cognitive coordination, its neural basis, and its relevance to psychopathology.

Social exchange is a pervasive feature of human social life. Models in evolutionary biology predict that for social exchange to evolve in a species, individuals must be able to detect cheaters (nonreciprocators). Previous research suggests that humans have a cognitive mechanism specialized for detecting cheaters. Here we provide neurological evidence indicating that social exchange reasoning can be selectively impaired while reasoning about other domains is left intact. The patient, R.M., had extensive bilateral limbic system damage, affecting orbitofrontal cortex, temporal pole, and amygdala. We compared his performance on two types of reasoning problem that were closely matched in form and equally difficult for control subjects: social contract rules (of the form, 'If you take the benefit, then you must satisfy the requirement') and precaution rules (of the form, 'If you engage in hazardous activity X, then you must take precaution Y'). R.M. performed significantly worse in social contract reasoning than in precaution reasoning, when compared both with normal controls and with other brain-damaged subjects. This dissociation in reasoning performance provides evidence that reasoning about social exchange is a specialized and separable component of human social intelligence, and is consistent with other research indicating that the brain processes information about the social world differently from other types of information.

This article examines epileptic children's social communication skills. Topics include neuropsychology, cognitive development, and an analysis of thought disorders.

Sixty undergraduate subjects were randomly assigned to one of three groups and completed the Seashore Rhythm Test (SRT) as part of an investigation regarding simulated neuropsychological impairment. A sophisticated simulator group was instructed to feign impairment and was provided information regarding traumatic brain injury (TBI) sequelae. A naive simulator group was instructed to feign impairment, but was given no such information. A control group was instructed to perform optimally. Additionally, SRT scores for 20 TBI subjects who completed neuropsychological evaluations were analyzed. Mean SRT scores for the sophisticated and naive simulators did not differ but were significantly lower when compared to control subjects and TBI subjects. A discriminate function analysis cutting score correctly classified 79% of subjects, while classification rates obtained with two previously investigated cutting scores were 64% and 72%. Implications of using these cutting scores are discussed. The findings indicate the SRT is a useful indicator of feigned neurological impairment.

Background. Factors related to physical health have been implicated in both normal and pathological aging of cognitive abilities. To substantiate this notion, we studied existing morbidity, as diagnosed by the general practitioner according to well-defined criteria, as a potential predictor of cognitive test performance. Methods. A sample of 1360 individuals, aged 24-81 years and living in the community, was stratified for age, sex, and general ability. Active and total morbidity in this group were classified according to the International Classification of Primary Care. Neurocognitive tests were used to assess the domains of verbal memory, sensorimotor speed, and cognitive flexibility. Results. Multiple regression analyses with adjustment for age, sex, and educational level showed both insulin-dependent and noninsulin-dependent diabetes to be negatively associated with all cognitive measures. More specific negative associations were found for chronic bronchitis (performance speed) and presbyacusia (memory). Single or aggregated cardiovascular morbidity (including hypertension) was unrelated to test performance. Conclusions. Existing morbidity as a whole contributes only modestly (up to 3.5%) to total variance in cognitive function. However, some specific, relatively common diseases of the elderly, such as diabetes and chronic bronchitis, may aggravate the age-related decline in cognitive ability.

Objective: we investigated the compensatory hypothesis that cognitive deficits in sober alcoholics would reveal differences in the organization Of their cognitive structures or functions relative to nonalcoholic peers with no deficits. Method: Following the method of Tracy and Bates, who tested a similar hypothesis in light versus heavy social drinkers, we used structural equation modeling (SEM: LISREL) to test the compensatory hypothesis. Alcoholics (n = 131, 83 male) and peer nonalcoholics (n = 83, 47 male) were given tests of verbal, visual-spatial and abstracting/problem-solving skills. Results: LISREL analyses indicated that the three factors (latent variables) representing the three skills and the loading of the tasks on these factors were invariant (i.e., similar) across groups. However, factor variances and covariances were noninvariant. Analyses identifying the sources of these differences revealed similarities between the heavy social drinkers of Tracy and sates, study and our alcoholic sample. Conclusions: Results from the present study on cognitive organization in alcoholics, as well as our interpretation of Tracy and sates, findings on the same in heavy social drinkers, support the notion of compensation and reorganization of cognitive function; however, other explanations cannot he ruled out (J. Stud. Alcohol 58: 67-74, 1997), Heavy social drinkers may be functional even though they suffer some brain damage because the brain can compensate for an injured function by switching to another, according to the compensatory hypothesis. This may be similar to the observation by Tracy and Bates that in alcoholics, cortical function is reorganized to cover defects. Researchers measured and statistically analyzed deficits in types of cognitive function in male and female alcoholics compared with controls. Although alcoholics had marked deficits, there appeared shifting from the most severely affected function to a similar but less damaged one., INVESTIGATORS throughout the Western world have reported cognitive deficits in posttreatment sober alcoholics that are similar to those found in other brain dysfunctional groups (Hunt and Nixon, 1993; Parsons et [...]