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OBJECTIVE: Determine the latent structure of health literacy in persons living with HIV (PLWH) and its association with health management and decision-making. METHOD: Participants included 220 PLWH and 123 seronegative participants from Southern California and Alabama who completed a battery of well-validated health literacy measures, along with assessments of health management self-efficacy, health-related decision-making, depression, and basic clinical laboratory measures. RESULTS: Exploratory factor analysis in HIV− participants showed that the shared variance between a battery of health literacy measures, including health word reading, verbal comprehension, numeracy, and self-reported problems was best explained by a single factor. Similarly, a confirmatory factor analysis in PLWH also supported a single factor structure, but for a re-specified four-test solution based on the core performance-based measures of health literacy. In analyses adjusting for demographics, PLWH demonstrated significantly lower health literacy composite scores as compared to their HIV− counterparts. Among PLWH, lower health literacy was independently associated with lower self-efficacy for health management and poorer health-related decision-making. CONCLUSIONS: Findings suggest that numeracy, word recognition, and verbal comprehension and reasoning comprise a unitary construct of health literacy that is lower in PLWH as compared to seronegatives and is independently associated with important downstream aspects of health management and decision-making.

Neuropsychological research has been limited in the representation of cultural diversity due to various issues, raising questions regarding the applicability of findings to diverse populations. Nonetheless, culture-dependent differences in fundamental psychological processes have been demonstrated. One of the most basic of these, self-construal (individualism, collectivism), is central to how many other differences are interpreted. Self-construals may have possible consequences on social interactions, emotions, motivation, and cognition. This study aimed to evaluate the impact of self-construal on neurocognitive functions in older adults. A total of 86 community-dwelling older adults 60 years and older were assessed with three common self-report measures of self-construal along individualism and collectivism (IC). A cognitive battery was administered to assess verbal and non-verbal fluency abilities. Latent profile analysis (LPA) was used to categorize individuals according to IC, and one-way analyses of covariance (ANCOVA), including relevant covariates (e.g., ethnicity, gender, linguistic abilities), were used to compare neurocognitive functions between individualists and collectivists. Collectivists outperformed individualists on left frontally-mediated measures of verbal fluency (action, phonemic) after controlling for relevant covariates, F(1,77) = 6.942, p = 0.010, η2 = 0.061. Groups did not differ on semantic fluency, non-verbal fluency, or attention/working memory (all ps > 0.05). These findings suggest a cognitive advantage in collectivists for verbal processing speed with an additional contribution of left frontal processes involved in lexicosemantic retrieval. Self-construal may provide a meaningful descriptor for diverse samples in neuropsychological research and may help explain other cross-cultural differences.

ObjectiveBrain atrophy has been correlated with objective cognitive dysfunction in multiple sclerosis but few studies have explored self-reported subjective cognitive concerns and their relationship to brain volume changes. This study explores the relationship between subjective cognitive concerns in multiple sclerosis and reduced brain volume in regions of interest implicated in cognitive dysfunction.MethodsA total of 158 patients with multiple sclerosis completed the Quality of Life in Neurologic Disorders Measures (Neuro-QoL) short forms to assess subjective cognitive concerns and underwent brain magnetic resonance imaging. Regional brain volumes from regions of interest implicated in cognitive dysfunction were measured using NeuroQuant automated volumetric quantitation. Linear regression was used to analyze the relationship between subjective cognitive concerns and brain volume.ResultsControlling for age, disease duration, gender, depression and fatigue, increased subjective cognitive concerns were associated with reduced thalamic volume (standardized β = 0.223, t150 =2.406, P = 0.017) and reduced cortical gray matter volume (standardized β = 0.240, t150 = 2.777, P = 0.006). Increased subjective cognitive concerns were not associated with any other regions of interest that were analyzed.ConclusionsSubjective cognitive concern in MS is associated with reduced thalamic and cortical gray matter volumes, areas of the brain that have been implicated in objective cognitive impairment. These findings may lend neuroanatomical significance to subjective cognitive concerns and patient-reported outcomes as measured by Neuro-QoL.

Indexación: Scopus. Evidence from small-scale studies indicates that impairments in postural stability are an early and disabling feature of Huntington’s disease (HD) and may be a useful clinical endpoint for disease modifying trials. Larger studies are needed to confirm these preliminary findings and the suitability of postural stability outcomes as clinical endpoints. Static and dynamic postural stability were evaluated in 54 premanifest HD, 36 manifest HD and 45 healthy individuals using the Sensory Organization Test (SOT) and Limits of Stability (LOS) test. Manifest HD displayed significantly lower scores on all SOT conditions and on the SOT composite score and had more falls than healthy and premanifest HD (p < 0.05). Premanifest and manifest HD demonstrated significantly lower endpoint excursion (p < 0.001), maximum excursion (p ≤ 0.001), and directional control (p ≤ 0.004) values than healthy individuals on the LOS test. Deficits in LOS were found to manifest on the left side of premanifest HD. Significant but low associations were observed between UHDRS-TMS, disease burden score, diagnostic confidence level, SOT conditions and SOT composite score. We confirm here that individuals with premanifest and manifest HD display significant impairments in static and dynamic postural stability. Dynamic posturography assessments should be considered as clinical endpoints for future disease modifying trials. © 2018, The Author(s). https://www.nature.com/articles/s41598-018-32924-y

Background/Aims: Biological markers of utility in tracking Alzheimer’s disease (AD) during the presymptomatic prodromal phase are important for prevention studies. Changes in cerebrospinal fluid (CSF) levels of 42-amino-acid β-amyloid (Aβ42), total tau protein (t-tau) and phosphorylated tau at residue 181 (p-tau181) during this state are incompletely characterized. Methods: We measured CSF markers in 13 carriers of familial AD (FAD) mutations that are fully penetrant for causing AD (PSEN1 and APP) and in 5 non-mutation-carrying family members. Results: Even among the entirely presymptomatic mutation carriers (n = 9), Aβ42 was diminished (388.7 vs. 618.4 pg/ml, p = 0.004), and t-tau (138.5 vs. 50.5 pg/ml, p = 0.002) and p-tau181 (71.7 vs. 24.6 pg/ml, p = 0.003) were elevated. There was a negative correlation between Aβ42 levels and age relative to the family-specific age of dementia diagnosis. Conclusions: Our data are consistent with a decline in CSF Aβ42 levels occurring at least 20 years prior to clinical dementia in FAD.

Background: Both familial and sporadic Alzheimer’s disease (AD) result in progressive cortical and subcortical atrophy. Familial autosomal dominant AD (FAD) allows us to study AD brain changes presymptomatically. Methods: 33 subjects at risk for FAD (25 for PSEN1 and 8 for APP mutations; 22 mutation carriers and 11 controls) and 3 demented PSEN1 mutation carriers underwent T1-weighted MPRAGE 1.5T MRI. Using the hippocampal radial distance and cortical pattern matching techniques, we investigated the effects of carrier status and dementia diagnosis on cortical and hippocampal atrophy. All analyses were corrected for age and relative age (years to median age of disease onset in the family). Results: The dementia cases had pronounced cortical atrophy in the lateral and medial parietal, posterior cingulate and frontal cortices and hippocampal atrophy bilaterally relative to both nondemented carriers and controls. Nondemented carriers did not show significant cortical thinning or hippocampal atrophy relative to controls. Conclusions: FAD is associated with thinning of the posterior association and frontal cortices and hippocampal atrophy. Larger sample sizes may be necessary to reliably identify cortical atrophy in presymptomatic carriers.

Familial Alzheimer’s disease (AD) due to PSEN1 mutations provides a unique opportunity to study the behavior of AD biomarkers in persons in whom the diagnosis is certain. Here we describe a 55 year-old woman with clinically probable AD and a novel PSEN1 mutation who underwent genetic, clinical, biochemical and imaging assessments, including nuclear imaging with FDDNP. Neuropsychological testing confirmed deficits in memory with more minor deficits in visuospatial and language function. CSF t-tau and p-tau181 were markedly elevated and Abeta42 levels reduced. FDG-PET revealed hypometabolism in the left parietotemporal cortex. FDDNP-PET showed increased global binding of tracer in medial temporal and parietal lobes and in the head of the caudate and anterior putamen bilaterally. Her similarly affected brother died and the diagnosis of AD was confirmed neuropathologically. The striatum demonstrated amyloid pathology and marked neurofibrillary pathology beyond that typically seen in late-onset AD. A novel S212Y substitution in PSEN1 was present in the index patient and in her affected brother but not in an older unaffected sister. An in-vitro assay in which the S212Y mutation was introduced in cell culture confirmed that it was associated with increased production of Abeta42.

The definition of mild cognitive impairment (MCI) as a precursor for Alzheimer's disease (AD) represented an important step forward in diagnosing the illness in its earliest stage. However, diagnoses based principally on cognitive performance have limitations in that there is variability between centers in which tests are employed and in how they are interpreted. Advances in our understanding of imaging and biochemical changes occurring early in the illness have improved our ability to diagnose AD in this early phase and diagnostic criteria for AD have been proposed recently based on such biomarkers. Persons inheriting autosomal dominant mutations causing familial AD (FAD) are essentially certain to develop the disease. In our studies of preclinical persons at-risk for inheriting FAD, we applied MCI diagnostic criteria to carriers of FAD mutations to ascertain the extent to which they identified persons in the earliest stages of the clinical illness. Our results indicate the relative prevalence of MCI subtypes varies considerably depending on the tests used to measure cognition. Furthermore, we found that cognitive complaints in such persons were less predictive of mutation status than were informants' reports of cognitive loss. The study of FAD provides an opportunity to test various criteria for early AD and these observations should be taken into consideration in future iterations of such diagnostic criteria.