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Objectives: The main objective of this study was to determine the directions of the relationships between apathy, cognitive deficits and lack of awareness. Methods: One hundred and twenty‐one older persons living in nursing homes, aged between 65 and 99 years old, participated in the study. Cognitive functioning, autonomy, depressive and anxious symptoms, general self‐efficacy, self‐esteem and apathy were evaluated through tests and questionnaires. Lack of awareness was calculated using the patient‐caregiver discrepancy method. The sample was divided into two groups (n1 = 60, n2 = 61) depending on cognitive functioning level (Dementia Rating Scale < median score: 120). We first explored the characteristics of each group. Then, we compared the mode of evaluation of apathy. Finally, we investigated the direction of relationships by applying mediation analyses. Results: Older persons in the low cognitive functioning group were less autonomous, had a lower cognitive functioning level, higher caregiver‐rated apathy and higher lack of awareness than the high cognitive functioning group (ps < 0.05). Evaluation differences were found only in the low cognition group. Caregiver‐rated apathy totally mediated the relationship between cognitive functioning (predictor) and lack of awareness (dependent variable) for the whole sample (90%) and for the low cognitive functioning group (100%). Conclusions: Cognitive deficits should be taken into account when evaluating apathy. Interventions should combine cognition training and emotion intervention to reduce lack of awareness. Future research should develop a therapy dedicated to apathy among older persons without pathologies. [ABSTRACT FROM AUTHOR]

Objectives: Impairment of type I interferon (IFN‐I) immunity has been reported in critically ill COVID‐19 patients. This defect can be explained in a subset of patients by the presence of circulating autoantibodies (auto‐Abs) against IFN‐I. We set out to improve the detection and the quantification of IFN‐I auto‐Abs in a cohort of critically ill COVID‐19 patients, in order to better evaluate the prevalence of these Abs as the pandemic progresses, and how they correlate with the clinical course of the disease. Methods: The concentration of anti‐IFN‐α2 Abs was determined in the serum of 84 critically ill COVID‐19 patients who were admitted to ICU in Hospices Civils de Lyon, France, using a commercially available kit (Thermo Fisher, Catalog #BMS217). Results: A total of 21 of 84 (25%) critically ill COVID‐19 patients had circulating anti‐IFN‐α2 Abs above cut‐off (> 34 ng mL−1). Among them, 15 of 21 had Abs with neutralising activity against IFN‐α2, that is 15 of 84 (18%) critically ill patients. In addition, we noticed an impairment of the IFN‐I response in the majority of patients with neutralising anti‐IFN‐α2 Abs. There was no significant difference in the clinical characteristics or outcome of with or without neutralising anti‐IFN‐α2 auto‐Abs. We detected anti‐IFN‐α2 auto‐Abs in COVID‐19 patients' sera throughout their ICU stay. Finally, we also found auto‐Abs against multiple subtypes of IFN‐I including IFN‐ω. Conclusions: We reported that 18% of critically ill COVID‐19 patients were positive for IFN‐I auto‐Abs, whereas all mild COVID‐19 patients were negative, confirming that the presence of these antibodies is associated with a higher risk of developing a critical COVID‐19 form. [ABSTRACT FROM AUTHOR]

We compared SimoaTM and EllaTM immunoassays to assess serum neurofilament‐light chain levels in 203 multiple sclerosis patients from the OFSEP HD study. There was a strong correlation (ρ = 0.86, p < 0.0001) between both platforms. The EllaTM instrument overestimated values by 17%, but as the data were linear (p = 0.57), it was possible to apply a correction factor to EllaTM results. As for SimoaTM, serum neurofilament‐light chain levels measured by EllaTM were correlated with age and EDSS and were significantly higher in active multiple sclerosis, suggesting that these assays are equivalent and can be used in routine clinical practice. [ABSTRACT FROM AUTHOR]

Background Executive function ( EF) impairment in alcohol dependence ( AD) has been related to the toxic effects of alcohol on frontal lobes. However, this impairment could be partially present before the onset of the disease and might constitute a vulnerability factor. Although a considerable body of research has investigated executive functioning among AD patients, much less attention has been directed toward high-risk individuals. Most studies were carried out among children or adolescents, and very few were conducted in adults. The aim of this study was to examine EF in a group of adult offspring of AD individuals. Methods One hundred and fifty-five nonalcoholic adults with (family history positive [FHP]) or without (family history negative [FHN]) family history of AD were included in the study. All participants were screened for past and current psychiatric diagnoses, and alcohol, tobacco, and other substance use. They were compared on self-rated impulsiveness using the Barratt Impulsiveness Scale-11 ( BIS-11) and EF using a neuropsychological test battery. Results Group comparison revealed that FHP participants had significantly higher BIS-11 scores than the FHN participants, while neuropsychological examination revealed lower EF scores for FHP participants. Hierarchical regression analysis revealed that the number of AD family members was a predictor of EF results, whereas impulsiveness was not. Conclusions Nonalcoholic adult offspring of AD individuals showed increased impulsiveness and decreased EF, suggesting weakness of 2 distinct neurobehavioral decision systems. Findings support evidence that EF weaknesses may qualify as a suitable endophenotype candidate for AD. [ABSTRACT FROM AUTHOR]