Dataset Information

Understanding Cognitive Deficits in People with Arthritis.

ABSTRACT: Cognitive deficits are commonly seen in people with arthritis. However, previous studies focused primarily on small-sized clinical samples. There is a need for cohort-based studies, which are characterized by high generalizability. In addition, these studies mainly focused on attention, memory, and executive function. However, cognition is not a single concept, but includes other cognitive domains, such as verbal fluency and arithmetic abilities. Thus, we aim to explore how arthritis can affect cognitive abilities, including episodic memory, semantic verbal fluency, fluid reasoning, and numerical ability by using a large cohort from the United Kingdom. The main findings were that people with arthritis have significantly lower immediate word recall (t(2257) = -6.40, p < 0.001, Cohen's d = -0.12, 95% C.I. = [-0.16, -0.08]), delayed word recall (t(2257) = -5.60, p < 0.001, Cohen's d = -0.11, 95% C.I. = [-0.14, -0.07]), semantic verbal fluency (t(2257) = -3.03, p < 0.01, Cohen's d = -0.06, 95% C.I. = [-0.10, -0.02]), fluid reasoning (t(2257) = -3.96, p < 0.001, Cohen's d = -0.07, 95% C.I. = [-0.11, -0.04]), and numerical ability (t(2257) = -3.85, p < 0.001, Cohen's d = -0.07, 95% C.I. = [-0.10, -0.03]) compared to what they would expect given their demographics. Interventions are needed to improve cognitive abilities in people with arthritis.

SUBMITTER: Kang W

PROVIDER: S-EPMC10178460 | biostudies-literature | 2023 May

REPOSITORIES: biostudies-literature

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Understanding Cognitive Deficits in People with Arthritis.

Kang Weixi W Whelan Edward E Malvaso Antonio A

Healthcare (Basel, Switzerland) 20230506 9

Cognitive deficits are commonly seen in people with arthritis. However, previous studies focused primarily on small-sized clinical samples. There is a need for cohort-based studies, which are characterized by high generalizability. In addition, these studies mainly focused on attention, memory, and executive function. However, cognition is not a single concept, but includes other cognitive domains, such as verbal fluency and arithmetic abilities. Thus, we aim to explore how arthritis can affect ...[more]

PMID: 37174879

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Project description:BackgroundThere is growing concern about possible cognitive consequences of COVID-19, with reports of 'Long COVID' symptoms persisting into the chronic phase and case studies revealing neurological problems in severely affected patients. However, there is little information regarding the nature and broader prevalence of cognitive problems post-infection or across the full spread of disease severity.MethodsWe sought to confirm whether there was an association between cross-sectional cognitive performance data from 81,337 participants who between January and December 2020 undertook a clinically validated web-optimized assessment as part of the Great British Intelligence Test, and questionnaire items capturing self-report of suspected and confirmed COVID-19 infection and respiratory symptoms.FindingsPeople who had recovered from COVID-19, including those no longer reporting symptoms, exhibited significant cognitive deficits versus controls when controlling for age, gender, education level, income, racial-ethnic group, pre-existing medical disorders, tiredness, depression and anxiety. The deficits were of substantial effect size for people who had been hospitalised (N = 192), but also for non-hospitalised cases who had biological confirmation of COVID-19 infection (N = 326). Analysing markers of premorbid intelligence did not support these differences being present prior to infection. Finer grained analysis of performance across sub-tests supported the hypothesis that COVID-19 has a multi-domain impact on human cognition.InterpretationInterpretation. These results accord with reports of 'Long Covid' cognitive symptoms that persist into the early-chronic phase. They should act as a clarion call for further research with longitudinal and neuroimaging cohorts to plot recovery trajectories and identify the biological basis of cognitive deficits in SARS-COV-2 survivors.FundingFunding. AH is supported by the UK Dementia Research Institute Care Research and Technology Centre and Biomedical Research Centre at Imperial College London. WT is supported by the EPSRC Centre for Doctoral Training in Neurotechnology. SRC is funded by a Wellcome Trust Clinical Fellowship 110,049/Z/15/Z. JMB is supported by Medical Research Council (MR/N013700/1). MAM, SCRW and PJH are, in part, supported by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London.

Project description:Background: Age-related cognitive deficits negatively affect quality of life and can presage serious neurodegenerative disorders. Despite sleep disruption’s well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep’s relationship to cognitive aging. Methodology: We measured sleep stages in young adult and aged F344 rats during inactive (enhanced sleep) and active (enhanced wake) periods. Animals were behaviorally characterized on the Morris water maze and gene expression profiles of their parietal cortices were taken. Principal Findings: Water maze performance was impaired, and inactive period deep sleep was decreased with age. However, increased deep sleep during the active period was most strongly correlated to maze performance. Transcriptional profiles were strongly associated with behavior and age, and were validated against prior studies. Bioinformatic analysis revealed increased translation and decreased myelin/ neuronal pathways. Conclusions: The F344 rat appears to serve as a reasonable model for some common sleep architecture and cognitive changes seen with age in humans, including the cognitively disrupting influence of active period deep sleep. Microarray analysis suggests that the processes engaged by this sleep are consistent with its function. Thus, active period deep sleep appears temporally misaligned but mechanistically intact, leading to the following: first, aged brain tissue appears capable of generating the slow waves necessary for deep sleep, albeit at a weaker intensity than in young. Second, this activity, presented during the active period, seems disruptive rather than beneficial to cognition. Third, this active period deep sleep may be a cognitively pathologic attempt to recover age-related loss of inactive period deep sleep. Finally, therapeutic strategies aimed at reducing active period deep sleep (e.g., by promoting active period wakefulness and/or inactive period deep sleep) may be highly relevant to cognitive function in the aging community. KEYWORDS: frontal cortex, rat, young or aged We implanted young and aged Fischer 344 rats (n = 6/ group) with wireless EEG, EMG and movement monitoring devices to measure sleep architecture. Animals were trained in the Morris water maze to assess cognitive function, and frontal cortices were removed for microarray analysis.sleep disruption and cognitive decline.

Dataset Information

Understanding Cognitive Deficits in People with Arthritis.

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Understanding Cognitive Deficits in People with Arthritis.

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