cognitive function
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Background and PurposeNon-alcoholic fatty liver disease (NAFLD) and cognitive impairment are common aging-related disorders. This study aims to explore the changes of cognitive function in middle-aged and elderly population with NAFLD from a Jidong impairment cohort.MethodsA total of 1,651 middle-aged and elderly participants (>40 years) without cognitive impairment were recruited into the current study in 2015 and were followed up until to 2019. Abdominal ultrasonography was used for diagnosis of NAFLD. Global cognitive function was assessed with the Mini-Mental State Examination (MMSE). Cognitive impairment was defined as a score <18 for illiterates, a score <21 for primary school graduates, and a score <25 for junior school graduates or above. Multivariable regression analysis was performed to evaluate the association between NAFLD and the four-year cognitive changes.ResultsOut of 1,651 participants, 795 (48.2%) of them had NAFLD in 2015. Cognitive impairment occurred in 241 (14.6%) participants in 2019. Patients with NAFLD had higher 4-year incidence of cognitive impairment than non-NAFLD patients did (17.7 vs. 11.7%, p < 0.001). Multivariable linear regression analysis showed significant association of baseline NAFLD with lower MMSE score in 2019 (β = −0.36, p < 0.05). Multivariable logistic analysis found that the adjusted odds ratio (OR) with 95% confidence interval (CI) of baseline NAFLD was 1.45 (1.00–2.11) for cognitive impairment in 2019 (p = 0.05). We also identified effects of baseline NAFLD on subsequent cognitive impairment as modified by age (interaction p < 0.01) and carotid stenosis (interaction p = 0.05) but not by gender.ConclusionsNAFLD is associated with cognitive decline, especially in middle-aged and with carotid stenosis population.

<b><i>Introduction:</i></b> The hippocampus is relevant to cognitive function in schizophrenia (SCZ) and mood disorder patients. Although not anatomically uniform, it is clearly divided into subfields. This study aimed to elucidate the relationship between hippocampal subfield volume and cognitive function in patients with SCZ, bipolar disorder (BP), and major depressive disorder (MDD). <b><i>Methods:</i></b> The study included 21 patients with SCZ, 22 with BP, and 21 with MDD and 25 healthy controls (HCs). Neurocognitive function was assessed using the Brief Assessment of Cognition in Schizophrenia. We obtained hippocampal subfield volumes using FreeSurfer 6.0. We compared the volumes of the hippocampal subfield between the 4 groups and ascertained correlation between the cognitive composite score and hippocampal subfield volume in each group. <b><i>Results:</i></b> The SCZ group had significantly lower cognitive composite score than the BP, MDD, and HC groups. In the SCZ group, the left and right hippocampus-amygdala transition area and right subiculum and right presubiculum volumes were significantly reduced compared to those in the HC group. The left presubiculum volumes in the SCZ group were significantly reduced compared to those in the MDD group. Subfield volumes did not significantly differ between the BP, MDD, and HC groups. Interestingly, in the SCZ group, volumes of the right CA1, right molecular layer of the hippocampus, and right granule cell and molecular layer of the dentate gyrus were significantly correlated with the cognitive composite score. <b><i>Conclusion:</i></b> Patients with SCZ had poorer cognitive function, which is related to their hippocampal pathology, than those with mood disorders.

Abstract Forkhead Box O 3 (FOXO3) genotype is strongly associated with human longevity and may be protective against neurodegeneration. Air pollution is a risk factor for cognitive decline and dementia. We aimed to study the individual and combined effects of FOXO3 and air pollution on cognitive function in a large prospective cohort with up to 14 years of follow-up. We measured cognitive function and impairment using the Mini-Mental State Examination (MMSE). We used tagging SNPs rs2253310, rs2802292, and rs4946936 to identify the FOXO3 gene, of which roughly half of the population had the longevity associated polymorphism. We matched annual average fine particulate matter (PM2.5) concentrations within 1 km^2 grid. We conducted cross-sectional and longitudinal analyses using multivariable linear and logistic regression models and generalized estimating equation. At baseline, carriers of the longevity associated homozygous minor alleles of FOXO3 SNPs had a higher MMSE score than the carriers of homozygous major alleles. In the longitudinal follow-up, carriers of FOXO3 homozygous minor alleles had lower odds of cognitive impairment compared to non-carriers. Higher PM2.5 was associated with a lower MMSE score and higher odds of cognitive impairment. The positive effects of FOXO3 were the strongest in females, older people, and residents in areas with lower air pollution.

Abstract Few studies have systematically explored the association between cognitive decline and mortality among the aged (above 80 years old) and also have limited evidence of the potential effect modifiers between them. Therefore, this study included 14,891 aged (mean age: 90.3±7.5 years) and 10,904 aged deaths with 34,486 person-years were observed. Cognitive decline was continuous and stratified into ten categories. Potential effect modifiers were identified as age, sex, blood pressure (BP) and high BP related diseases, including hypertension and cardiovascular disease (CVD) mortality. Cox proportional hazards model was used to evaluate the relationship between them after adjusting for demographic characteristics, socioeconomic status, lifestyle factors, leisure activities and health conditions. Compared to those with maintained high normal cognitive function, participants who have declined to severe cognitive impairment from a high normal cognitive function, low normal cognitive function and mild cognitive impairment have 55%, 56% and 63% mortality risks respectively. The multivariable-adjusted model indicated that the aged with decreasing one more point in MMSE score per year, had around 4% higher risk of mortality. There was a significant association of interaction of cognitive decline-mortality and sex (P=0.013) as well as hypertension (P=0.004) but with no significant association among age (P=0.277), high BP (P=0.082), and CVD mortality (P=0.058). Our findings suggest that periodic screen cognitive decline and strengthen BP control may be necessary for public health.

Abstract Study Objectives Untreated obstructive sleep apnea (OSA) is associated with cognitive deficits and altered brain electrophysiology. We evaluated the effect of continuous positive airway pressure (CPAP) treatment on quantitative sleep electroencephalogram (EEG) measures and cognitive function. Methods We studied 162 OSA patients (age 50±13, AHI 35.0±26.8) before and after 6 months of CPAP. Cognitive tests assessed working memory, sustained attention, visuospatial scanning and executive function. All participants underwent overnight polysomnography at baseline and after CPAP. Power spectral analysis was performed on EEG data (C3-M2) in a sub-set of 90 participants. Relative delta EEG power and sigma power in NREM and EEG slowing in REM were calculated. Spindle densities (events p/min) in N2 were also derived using automated spindle event detection. All outcomes were analysed as change from baseline. Results Cognitive function across all cognitive domains improved after six months of CPAP. In our sub-set, increased relative delta power (p&lt;0.0001) and reduced sigma power (p=0.001) during NREM were observed after the 6-month treatment period. Overall, fast and slow sleep spindle densities during N2 were increased after treatment. Conclusions Cognitive performance was improved and sleep EEG features were enhanced when assessing the effects of CPAP. These findings suggest the reversibility of cognitive deficits and altered brain electrophysiology observed in untreated OSA following six months of treatment.