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Objectives: This study investigates the mediating roles of autonomic function and mental health in the association between sleep and cognitive decline in adults aged 50 and above. Method: A total of 2,697 participants with observations on sleep and mediators at baseline and repeated measures of cognitive function (MMSE) were included. Clusters of individuals with similar cognitive trajectories (high-stable, mid-stable and low-declining) were identified. Multinomial logistic regressions were used to estimate the likelihood of membership to each trajectory group based on sleep duration and disturbance. Finally, mediation analysis tested potential mediating effects of autonomic function and mental health underpinning the sleep–cognition relationship. Results: Short (p =.028), long (p =.019), and disturbed sleep (p =.008) increased the likelihood of a low-declining cognitive trajectory. Mental health measures fully attenuated relationships between cognitive decline and short or disturbed sleep but not long sleep. No autonomic function mediation was observed. Conclusion: Older adults with short or disturbed sleep are at risk of cognitive decline due to poor mental health. Individuals with long sleep are also at risk, however, the acting pathways remain to be identified. These outcomes have clinical implications, potentially identifying intervention strategies targeting mental health and sleep as prophylactic measures against dementia. [ABSTRACT FROM AUTHOR]

The aim of this study is to investigate whether 25-hydroxyvitamin D (25(OH)D) is associated with periodontitis and tooth loss in older adults. A total of 2346 adults underwent a detailed dental examination as part of the health assessment of a national population study – The Irish Longitudinal Study of Ageing. 25(OH)D analysis was performed on frozen non-fasting total plasma using LC-MS. The analysis included both multiple logistic regression and multinominal logistic regression to investigate associations between 25(OH)D concentration, periodontitis and tooth loss, adjusting for a range of potential confounders. Results of the analysis found the mean age of participants was 65·3 years (sd 8·2) and 55·3 % of the group were female. Based on the quintile of 25(OH)D concentration, participants in the lowest v. highest quintile had an OR of 1·57 (95 % CI 1·16, 2·13; P < 0·01) of having periodontitis in the fully adjusted model. For tooth loss, participants in the lowest v. highest quintile of 25(OH)D had a RRR of 1·55 (95 % CI 1·12, 2·13; P < 0·01) to have 1–19 teeth and a RRR of 1·96 (95 % CI 1·20, 3·21; P < 0·01) to be edentulous, relative to those with ≥ 20 teeth in the fully adjusted models. These findings demonstrate that in this cross-sectional study of older men and women from Ireland, 25(OH)D concentration was associated with both periodontitis and tooth loss, independent of other risk factors. [ABSTRACT FROM AUTHOR]

Objective: To examine associations of plasma folate concentrations and risk of global and domain-specific cognitive decline in older people.Methods: Data of 3140 participants from The Irish Longitudinal Study on Ageing (TILDA), a nationally-representative cohort of adults aged ≥50 years were used over 8-year follow-up. Biannual cognitive assessments included the Mini-Mental State Examination (MMSE), verbal fluency and immediate and delayed word recall tests (Waves 1-5) and the Montreal Cognitive Assessment, (MoCA) (Waves 1 and 3). Plasma folate concentrations were measured in stored blood collected at baseline. Mixed effects Poisson and linear regression determined associations between baseline folate concentrations and cognition.Results: In multivariable-adjusted models of those aged ≥50 years at baseline, low folate at baseline (<11.2 nmol/L) was associated with higher proportions of MMSE errors (incidence rate ratio [IRR] = 1.10; 95% confidence interval [CI] (1.00, 1.21), lowest vs. highest quintile) over 8 years. Plasma folate <21.8 nmol/L predicted declines in episodic memory for immediate (beta [β] = -0.26; 95% CI (-0.48, -0.03), β = -0.29; 95% CI (-0.50, 0.08) and β = -0.29; (-0.50, -0.08), for lowest three vs. highest quintile) and delayed recall (β = -0.20; 95% CI (-0.38, -0.01), β = -0.18; 95% CI (-0.37, -0.01) and β = -0.19; (-0.36, -0.01) lowest three vs. highest quintile). There were no significant associations in a subsample aged ≥65 years.Conclusion: In those aged ≥50 years, lower concentrations of folate may have differential relationships with cognitive domains. Folate <11.2 nmol/L predicted a decline in global cognitive function, while <21.8 nmol/L predicted poorer episodic memory. Low folate was associated with accelerated decline in cognitive function and is an important marker for cognitive decline among older people. [ABSTRACT FROM AUTHOR]

Objective: Cognitive impairment is prevalent in older ages. Associations with sleep are well established; however, ambiguity remains in which sleep characteristics contribute to this impairment. We examined cross‐sectional associations between both self‐reported and actigraphy‐based sleep and cognitive performance across a number of domains in community‐dwelling older adults. Methods: 1520 participants aged 50 and older with self‐reported and actigraphy‐based total sleep time (TST) (≤5, 6, 7–8, 9 and ≥10 h) and self‐reported sleep problems were analysed. Cognitive function was assessed using the Mini‐Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), verbal fluency, immediate and delayed recall memory, colour trails tests, and choice reaction tests (CRT). Associations between sleep and cognition were modelled using linear and negative binomial regression. Results: Negative associations were found between ≥10 h of self‐reported TST and MoCA error rate (incidence rate ratio [IRR] = 1.42; 95% confidence interval [CI] = 1.18, 1.71; p < 0.001); verbal fluency (beta [B] = −2.32 words; 95% CI = −4.00, −0.65; p < 0.01); and delayed recall (B = −0.91 words; 95% CI = −1.58, −0.25; p < 0.05) compared to 7–8 h. Significant associations with actigraphy‐based TST were limited to MoCA error rate in ≤5 h (IRR = 1.22; 95% CI = 1.02, 1.45; p < 0.05) compared to 7–8 h. Higher numbers of sleep problems were associated with slower performance in CRT cognitive response time (IRR = 1.02; 95% CI = 1.00, 104; p < 0.05) and total response time (IRR = 1.02; 95% CI = 1.00, 1.04; p < 0.05). Conclusions: Self‐reported long sleep duration was consistently associated with worse cognitive performance across multiple domains. Marginal associations between cognition and both actigraphy‐based sleep and self‐reported sleep problems were also apparent. These results further affirm poor sleep as a risk factor for cognitive impairment. [ABSTRACT FROM AUTHOR]

Background Orthostatic hypotension (OH) can be assessed with non-invasive continuous beat-to-beat haemodynamic monitoring during active stand (AS) testing; this yields large volumes of data outside the scope of the traditional OH definition. We explored clinical associations of different AS patterns in participants from Wave 1 of the Irish Longitudinal Study on Ageing. Methods AS patterns were generated based on three sequential binary systolic blood pressure features: drop ≥40 mmHg within 10 sec post-stand ("immediate deficit"), failure to return to within 20 mmHg of supine level at 40 sec after standing ("stabilisation deficit") and drop ≥20 mmHg between >40 and 120 sec post-stand ("late deficit"). Eight AS groups resulted from combining the presence/absence of these three features. The groups were cross-sectionally characterised, and their ability to independently predict orthostatic intolerance (OI) during AS, and falls or syncope in the past year, was evaluated using multivariate logistic regression models. Results A total of 4,899 participants were included (mean age 61), of which 3,312 (68%) had no deficits. Older age was associated with stabilisation deficit and late deficits were seen in groups with higher proportions of beta blockers and psychotropic medications. Regression models identified independent associations between OI and three immediate-deficit groups; associations seemed stronger as more deficits were present. There was a significant association between falls history and the three-deficit group (odds ratio 1.54, 95% confidence interval: 1.15–2.07, P  = 0.004). Conclusions More deficits seemed associated with the higher risk of OI and falls history. Observations are not causal but the recognition of these patterns may help clinicians focus on careful prescribing. [ABSTRACT FROM AUTHOR]

Background Fried's frailty phenotype is defined by five criteria: exhaustion, unexplained weight loss, weakness, slowness and low physical activity. Prefrailty (PF) meets one or two criteria. PF is of interest as a target for preventative interventions, but it is not known if it is a homogenous syndrome. Objective to compare the longitudinal trajectories of two PF groups: one defined by exhaustion and/or unexplained weight loss (PF1) and one defined by one or two of the following: weakness, slowness, low physical activity (PF2). Design and setting population-based longitudinal study of ageing. Subjects One-thousand four-hundred seventy-six PF participants aged ≥50 years from wave 1 of the study (2010), followed 2-yearly over four longitudinal waves (2012, 2014, 2016, 2018). Methods generalised estimating equations (GEEs) were used to assess the effect of PF type across waves to predict cumulative mortality and disability in basic activities of daily living (ADL) and independent ADL (IADL), adjusting for baseline characteristics (age, sex, education, living alone, self-rated health, comorbidity, body mass index). Results in wave 1, there were 503 PF1 and 973 PF2 participants. By wave 5, 38 (7.6%) PF1 and 145 (14.9%) PF2 participants had died. In PF1 participants, mean numbers of ADL and IADL disabilities both increased from 0.1 to 0.2 from wave 1 to wave 5, whilst in PF2 increases were from 0.2 to 0.5. Adjusted GEE models suggested significantly divergent trajectories of IADL disability by wave 2, ADL disability by wave 3 and mortality by wave 3. Conclusion PF may not be a homogenous biological syndrome. [ABSTRACT FROM AUTHOR]