Higher Risk Of Dementia Research Articles

Sleep disorders and incident dementia: a nationwide observational cohort study

AbstractBackgroundIn recent years, significant research efforts have focused on identifying modifiable risk factors to be leveraged for dementia prevention. Sleep is required for memory consolidation and normal brain functioning, and various mechanisms are proposed between poor sleep quality and cognitive impairment. Several studies have examined the role of sleep disturbances as a risk factor for dementia; however, most of these studies have involved smaller cohorts and short time intervals, and often rely on retrospective surveys and self‐reported exposure data. Our aim was to examine the association between sleep disorders and late‐onset dementia in an entire population.MethodIn a nationwide cohort with a 40‐year follow up, we linked nationwide population data with information on hospital‐based sleep disorder diagnoses and late‐onset dementia from the extensive Danish health registers. Incidence rate ratios (IRR) were calculated using Poisson regression analysis. Analyses were adjusted for age, sex, calendar year, education, and somatic and psychiatric comorbidities.ResultThe cohort consisted of 1,491,276 people. Those with any hospital‐diagnosed sleep disorder had a 17% higher risk of dementia (IRR 1.17, 95% CI 1.11‐1.24) compared to people with no sleep disorder diagnosis. The highest risk was found for men with ‘other specific disorders’ (e.g. insomnia, hypersomnia, non‐organic sleep disorders) with an IRR of 2.00 (95% CI 1.71‐2.32). The risk of dementia was significantly increased 0 to 5 years after sleep disorder diagnosis (IRR 1.35, 95% CI 1.25‐1.47), while the association after 5 years or more was non‐significant (1.05, 95% CI 0.97‐1.13).ConclusionOur findings indicate an increased short‐term risk of dementia following a hospital‐based sleep disorder diagnosis, while we found weaker evidence of a long‐term risk. While this may indicate that sleep disorders could be early symptoms of dementia as well as a risk factor, further research is needed to evaluate sleep disorders as potential early symptoms of dementia, risk factors for dementia, or both, and characterize how this may change at different points along the dementia course. Increased knowledge of the role of sleep disorders in dementia could help inform efforts towards diagnosing dementia in the early stages of the disease or even in dementia prevention.

Air pollution and dementia using longitudinal electronic health record data from the Indian Health Service

AbstractBackgroundAir pollution has been identified as an important risk factor for dementia in previous studies. As a unique population with a history of colonization, American Indians have long been disproportionately affected by air pollution. However, few studies have investigated the effects of air pollution on the risk of developing dementia in American Indians. This study aims to address this important knowledge gap.MethodCounty‐level average air pollution data in 2003‐2007 were downloaded from the land‐use regression models developed by the Center for Air, Climate, & Energy Solutions (CACES) and merged with data from the Indian Health Service (IHS) National Data Warehouse and related electronic health record databases between fiscal year (FY) 2007‐2013. We assigned air pollution exposure to IHS users based on their county of residence and calculated 5‐year averages of PM2.5, O3, CO, and NO2 in each county. A total of 14,910 American Indians who were 65+ years old in FY2007, used IHS services at least once each year, and were dementia free between FY2007‐2009 were included in the main analysis. Cox proportional hazard models with age as the time scale were employed to examine the association of air pollution with dementia incidence, adjusting for potential confounders.ResultThe PM2.5 levels in the IHS counties were lower than those in all US counties during 2003‐2013, while the levels of other air pollutants were similar to the US (Figure 1). More dementia incident cases were found in IHS counties with higher O3 levels (Figure 2). In multivariable Cox regression models (Table1), we found a significant positive association between dementia and O3 with a hazard ratio (HR) of 1.26 (95% CI: 1.02‐1.55) per 1 ppb standardized O3, while the associations between dementia and PM2.5, and CO were not statistically significant. We found similar results in sensitivity analyses using longer lags between air pollution and dementia or replacing CO by NO2 in the regression model.ConclusionOur study suggests that exposure to O3 is associated with the higher risk of dementia in American Indians. Future efforts to reduce exposure to air pollution might help lower dementia risk in American Indian communities.

Present mind in aging brain: Neural associations of dispositional mindfulness in cognitive decline

AbstractBackgroundSubjects at risk of dementia, such as subjective cognitive decline (SCD) and mild cognitive impairment (MCI), present with specific clinical symptoms, as well as functional and structural changes within the brain. Dispositional mindfulness (DM) has been linked to better cognitive performance and is associated with activation and grey matter volume of specific brain regions. It is yet unknown how DM is related to cognitive and neural parameters of those at risk of dementia.ObjectiveTo estimate the association of DM with cognitive functions, brain volumetry, functional connectivity and gray matter integrity in key regions relevant for cognition (hippocampus, anterior cingulate cortex) and self‐awareness (ventromedial prefrontal cortex (vmPFC), posterior cingulate cortex) in SCD and MCI subjects.Methods79 non‐demented older adults with memory complaints ((SCD = 48, MCI = 31) were assessed by neuropsychological tests, MRI volumetry, resting‐state fMRI‐derived connectivity and DTI. Dispositional mindfulness was examined with Breath Counting Task (BCT).ResultsParticipants with MCI showed significantly worse BCT performance in comparison to SCD (p˂0.001). In MCI, BCT performance was positively associated with connectivity (p˂0.001) and negatively related to mean gray matter diffusivity (p˂0.05) in vmPFC. No other significant associations were found between DM, MRI measures and neuropsychological variables in either group.ConclusionWorse cognition in subjects at risk of dementia may be reflected in changes in DM. Lower connectivity and worse gray matter integrity of vmPFC in MCI could play a role in the worsening of DM in this population. Longitudinal studies are needed to further clarify the relatedness of DM and neural changes elicited by neurodegeneration in people at higher risk of dementia.

House dust mite‐induced asthma exacerbates Alzheimer's disease by increasing amyloid beta accumulation and neuroinflammation

AbstractBackgroundAlzheimer's disease (AD) is an age‐related neurodegenerative disorder affecting around 35 million individuals worldwide. Besides aging, various comorbid factors increase the risk of AD, including air pollution and asthma. Epidemiological studies have reported a 2.17‐fold higher risk of dementia in asthmatic patients. However, the molecular mechanism(s) underlying this asthma‐associated AD exacerbation is unknown. This study was designed to explore house dust mite‐induced asthma effects on AD‐related brain changes using the App NL‐G‐F transgenic mouse model.MethodMale and female C57BL/6 wild type and AppNL‐G‐F mice (8‐9 months old) were exposed to either saline or house dust mite (dose: 833μg/kg in saline) every alternate day for 16 weeks. Mice were sacrificed at the end of the experiment, and broncho‐alveolar lavage fluid (BALF), blood, and brains were collected. BALF was analyzed for immune cell markers, inflammatory mediators and total protein content. Serum was analyzed for cytokine and soluble Aβ1‐40/42 levels. In addition, brain sections were immunostained for Aβ and GFAP. Finally, frozen hippocampi and cortices were used to perform Aβ ELISAs and cytokine arrays, respectively.ResultAs expected, dust mite exposure increased inflammatory cells, cytokine levels, and total protein content in the BALF from both sexes and genotypes, suggesting induction of a severe asthma‐like condition. This correlated with increased levels of serum cytokines in all dust‐mite exposed groups. Serum from the AppNL‐G‐F dust mite‐induced asthma group also had significantly increased soluble Aβ1‐42 levels in both sexes. In agreement with this peripheral change, hippocampi from asthma‐induced male and female AppNL‐G‐F mice demonstrated elevated Aβ plaque load and increased soluble Aβ 1‐40/42 and insoluble Aβ 1‐40 levels. Dust mite exposure also increased astrogliosis in both sexes of AppNL‐G‐F mice, as indicated by GFAP immunoreactivity. Finally, dust mite exposure‐induced asthma elevated cortical levels of several cytokines in both sexes and genotypes.ConclusionDust mite exposure was responsible for a severe asthma‐like condition in the lungs that exacerbated Aβ pathology, astrogliosis, and cytokine changes in the brains of male and female App NL‐G‐F mice. Defining mechanisms of asthma effects on the brain may provide a novel therapeutic approach for both asthma and AD.

Exploration of Multidimensional Poverty and Dementia in Adults older than 50 years old in South Africa

AbstractBackgroundMultidimensional poverty is associated with chronic health conditions. However, limited research exists investigating the association between multidimensional poverty and dementia on a population level in low‐and middle‐income countries (LMICs).MethodThis study was conducted in Soweto between 11 November 2019 and 28 February 2020. Participants included older adults above 50 years old. Data analysis was concluded in August 2021. We calculated a measure of multidimensional poverty that includes seven dimensions and eleven indicators. Assessing Dementia 8 (AD8) and the Rowland Universal Dementia Assessment Scale (RUDAS) were used to measure dementia. Differences in level and depth of poverty between adults with no dementia and those with a score above the threshold for either AD8 or RUDAS, or for both AD8/RUDAS, and for comparing gender, age group and marital status were examined. Correlation analyses to assess overlap of dimensions of deprivation were carried out. Association between dementia and multidimensional poverty were investigated using multivariate regression model.ResultAmong 227 participants living in Soweto, South Africa, 151 adults were identified with dementia by the AD8 (66.5%), 64 by the RUDAS (28.2%) and 50 by both AD8 and RUDAS (22.0%). More men (32.1%) had no dementia compared to women (24.7%); and 20% of adults with dementia compared to 9.7% of those without dementia were found to be poor on four dimensions or more. The difference in multidimensional poverty index for k = 3 was 77.1% and 67.3% between adults with and without dementia. Education, health and employment were the main contributors of poverty. Multidimensional poverty was strongly associated with dementia as measured by AD8/RUDAS (adjusted OR 2.31, 95% CI 1.08‐4.95), with higher odds for older female (OR 2.03, 95% CI 1.00‐4.12) or those living in large households (OR 1.27, 95% CI 1.05‐1.53).ConclusionThis study found that the prevalence and depth of poverty is higher among older adults with dementia. A lack of education, poor health and unemployment are major dimensions of poverty which was associated with higher risk of dementia. These findings suggest that early improvement in social determinants of health through targeted structural policies may prevent dementia later in life.

Increased incidence of dementia following herpesvirus infection in the Korean population

AbstractBackgroundHerpesviruses affect the development of dementia. We investigated the association between herpes infection and subsequent diagnoses of dementia.MethodData from the National Health Insurance Service of South Korea were used. Patients aged ≥ 50 years with the relevant diagnostic codes in the reference year 2009 were included and prospectively reviewed from January 2010 to December 2018. All study participants were followed from the index date until the onset of dementia, death, or the study endpoint.ResultThe three cohorts comprised 92,095 patients with herpes simplex virus (HSV) infections, 97,323 patients with varicella‐zoster virus (VZV) infections, and 183,779 controls. During the follow‐up period, 15,831 (17.19%) subjects with HSV infection and 17,082 (17.55%) VZV‐infected subjects, compared to 27,028 (14.17%) control subjects, were subsequently diagnosed with dementia (all, P<0.001). The adjusted hazard ratio for developing dementia was found to be 1.18 (95% confidence interval [CI]; 1.16‐1.20) in HSV and 1.09 (95% CI; 1.07‐1.11) in VZV patients (all, P<0.001). HSV1 infections such as oral or ocular subtypes, but not HSV2, anogenital subtype, were associated with dementia, including several subtypes such as Alzheimer’s disease (AD), vascular dementia, and dementia with Lewy bodies. VZV infection is also associated with AD.ConclusionIn this Korean nationwide population‐based cohort study, both HSV and VZV infections were associated with a higher risk of dementia, particularly AD. Among the subtypes of HSV infection, HSV1 is associated with a risk of dementia. Further studies including appropriate public health interventions could evaluate the causality of these relationships.

Associations between dual‐decline in cognition and gait speed with risk of dementia – results from the ASPREE trial cohort

AbstractBackgroundDual decline in gait speed and cognition is associated with an increased risk of dementia. However, it is unclear if risks are conferred by decline in domain‐specific cognition and gait. We aimed to examine associations between dual decline in gait speed and cognition (global cognition, memory, processing speed and verbal fluency) with risk of dementia.MethodsProspective cohort study. Participants were from the ASPREE (ASPirin in Reducing Events in the Elderly) study, a double‐blind, randomized, placebo‐controlled trial of low dose aspirin in older adults (≥70 years; ≥65 if US minority). Of 19,114 randomized participants, 16,855 (88%) had longitudinal gait and cognitive data. Gait speed was measured at 0, 2, 4, 6 years and close‐out. Cognitive measures included Modified Mini‐Mental State examination (3MS, global cognition), Hopkins Verbal Learning Test‐Revised (HVLT‐R, memory), Symbol Digit Modalities (SDMT, processing speed) and Controlled Oral Word Association Test (COWAT‐F, verbal fluency), assessed at years 0, 1, 3, 5, and close‐out. Participants were classified into four groups: 1) dual decline in gait and cognition; 2) gait decline only; 3) cognitive decline only and 4) non‐decliners. Cognitive decline was defined as membership of the lowest tertile of annual change. Gait decline was defined as decline in gait speed ≥0.05 m/s per year across the study. Dementia (DSM‐IV criteria) was adjudicated by an expert panel using cognitive tests, functional status and clinical records. Cox proportional hazard models were used to estimate risk of dementia adjusting for covariates with death as competing risk.ResultsThe mean age of participants was 75.0 (SD4.4) years. Compared with non‐decliners, risk of dementia was highest in the gait+HVLT‐R decliners (HR 24.7; 95% CI 16.3‐37.3), followed by the gait+3MS (HR 22.2; 95% CI 15.0‐32.9), gait+COWAT‐F (HR 4.66 95%; CI 3.5‐6.3) and gait+SDMT (HR 4.3 95% CI 3.2‐5.8) groups. Dual decliners also had higher risk of dementia than those with either gait or cognitive decline alone for 3MS and HVLT‐R.ConclusionThe combination of decline in gait speed and memory may be the best suited to predict future dementia risk.

Socioeconomic Deprivation, Genetics and Risk of Dementia

AbstractBackgroundThe risk of Alzheimer’s disease and other subtypes of dementia is determined by multiple pathways including genetic, environmental and lifestyle factors. With higher risk in socioeconomically deprived individuals, it remains unclear whether associations of genetic risk with dementia incidence may be modified by individual‐ or area‐level socioeconomic deprivation.MethodParticipants of the UK Biobank study attended baseline assessments at 22 assessment centers between 2006 and 2010 and were followed‐up until 2016 or 2017. Cox proportional‐hazards regressions with area‐level socioeconomic deprivation based on the Townsend Deprivation Index and individual‐level socioeconomic deprivation based on car and home ownership, housing type, and income were run. A comprehensive polygenic risk score was employed and potential mediation through lifestyle and depressive symptoms was assessed. In an imaging substudy, associations of socioeconomic deprivation with six imaging‐derived phenotypes including white matter hyperintensities were examined.Result196,368 participants (mean [standard deviation] age, 64.1 [2.9] years, 52.7% female) aged 60 years and older, of European ancestry, without dementia diagnosis or cognitive impairment at baseline were followed‐up for 1,545,316 person‐years (median [interquartile range] follow‐up, 8.0 [7.4‐8.6] years). In high genetic risk and high area‐level deprivation 1.71% (95% confidence interval, 1.44% to 2.01%) developed dementia compared to 0.56% (95% confidence interval, 0.48% to 0.65%) in low genetic risk and low‐to‐moderate area‐level deprivation (hazard ratio, 2.31; 95% confidence interval, 1.84 to 2.91). In high genetic risk and high individual‐level deprivation 1.78% (95% confidence interval, 1.50% to 2.09%) developed dementia compared to 0.31% (95% confidence interval, 0.20% to 0.45%) in low genetic risk and low individual‐level deprivation (hazard ratio, 4.06; 95% confidence interval, 2.63 to 6.26). There was no significant interaction between genetic risk and area‐level (P =.77) or individual‐level (P =.07) deprivation. An imaging substudy including 11,083 participants found greater burden of white matter hyperintensities associated with higher socioeconomic deprivation.ConclusionIn older adults without dementia area‐level and individual‐level socioeconomic deprivation and genetic risk were significantly and independently associated with a higher risk of dementia. Dementia prevention interventions may be particularly effective if targeted to people living in deprived households and areas, regardless of genetic vulnerability.

GCase activity and long‐term risk of dementia in Parkinson’s disease

AbstractBackgroundClinically, patients with Parkinson disease (PD) carrying a mutation in the glucocerebrosidase (GCase) gene (GBA) are at higher risk of dementia, suggesting that GCase dysfunction may contribute to a more severe disease course, although evidence is lacking. We aimed to discover if cerebrospinal fluid (CSF) GCase activity is altered in newly diagnosed PD patients and if GCase activity at diagnosis predicts the future development of dementia.MethodWe measured CSF GCase activity in 117 PD patients from the Norwegian ParkWest study, a population‐based study of incident PD with 10 years of biannual, prospective follow up, and 50 control subjects without neurological disease. PD dementia diagnosis was set according to established clinical criteria. Parametric accelerated failure time models were applied to analyze the association of GCase activity at the time of PD diagnosis with dementia free survival.ResultGCase activity was reduced in PD patients with (0.92±0.40 mU/mg) or without GBA mutations (1.00±0.37 mU/mg) compared to controls (1.20±0.35 mU/mg). GCase activity at the time of diagnosis was lower in PD patients who developed dementia within 10 years (n=41, 35%) than in those who remained free of dementia (p = 0.001). Further, patients in the lowest tertile of GCase activity at PD diagnosis were at 3‐fold increased risk of developing dementia in the next ten years (HR 3.10; 95% 0.72 to 4.68; P= .014; Figure), a finding that was also independent of GBA carrier status.ConclusionThis is the first study to show both that GCase dysfunction is evident in idiopathic PD at the time of diagnosis and that low GCase activity is associated with greater risk of developing dementia over the next ten years. GCase‐targeting compounds are among the most promising strategies towards disease‐modifying treatments in PD, and evidence for the association of CSF GCase activity with disease progression, independent of GBA mutation status, will have important implications for clinical trial design and patient management.

Cardiometabolic multimorbidity, genetic risk and dementia

AbstractBackgroundThe extent to which multiple cardiovascular and metabolic co‐morbidity and genetic factors combine or interact to increase dementia risk is unknown.MethodWe analysed 435 105 participants from the UK Biobank prospective cohort of European ancestry, aged 40 to 72 years, without dementia at baseline (2006‐2010), followed until 2021. A cardiometabolic multimorbidity index with a point given for co‐morbid stroke, diabetes and heart disease (myocardial infarction, atrial fibrillation or heart failure) was calculated for each participant along with a polygenic risk score for dementia with low (lowest quintile), intermediate (quintiles 2 to 4) and high (highest quintile) risk categories. The primary outcome was incident all‐cause dementia during follow‐up.ResultParticipants with both a high genetic risk and a cardiometabolic multimorbidity index of two or greater had an increased risk of developing dementia, hazard ratio of 5.01(95% confidence interval 3.35 ‐ 7.49), compared to those with a low genetic risk and no cardiometabolic conditions. The risk of developing dementia increased monotonically with increasing cardiometabolic morbidity. Crucially, there was no interaction between cardiometabolic multimorbidity and polygenic risk (P = 0.11).ConclusionCardiometabolic multimorbidity was independently associated with higher dementia risk, compared with genetic dementia risk. Addressing cardiometabolic multimorbidity may help to reduce dementia risk regardless of genetic risk.

C‐reactive protein, APOE status, and cognitive impairment in older adults

AbstractBackgroundThe aim of this study was to investigate the impact of Apolipoprotein ε4 (APOEε4) on the possible relationship between high sensitive serum CRP (hsCRP) and risk of incident dementia, Alzheimer’s disease (AD), and cognitive impairment over seven years in a longitudinal, population based study of community dwelling older adults.MethodSerum hsCRP was measured at baseline in 304 dementia‐free individuals aged 65‐79 years derived from the Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study. Participants were re‐examined seven years later, and global cognition, episodic memory, executive functioning, verbal expression, and psychomotor speed were assessed both at baseline and at follow‐up. Incident dementia was diagnosed using DSM‐IV criteria. Multiple linear regression and logistic‐regression models were used to investigate the association of serum hsCRP and its interaction with APOEε4 status on cognitive performance and incident dementia at follow‐up, after adjusting for several potential confounders, including common vascular risk factors.ResultAfter adjustment for age, sex, education, duration of follow‐up, systolic blood pressure, diastolic blood pressure, body mass index, prevalent stroke, and smoking status, odds ratio (95% confidence intervals (CI)) was 3.02 (1.18 – 7.73) for those who had at least one alle of APOEε4 compared to those who did not. The odds ratio (95%CI) for incident dementia was 1.00 (0.96 – 1.04) oer unit increase in hsCRP. No associations between hsCRP and cognitive impairment seven years later was detected. However, raised hsCRP values were related to worse performance in episodic memory seven years later in participants who had at least one allele of APOEε4 (β (standard error): ‐0.005 (0.002); p = 0.025).ConclusionRaised values of hsCRP is associated with higher risk of cognitive impairment seven years later among individuals who carry at least one allele of APOEε4. Randomized controlled trials are needed to determine this issue.

Plasma amyloid β 42/40 associations on episodic memory: Moderations with depressive symptoms and marital status

AbstractBackgroundPlasma amyloid β (aβ) 42/40 is a non‐invasive and cost‐effective biomarker associated with aβ accumulation and cognitive performance in normal aging and Alzheimer’s disease. Recent studies have linked plasma aβ 42/40 to well established modifiable risk factors for dementia. Specifically, depressive symptoms (DS) and marital status have been associated with steeper cognitive decline and increased dementia onset. We examine whether the association between plasma aβ 42/40 and episodic memory (EM) is moderated by (1) DS, (2) marital status, and (3) additive risk of DS+ marital status.MethodWe used an ethnically and clinically diverse longitudinal cohort of older adults (n=473, mean baseline age=74.81(7.22) years, 60.5% women) from University of California, Davis‐Alzheimer’s Disease Research Center (Table 1). Statistical analyses included latent growth modeling to establish a latent EM growth model, and regression analyses to test independent associations and moderations with DS (measured with Geriatric Depression Scale; low<5/ high≥5), marital status (married/not married), and combined DS+marital status risk (low: low DS+married/intermediate: high DS+married or low DS+not married/high: high DS+not married). Age was centered at 75 years. Sex and education were included as covariates.ResultLower aβ42/40 was associated with lower EM performance and steeper decline (level: β=6.195, SE=3.065, p=0.041, slope: β=0.284, SE=0.134, p=0.034). DS and marital status independently moderated this association. Specifically, lower aβ42/40 was associated with (1) poorer EM performance in the high DS groups (n=80; level: β=8.914, SE=4.353, p=0.014) and (2) poorer EM performance and steeper decline in the married group (n=115; level: β=11.157, SE=4.477, p=0.013, slope: β=0.524, SE=0.219, p=0.017). The effects of these independent associations were magnified with combined DS + marital status. Specifically, lower aβ42/40 was associated with poorer EM performance and steeper decline in the low (n=62; level: β=15.445, SE=5.650, p=0.006, slope: β=0.642, SE=0.305, p=0.035) risk group but this association was absent in the intermediate (n=171) and high (n=56) groups.ConclusionThe impact of amyloidosis, as measured by plasma aβ42/40 on cognition, may be more prominent in married older adults with low DS. Examining multimodal associations of non‐invasive plasma biomarkers with modifiable risk factors may identify older adults with high cognitive decline and dementia risk profiles.

Monitoring cognitive and psychological alterations in COVID-19 patients: A longitudinal neuropsychological study

BackgroundSARS-COV-2 infection has been associated to long-lasting neuropsychiatric sequelae, including cognitive deficits, that persist after one year. However, longitudinal monitoring has been scarcely performed. Here, in a sample of COVID-19 patients, we monitor cognitive, psychological and quality of life-related profiles up to 22 months from resolution of respiratory disease. MethodsOut of 657 COVID-19 patients screened at Manzoni Hospital (Lecco, Italy), 22 underwent neuropsychological testing because of subjective cognitive disturbances at 6 months, 16 months, and 22 months. Tests of memory, attention, and executive functions were administered, along with questionnaires for depressive and Post-traumatic stress disorder (PTSD) symptoms, psychological well-being and quality of life. Cross-sectional descriptives, correlational, as well as longitudinal analyses considering COVID19-severity were carried out. A preliminary comparison with a sample of obstructive sleep apneas patients was also performed. ResultsAround 50% of COVID-19 patients presented with cognitive deficits at t0. The most affected domain was verbal memory. Pathological scores diminished over time, but a high rate of borderline scores was still observable. Longitudinal analyses highlighted improvements in verbal and non-verbal long term memory, as well as attention, and executive functioning. Depression and PTSD-related symptoms were present in 30% of patients. The latter decreased over time and were associated to attentional-executive performance. ConclusionsCognitive dysfunctions in COVID-19 patients may extend over 1 year, yet showing a significant recovery in several cases. Cognitive alterations are accompanied by a significant psychological distress. Many patients displaying borderline scores, especially those at higher risk of dementia, deserve clinical monitoring.

Multimorbidity burden and developmental trajectory in relation to later-life dementia: A prospective study.

This study assessed the associations of multimorbidity burden and its developmental trajectory with later-life dementia. Among 5923 Health and Retirement Study participants, major chronic conditions including hypertension, diabetes mellitus, cancer, lung diseases, heart disease, stroke, psychological disorders, and arthritis were self- orproxy-reported in 1994-2008. Dementia diagnosis was self- or proxy-reported in 2008-2018. We used Cox regression to assess the associations of multimorbidity with incident dementia. During follow-up (median = 8 years), 701 participants developed dementia. Each additional chronic condition in 2008 was related to 15% (confidence interval: 9% to 22%) higher hazard of dementia. Multimorbidity trajectories in 1994-2008 were classified as "rapid growth", "steady growth", "slow growth", and "no new condition" by the group-based trajectory modelling methods. Compared to "no new condition", the "rapid growth" trajectory was related to 32% (3% to 69%) higher dementia risk. Both multimorbidity burden and its developmental trajectory were prospectively associated with risk of dementia.

The Association Between Exposure to Air Pollution and Dementia Incidence: The Modifying Effect of Smoking.

The influence of overall air pollution on dementia risk and the potential effect modification by other risk factors remain to be clarified. We included 459844 UK residents who were free of dementia and had data on the exposure to particulate matter (PM)2.5, PM2.5-10, PM10, NO2, and NOx during baseline recruitment. The combined exposure to various PMs and NOx was estimated by using an air pollution score. Hazard ratios (HRs) and 95% confidence intervals (CIs) for incident dementia were estimated by multivariable Cox models. During a median 11.7years follow-up, 5905 incident cases of all-cause dementia were identified. With the exception of PM2.5-10, all other air pollutants were separately associated with a higher risk of all-cause dementia (all p-trend < .001) with generally similar associations for dementia subtypes. An increasing air pollution score was associated with higher risks of all-cause as well as individual dementia outcomes, with adjusted HRs (95% CI) of 1.27 (1.18, 1.37) for all-cause dementia, 1.27 (1.14, 1.43) for Alzheimer's disease, and 1.35 (1.16, 1.57) for vascular dementia when comparing the highest with the lowest quartile of the score (all p-trend < .001). These associations of air pollution score with dementia and its subtypes were observed among never and former smokers but not among current smokers (all p-interaction < .030). Air pollution was associated with a higher risk of dementia among nonsmokers but not current smokers. Additional studies are required to confirm our findings and to explore the potential mechanisms underlying the possible effect modification by smoking status.

Self-reported sleep in relation to risk of dementia a quarter of a century later at age 90+: The 90+ Study

ABSTRACT Objective To examine sex-specific associations of sleep duration and napping self-reported at mean age of 69 years (range: 53–81) with risk of incident dementia 24 years later at age 90 +. Method Analytic sample included individuals from a population-based study who reported sleep and napping once in the 1980s and 24 years later (range: 16–38) joined The 90+ Study and were evaluated in-person. Those without dementia at baseline of The 90+ Study were prospectively followed. Hazard ratios [HR] and 95% confidence intervals [CI] of dementia risk were estimated by Cox regression. Results Of 574 participants 71% were women, mean age at start of dementia follow-up with The 90+ Study was 93 years (range: 90–102). After 3.3 years (range: 0.4–13.8) of follow-up 47% developed dementia. Higher risk of dementia at age 90+ was seen in women with <6 hours of self-reported sleep per night (adjusted HR = 2.00; 95% CI = 1.15–3.50; p = .01) compared with 8 hours. Lower risk of dementia at 90+ was seen in men with short-to-moderate (<60 minutes) self-reported naps compared with no naps (HR = 0.33; 95% CI = 0.18–0.63; p < .01). Conclusions Sleep and nap 24 years earlier are important risk factors for dementia after age 90.

Low dietary vitamin E intake is associated with high risk of incident dementia among older adults: The Shanghai Aging Study.

Growing evidence has shown the association between vitamin E intake and the risk of cognitive decline, but the conclusions were inconsistent. This study aimed to verify the hypothesis that vitamin E intake is associated with incident dementia and deterioration of global cognition. We followed 1,550 non-demented community residents aged ≥60 years for an average of 5.2 years in the Shanghai Aging Study. Baseline vitamin E intake were measured by the Food Frequency Questionnaire. Cognitive function was evaluated by a battery of neuropsychological tests. Consensus diagnosis of incident dementia was made based on the DSM-IV criteria. During the follow-up, 135 cases (8.7%) of incident dementia were identified. The incidence rates of dementia in low, low-medium, medium-high, and high vitamin E intake groups were 2.8, 1.5, 1.6, and 0.7 per 100 person-years, respectively (P < 0.001). Participants with low vitamin E intake had a significantly higher risk of incident dementia than those with higher intake [compared with the highest intake group: hazard ratio (HR) 2.34, 95% confidence interval (CI) 1.20-4.57] after adjusting for confounders. Vitamin E intake was negatively correlated to the rate of annual decline of Mini-Mental State Examination score with the adjustment of confounders (β = 0.019, p = 0.001). Vitamin E intake is negatively correlated with the risk of dementia in older adults. An appropriate high amount of vitamin E intake from the diet might be helpful to prevent future cognitive decline.

Word Recognition Program for Thai Older People with High Risk of Dementia: A Quasi-Experimental One-Group Study

Introduction: Dementia is one of the most common disorders among older people. This condition causes cognitive impairment, which can affect memory, thinking, expressive or comprehension language. It affects work and daily life. The purpose of this study was to examine the effects of a word recognition program on naming and quality of life in older people with high risk of dementia. The purpose of this study was to examine the effects of a word recognition program on naming and quality of life in older people with high risk of dementia. Methods: A one-group, quasi-experimental pretest-posttest study was conducted at Maeka Subdistrict Administrative Organization, Chiang Mai, Thailand, and participants’ home setting from December 2021 to March 2022. Participants were 6 Thai elderly persons with a high risk of dementia according to MEST10 cut-off score, including 1 (16.66%) male and 5 (83.34%) females. They were assessed on naming using the WAB test. Additionally, they were assessed on quality of life using the WHOQOL-BREF-THAI. The word recognition program delivered 30 min per day for 5-week duration. The results were analyzed by using descriptive statistics and the Wilcoxon signed-rank test to compare the effect on the intervention program. Results: The older people with high risk of dementia significantly gained in naming after receiving the word recognition program (MD = −9.00 ± 2.344; 95% CI: −20.00 to −4.00; p = 0.031). However, they did not significantly gain in quality of life after receiving the word recognition program (MD = −4.50 ± 3.393; 95% CI: −10.50 to 1.00; p = 0.418). Discussion/Conclusion: The current study demonstrates that a 5-week intervention of the word recognition program may be effective in naming to enhance language skills for Thai older people with high risk of dementia.

Effects of Eligibility Criteria on Patient Selection and Treatment Implications from 10 Multidomain Dementia Prevention Trials: A Population-Based Study

Introduction: Dementia prevention trials have so far shown little benefit of multidomain interventions against cognitive decline. Recruitment strategies in these trials often centre around dementia risk or cardiovascular risk profile, but it is uncertain whether this leads to inclusion of individuals who may benefit most from the intervention. We determined the effects of eligibility criteria on the recruitment of potential trial participants in the general population. Methods: In a systematic search until January 1, 2022, we identified all published and ongoing large (≥500 participants), phase-3 multidomain trials for the prevention of cognitive decline or dementia. We applied trial eligibility criteria to 5,381 participants of the population-based Rotterdam Study (mean age: 72 years, 58% women), to compare participant characteristics, predicted risk of cardiovascular disease, and dementia risk, between trial eligible and ineligible persons. Results: We identified 10 trials, of which 5 had been published (DR’s EXTRA, FINGER, preDIVA, MAPT, and HATICE) and 5 are ongoing (US-POINTER, MIND-CHINA, MYB, AgeWell.de, and J-Mint). Among all Rotterdam Study participants, eligibility across published trials ranged from 48% for MAPT to 87% for preDIVA, in line with original trial reports. Variability in eligibility was wider for ongoing trials, from 1% for US-POINTER to over 94% for MYB trial. Over 70% of trial eligible individuals are recommended preventive intervention in routine care based on their cardiovascular risk, similar for lipid-lowering (71%) and blood pressure-lowering treatment (73%). Ten-year risks of dementia were similar for eligible compared to ineligible individuals (12 vs. 11%). Conclusion: Multidomain dementia prevention trials fail to preferentially include those at the highest risk of dementia and mostly include individuals who qualify for interventions already on the basis of cardiovascular prevention guidelines. These findings call for better targeted enrolment of individuals for whom trial results can improve clinical decision-making.

Pathways explaining racial/ethnic and socio-economic disparities in incident all-cause dementia among older US adults across income groups

Differential racial and socioeconomic disparities in dementia incidence across income groups and their underlying mechanisms remain largely unknown. A retrospective cohort study examining all-cause dementia incidence across income groups was conducted linking third National Health and Nutrition Examination Surveys (NHANES III) to Centers for Medicare and Medicaid Services-Medicare data over ≤26 y of follow-up (1988–2014). Cox regression and generalized structural equations models (GSEM) were constructed among adults aged≥60 y at baseline (N = 4,592). Non-Hispanic Black versus White (NHW) adults had higher risk of dementia in age and sex-adjusted Cox regression models (HR = 1.34, 95%CI: 1.15–1.55, P < 0.001), an association that was attenuated in the SES-adjusted model (HR = 1.15, 95%CI: 1.01–1.34, P = 0.092). SES was inversely related to dementia risk overall (per Standard Deviation, HR = 0.80, 95% CI:0.69–0.92, P = 0.002, Model 2), mainly within the middle-income group. Within the lowest and middle-income groups and in socio-economic status (SES)-adjusted models, Mexican American participants were at lower all-cause dementia risk compared with their NHW counterparts. GSEM models further detected 3 pathways explaining >55% of the total effect of SES on dementia risk (Total effect = −0.160 ± 0.067, p = 0.022), namely SES→LIFESTYLE→DEMENTIA (Indirect effect (IE) = −0.041 ± 0.014, p = 0.004), SES→LIFESTYLE→COGN→DEMENTIA (IE = −0.006 ± 0.001, p < 0.001), SES→COGN→DEMENTIA(IE = −0.040 ± 0.008, p < 0.001), with the last two remaining significant or marginally significant in the uppermost income groups. Diet and social support were among key lifestyle factors involved in socio-economic disparities in dementia incidence. We provide evidence for modifiable risk factors that may delay dementia onset differentially across poverty-income ratio groups, underscoring their importance for future observational and intervention studies.