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Background: Population-based research on the prevalence and determinants of dementia, Alzheimer's disease, and cognitive impairment is scarce in East Africa. Objective: To provide an overview of community- and population-based studies among older adults on the prevalence of dementia and cognitive impairment in East Africa, and identify research gaps. Methods: We carried out a literature search using three electronic databases (PubMed, Scopus, Google Scholar) using pertinent search terms. Results: After screening 445 publications, we identified four publications on the population-based prevalence of dementia, and three on cognitive impairment. Prevalence rates varied from 6– 23% for dementia, and 7– 44% for cognitive impairment, among participants aged≥50–70 years. Old age and a lower education level were risk factors for dementia and cognitive impairment. Physical inactivity, lack of a ventilated kitchen, and history of central nervous system infections and chronic headache were associated with increased odds of dementia. Female sex, depression, having no spouse, increased lifetime alcohol consumption, low income, rural residence, and low family support were associated with increased odds of cognitive impairment. Potential misclassification and non-standardized data collection methods are research gaps that should be addressed in future studies. Conclusions: Establishing collaborative networks and partnering with international research institutions may enhance the capacity for conducting population-based studies on dementia and cognitive impairment in East Africa. Longitudinal studies may provide valuable insights on incidence, as well as potential risk and protective factors of dementia and cognitive impairment, and may inform the development of targeted interventions including preventive strategies in the region. [ABSTRACT FROM AUTHOR]

Background: Studies that assess cognition prospectively and study in detail anxiety history in the participants' medical records within the context of brain aging and Alzheimer's disease are limited. Objective: To examine the associations of anxiety and unspecified emotional distress (UED) acquired throughout a person's life with prospectively collected cognitive outcomes. Methods: Mayo Clinic Study of Aging participants who were cognitively unimpaired at baseline were included. Anxiety and UED data were abstracted from the medical record using the Rochester Epidemiology Project (REP) resources and were run separately as predictors in our models. The data were analyzed using Cox proportional hazards models for the outcomes of incident mild cognitive impairment (MCI) and dementia and using linear mixed effects models for the outcomes of global and domain specific cognitive z-scores and included key covariates. Results: The study sample (n = 1,808) had a mean (standard deviation) age of 74.5 (7.3) years and 51.4% were male. Anxiety was associated with increased risk of MCI and dementia and was associated with lower baseline cognitive z-scores and accelerated decline over time in the global, memory, and attention domains. UED was associated with faster decline in all domains except visuospatial but did not show evidence of association with incident cognitive outcomes. These results varied by medication use and timing of anxiety. Conclusions: Anxiety and UED both showed inverse associations with cognition. Utilization of anxiety and UED data from across the life course, as available, from the REP system adds robustness to our results. [ABSTRACT FROM AUTHOR]

Background: We investigated a potential sex difference in the relationship between alcohol consumption, brain age gap and cognitive function in older adults without cognitive impairment from the population-based Mayo Clinic Study of Aging. Methods: Self-reported alcohol consumption was collected using the food-frequency questionnaire. A battery of cognitive testing assessed performance in four different domains: attention, memory, language, and visuospatial. Brain magnetic resonance imaging (MRI) was conducted using 3-T scanners (Signa; GE Healthcare). Brain age was estimated using the Brain-Age Regression Analysis and Computational Utility Software (BARACUS). We calculated the brain age gap as the difference between predicted brain age and chronological age. Results: The sample consisted of 269 participants [55% men (n=148) and 45% women (n=121) with a mean age of 79.2 ± 4.6 and 79.5 ± 4.7 years respectively]. Women had significantly better performance compared to men in memory, (1.12 ± 0.87 vs 0.57 ± 0.89, P<0.0001) language (0.66 ± 0.8 vs 0.33 ± 0.72, P=0.0006) and attention (0.79 ± 0.87 vs 0.39 ± 0.83, P=0.0002) z-scores. Men scored higher in visuospatial skills (0.71 ± 0.91 vs 0.44 ± 0.90, P=0.016). Compared to participants who reported zero alcohol drinking (n=121), those who reported alcohol consumption over the year prior to study enrollment (n=148) scored significantly higher in all four cognitive domains [memory: F3,268 = 5.257, P=0.002, Language: F3,258 = 12.047, P<0.001, Attention: F3,260 = 22.036, P<0.001, and Visuospatial: F3,261 = 9.326, P<0.001] after correcting for age and years of education. In addition, we found a significant positive correlation between alcohol consumption and the brain age gap (P=0.03). Post hoc regression analysis for each sex with language z-score revealed a significant negative correlation between brain age gap and language z-scores in women only (P=0.008). Conclusion: Among older adults who report alcohol drinking, there is a positive association between higher average daily alcohol consumption and accelerated brain aging despite the fact that drinkers had better cognitive performance compared to zero drinkers. In women only, accelerated brain aging is associated with worse performance in language cognitive domain. Older adult women seem to be vulnerable to the negative effects of alcohol on brain structure and on certain cognitive functions. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) affects Latinos disproportionately. One of the reasons underlying this disparity may be type 2 diabetes (T2D) that is a risk factor for AD. The purpose of this study was to examine the associations of T2D and AD blood biomarkers and the differences in these associations between Mexican Americans and non-Hispanic Whites. This study was a secondary analysis of baseline data from the observational Health and Aging Brain Study: Health Disparities (HABS-HD) that investigated factors underlying health disparities in AD in Mexican Americans in comparison to non-Hispanic Whites. HABS-HD participants were excluded if they had missing data or were large outliers (z-scores >|4|) on a given AD biomarker. Fasting blood glucose and glycosylated hemoglobin (HbA1c) levels were measured from clinical labs. T2D was diagnosed by licensed clinicians. Plasma amyloid-beta 42 and 40 (Aβ42/42) ratio, total tau (t-tau), and neurofilament light (NfL) were measured via ultra-sensitive Simoa assays. The sample sizes were 1,552 for Aβ42/40 ratio, 1,570 for t-tau, and 1,553 for NfL. Mexican Americans were younger (66.6±8.7 vs. 69.5±8.6) and had more female (64.9% female vs. 55.1%) and fewer years of schooling (9.5±4.6 vs. 15.6±2.5) than non-Hispanic Whites. Mexican Americans differed significantly from non-Hispanic Whites in blood glucose (113.5±36.6 vs. 99.2±17.0) and HbA1c (6.33±1.4 vs. 5.51±0.6) levels, T2D diagnosis (35.3% vs. 11.1%), as well as blood Aβ42/40 ratio (.051±.012 vs..047±.011), t-tau (2.56±.95 vs. 2.33±.90), and NfL levels (16.3±9.5 vs. 20.3±10.3). Blood glucose, blood HbA1c, and T2D diagnosis were not related to Aβ42/40 ratio and t-tau but explained 3.7% of the variation in NfL (p <.001). Blood glucose and T2D diagnosis were not, while HbA1c was positively (b = 2.31, p <.001, β = 0.26), associated with NfL among Mexican Americans. In contrast, blood glucose, HbA1c, and T2D diagnosis were negatively (b = -0.09, p <.01, β = -0.26), not (b = 0.34, p =.71, β = 0.04), and positively (b = 3.32, p <.01, β = 0.33) associated with NfL, respectively in non-Hispanic Whites. To conclude, blood glucose and HbA1c levels and T2D diagnosis are associated with plasma NfL levels, but not plasma Aβ and t-tau levels. These associations differ in an ethnicity-specific manner and need to be further studied as a potential mechanism underlying AD disparities. [ABSTRACT FROM AUTHOR]

Background: Traumatic encephalopathy syndrome (TES) is defined as the clinical manifestation of the neuropathological entity chronic traumatic encephalopathy (CTE). A core feature of TES is neurobehavioral dysregulation (NBD), a neuropsychiatric syndrome in repetitive head impact (RHI)-exposed individuals, characterized by a poor regulation of emotions/behavior. To discover biological correlates for NBD, we investigated the association between biomarkers of inflammation (interleukin (IL)-1β, IL-6, IL-8, IL-10, C-reactive protein (CRP), tumor necrosis factor (TNF)-α) in cerebrospinal fluid (CSF) and NBD symptoms in former American football players and unexposed individuals. Methods: Our cohort consisted of former American football players, with (n = 104) or without (n = 76) NBD diagnosis, as well as asymptomatic unexposed individuals (n = 55) from the DIAGNOSE CTE Research Project. Specific measures for NBD were derived (i.e., explosivity, emotional dyscontrol, impulsivity, affective lability, and a total NBD score) from a factor analysis of multiple self-report neuropsychiatric measures. Analyses of covariance tested differences in biomarker concentrations between the three groups. Within former football players, multivariable linear regression models assessed relationships among log-transformed inflammatory biomarkers, proxies for RHI exposure (total years of football, cumulative head impact index), and NBD factor scores, adjusted for relevant confounding variables. Sensitivity analyses tested (1) differences in age subgroups (< 60, ≥ 60 years); (2) whether associations could be identified with plasma inflammatory biomarkers; (3) associations between neurodegeneration and NBD, using plasma neurofilament light (NfL) chain protein; and (4) associations between biomarkers and cognitive performance to explore broader clinical symptoms related to TES. Results: CSF IL-6 was higher in former American football players with NBD diagnosis compared to players without NBD. Furthermore, elevated levels of CSF IL-6 were significantly associated with higher emotional dyscontrol, affective lability, impulsivity, and total NBD scores. In older football players, plasma NfL was associated with higher emotional dyscontrol and impulsivity, but also with worse executive function and processing speed. Proxies for RHI exposure were not significantly associated with biomarker concentrations. Conclusion: Specific NBD symptoms in former American football players may result from multiple factors, including neuroinflammation and neurodegeneration. Future studies need to unravel the exact link between NBD and RHI exposure, including the role of other pathophysiological pathways. [ABSTRACT FROM AUTHOR]

Introduction: We examined the association between cerebrospinal fluid (CSF)‐derived biomarkers of Alzheimer's disease and neuropsychiatric symptoms (NPS) in older non‐demented adults. Methods: We included 784 persons (699 cognitively unimpaired, 85 with mild cognitive impairment) aged ≥ 50 years who underwent CSF amyloid beta (Aβ42), hyperphosphorylated tau 181 (p‐tau), and total tau (t‐tau) as well as NPS assessment using Beck Depression and Anxiety Inventories (BDI‐II, BAI), and Neuropsychiatric Inventory Questionnaire (NPI‐Q). Results: Lower CSF Aβ42, and higher t‐tau/Aβ42 and p‐tau/Aβ42 ratios were associated with BDI‐II and BAI total scores, clinical depression (BDI‐II ≥ 13), and clinical anxiety (BAI ≥ 10), as well as NPI‐Q–assessed anxiety, apathy, and nighttime behavior. Discussion: CSF Aβ42, t‐tau/Aβ42, and p‐tau/Aβ42 ratios were associated with NPS in community‐dwelling individuals free of dementia. If confirmed by a longitudinal cohort study, the findings have clinical relevance of taking into account the NPS status of individuals with abnormal CSF biomarkers. [ABSTRACT FROM AUTHOR]

Introduction: We investigated the association of the area deprivation index (ADI) with cognitive decline, mild cognitive impairment (MCI), and dementia in older adults (≥50 years old). ADI is a neighborhood socioeconomic disadvantage measure assessed at the census block group level. Methods: The study included 4699 participants, initially without dementia, with available ADI values for 2015 and at least one study visit in 2008 through 2018. Using logistic regression and Cox proportional hazards models with age as the time scale, we assessed the odds for MCI and the risk for dementia, respectively. Results: In cognitively unimpaired (CU) adults at baseline, the risk for progression to dementia increased for every decile increase in the ADI state ranking (hazard ratio = 1.06, 95% confidence interval (1.01–1.11), P =.01). Higher ADI values were associated with subtly faster cognitive decline. Discussion: In older CU adults, higher baseline neighborhood socioeconomic deprivation levels were associated with progression to dementia and slightly faster cognitive decline. Highlights: The study used area deprivation index, a composite freely available neighborhood deprivation measure.Higher levels of neighborhood deprivation were associated with greater mild cognitive impairment odds.Higher neighborhood deprivation levels were associated with higher dementia risk. [ABSTRACT FROM AUTHOR]