@article {766, title = {Cognitive impairment and decline are associated with carotid artery disease in patients without clinically evident cerebrovascular disease.}, journal = {Ann Intern Med}, volume = {140}, year = {2004}, month = {2004 Feb 17}, pages = {237-47}, abstract = {

BACKGROUND: Whether carotid artery disease is a cause of cognitive impairment in persons who have not had stroke is unknown. If this is the case, diminished performance on the Modified Mini-Mental State Examination should be more common in persons with left carotid artery disease than in those with right carotid artery disease.

OBJECTIVE: To determine whether left carotid artery disease is associated with cognitive impairment.

DESIGN: Cross-sectional and cohort study.

SETTING: Four U.S. communities participating in the Cardiovascular Health Study.

PATIENTS: 4006 right-handed men and women 65 years of age or older without history of stroke, transient ischemic attack, or carotid endarterectomy.

MEASUREMENTS: Internal carotid artery stenosis and intima-media thickness of the common carotid artery were assessed by using duplex ultrasonography. Cognitive impairment was defined as a score less than 80 on the Modified Mini-Mental State Examination, and cognitive decline was defined as an average decrease of more than 1 point annually in Modified Mini-Mental State Examination score during up to 5 years of follow-up. Multivariate logistic regression models were used to estimate the risk for cognitive impairment and decline associated with left internal carotid artery stenosis and intima-media thickness, after adjustment for measures of right-sided disease and risk factors for vascular disease.

RESULTS: After adjustment for right-sided stenosis, high-grade (> or =75\% narrowing of diameter) stenosis of the left internal carotid artery (32 patients) was associated with cognitive impairment (odds ratio, 6.7 [95\% CI, 2.4 to 18.1] compared with no stenosis) and cognitive decline (odds ratio, 2.6 [CI, 1.1 to 6.3]). Intima-media thickness of the left common carotid artery was associated with cognitive impairment and decline in univariate analysis, but this effect did not persist after adjustment.

CONCLUSIONS: Cognitive impairment and decline are associated with asymptomatic high-grade stenosis of the left internal carotid artery. The persistence of the association after adjustment for right-sided stenosis indicates that the association is not due to underlying vascular risk factors or atherosclerosis in general.

}, keywords = {Aged, Carotid Stenosis, Cognition Disorders, Cohort Studies, Cross-Sectional Studies, Female, Humans, Male, Neuropsychological Tests, Odds Ratio, Risk Factors, Tunica Intima}, issn = {1539-3704}, doi = {10.7326/0003-4819-140-4-200402170-00005}, author = {Johnston, S Claiborne and O{\textquoteright}Meara, Ellen S and Manolio, Teri A and Lefkowitz, David and O{\textquoteright}Leary, Daniel H and Goldstein, Steven and Carlson, Michelle C and Fried, Linda P and Longstreth, W T} } @article {1157, title = {Secondhand smoke, vascular disease, and dementia incidence: findings from the cardiovascular health cognition study.}, journal = {Am J Epidemiol}, volume = {171}, year = {2010}, month = {2010 Feb 01}, pages = {292-302}, abstract = {

Recent studies have found that smoking is associated with an increased risk of dementia, but the effects of secondhand smoke (SHS) on dementia risk are not known to have previously been studied. The authors used Cox proportional hazards marginal structural models to examine the association between self-reported lifetime household SHS exposure and risk of incident dementia over 6 years among 970 US participants in the Cardiovascular Health Cognition Study (performed from 1991 to 1999) who were never smokers and were free of clinical cardiovascular disease (CVD), dementia, and mild cognitive impairment at baseline. In addition, because prior studies have found that SHS is associated with increased risk of CVD and that CVD is associated with increased risk of dementia, the authors tested for interactions between SHS and measures of clinical and subclinical CVD on dementia risk. Moderate (16-25 years) and high (>25 years) SHS exposure levels were not independently associated with dementia risk; however, subjects with >25 years of SHS exposure and >25\% carotid artery stenosis had a 3-fold increase (hazard ratio = 3.00, 95\% confidence interval: 1.03, 9.72) in dementia risk compared with subjects with no/low (0-15 years) SHS exposure and < or =25\% carotid artery stenosis. High lifetime SHS exposure may increase the risk of dementia in elderly with undiagnosed CVD.

}, keywords = {Aged, Dementia, Female, Humans, Incidence, Male, Risk Factors, Tobacco Smoke Pollution, Vascular Diseases}, issn = {1476-6256}, doi = {10.1093/aje/kwp376}, author = {Barnes, Deborah E and Haight, Thaddeus J and Mehta, Kala M and Carlson, Michelle C and Kuller, Lewis H and Tager, Ira B} } @article {6596, title = {Multisystem physiologic impairments and changes in gait speed of older adults.}, journal = {J Gerontol A Biol Sci Med Sci}, volume = {70}, year = {2015}, month = {2015 Mar}, pages = {319-24}, abstract = {

BACKGROUND: Slowed gait is an important health indicator in older adults but a single identifiable cause is often lacking. We assessed whether a summary index measuring impairments across multiple physiologic systems was associated with slowed gait in older individuals.

METHODS: Data from the Cardiovascular Health Study (n = 3,010) were used to assess associations between baseline physiologic index (measuring vasculature, brain, kidneys, lungs, and glucose metabolism; range 0-10 with 0-2 points/system and lower score indicating higher function) and annual gait speed (m/s) over 6 years. Participants with complete data on the physiologic index and at least two gait speed measures were included. Mean gait speed and 95\% confidence intervals (CI) by category of index were calculated using mixed effects models.

RESULTS: Those with scores of three or higher on the index had significantly slower gait speed at baseline compared to those with scores of 0-2 (7-10: mean speed = 0.83 m/s, 95\% CI: 0.80, 0.84; 0-2: mean speed = 1.01 m/s, 95\% CI: 0.99, 1.03). Those with higher indices also had faster decline in gait speed compared to those with lower scores after adjustment for demographic and health characteristics (7-10: change in speed = -0.020 m/s/year, 95\% CI: -0.024, -0.016; 0-2: change in speed= -0.010 m/s/year, 95\% CI: -0.014, -0.006).

CONCLUSIONS: Greater impairment across five organ systems was associated with slower gait speed and greater declines in gait speed over 6 years. Impairments accumulated over multiple physiologic systems may make older adults more vulnerable to slow gait speed.

}, keywords = {Age Factors, Aged, Aged, 80 and over, Brain, Cardiovascular Physiological Phenomena, Cohort Studies, Female, Gait, Geriatric Assessment, Glucose, Health Status Indicators, Humans, Kidney, Lung, Male, Sensitivity and Specificity, Time Factors}, issn = {1758-535X}, doi = {10.1093/gerona/glu176}, author = {Rosso, Andrea L and Sanders, Jason L and Arnold, Alice M and Boudreau, Robert M and Hirsch, Calvin H and Carlson, Michelle C and Rosano, Caterina and Kritchevsky, Stephen B and Newman, Anne B} } @article {9480, title = {CogDrisk, ANU-ADRI, CAIDE, and LIBRA Risk Scores for Estimating Dementia Risk.}, journal = {JAMA Netw Open}, volume = {6}, year = {2023}, month = {2023 Aug 01}, pages = {e2331460}, abstract = {

IMPORTANCE: While the Australian National University-Alzheimer Disease Risk Index (ANU-ADRI), Cardiovascular Risk Factors, Aging, and Dementia (CAIDE), and Lifestyle for Brain Health (LIBRA) dementia risk tools have been widely used, a large body of new evidence has emerged since their publication. Recently, Cognitive Health and Dementia Risk Index (CogDrisk) and CogDrisk for Alzheimer disease (CogDrisk-AD) risk tools have been developed for the assessment of dementia and AD risk, respectively, using contemporary evidence; comparison of the relative performance of these risk tools is limited.

OBJECTIVE: To evaluate the performance of CogDrisk, ANU-ADRI, CAIDE, LIBRA, and modified LIBRA (LIBRA with age and sex estimates from ANU-ADRI) in estimating dementia and AD risks (with CogDrisk-AD and ANU-ADRI).

DESIGN, SETTING, AND PARTICIPANTS: This population-based cohort study obtained data from the Rush Memory and Aging Project (MAP), the Cardiovascular Health Study Cognition Study (CHS-CS), and the Health and Retirement Study-Aging, Demographics and Memory Study (HRS-ADAMS). Participants who were free of dementia at baseline were included. The factors were component variables in the risk tools that included self-reported baseline demographics, medical risk factors, and lifestyle habits. The study was conducted between November 2021 and March 2023, and statistical analysis was performed from January to June 2023.

MAIN OUTCOMES AND MEASURES: Risk scores were calculated based on available factors in each of these cohorts. Area under the receiver operating characteristic curve (AUC) was calculated to measure the performance of each risk score. Multiple imputation was used to assess whether missing data may have affected estimates for dementia risk.

RESULTS: Among the 6107 participants in 3 validation cohorts included for this study, 2184 participants without dementia at baseline were available from MAP (mean [SD] age, 80.0 [7.6] years; 1606 [73.5\%] female), 548 participants without dementia at baseline were available from HRS-ADAMS (mean [SD] age, 79.5 [6.3] years; 288 [52.5\%] female), and 3375 participants without dementia at baseline were available from CHS-CS (mean [SD] age, 74.8 [4.9] years; 1994 [59.1\%] female). In all 3 cohorts, a similar AUC for dementia was obtained using CogDrisk, ANU-ADRI, and modified LIBRA (MAP cohort: CogDrisk AUC, 0.65 [95\% CI, 0.61-0.69]; ANU-ADRI AUC, 0.65 [95\% CI, 0.61-0.69]; modified LIBRA AUC, 0.65 [95\% CI, 0.61-0.69]; HRS-ADAMS cohort: CogDrisk AUC, 0.75 [95\% CI, 0.71-0.79]; ANU-ADRI AUC, 0.74 [95\% CI, 0.70-0.78]; modified LIBRA AUC, 0.75 [95\% CI, 0.71-0.79]; CHS-CS cohort: CogDrisk AUC, 0.70 [95\% CI, 0.67-0.72]; ANU-ADRI AUC, 0.69 [95\% CI, 0.66-0.72]; modified LIBRA AUC, 0.70 [95\% CI, 0.68-0.73]). The CAIDE and LIBRA also provided similar but lower AUCs than the 3 aforementioned tools (eg, MAP cohort: CAIDE AUC, 0.50 [95\% CI, 0.46-0.54]; LIBRA AUC, 0.53 [95\% CI, 0.48-0.57]). The performance of CogDrisk-AD and ANU-ADRI in estimating AD risks was also similar.

CONCLUSIONS AND RELEVANCE: CogDrisk and CogDrisk-AD performed similarly to ANU-ADRI in estimating dementia and AD risks. These results suggest that CogDrisk and CogDrisk-AD, with a greater range of modifiable risk factors compared with other risk tools in this study, may be more informative for risk reduction.

}, keywords = {Aged, Aged, 80 and over, Alzheimer Disease, Australia, Cohort Studies, Female, Heart Disease Risk Factors, Humans, Male, Risk Factors}, issn = {2574-3805}, doi = {10.1001/jamanetworkopen.2023.31460}, author = {Huque, Md Hamidul and Kootar, Scherazad and Eramudugolla, Ranmalee and Han, S Duke and Carlson, Michelle C and Lopez, Oscar L and Bennett, David A and Peters, Ruth and Anstey, Kaarin J} } @article {9737, title = {Associations between toxicity-weighted concentrations and dementia risk: Results from the Cardiovascular Health Cognition Study.}, journal = {Sci Total Environ}, volume = {945}, year = {2024}, month = {2024 Oct 01}, pages = {173706}, abstract = {

BACKGROUND: Air pollution is a modifiable risk factor for dementia. Yet, studies on specific sources of air pollution (i.e., toxic chemical emissions from industrial facilities) and dementia risk are scarce. We examined associations between toxicity-weighted concentrations of industrial pollution and dementia outcomes among a large, multi-site cohort of older adults.

METHODS: Participants (n~=~2770) were~>=~65~years old (Mean~=~75.3, SD~=~5.1~years) from the Cardiovascular Health Cognition Study (1992-1999). Toxicity-weighted concentrations were estimated using the Risk Screening Environmental Indicator (RSEI) model which incorporates total reported chemical emissions with toxicity, fate, and transport models. Estimates were aggregated to participants{\textquoteright} baseline census tract, averaged across 1988-1992, and log2-transformed. Dementia status was clinically adjudicated in 1998-1999 and categorized by subtype (Alzheimer{\textquoteright}s, vascular, mixed). We assessed whether RSEI-estimated toxicity-weighted concentrations were associated with 1) odds of prevalent dementia and 2) incident dementia risk by subtype.

RESULTS: After adjusting for individual and census-tract level covariates, a doubling in toxicity-weighted concentrations was associated with 9~\% higher odds of prevalent dementia (OR~=~1.09, 95~\% CI: 1.00, 1.19). In discrete-time survival models, each doubling in toxicity-weighted concentrations was associated with a 16~\% greater hazard of vascular dementia (HR~=~1.16, 95~\% CI: 1.01, 1.34) but was not significantly associated with all-cause, Alzheimer{\textquoteright}s disease, or mixed dementia (p{\textquoteright}s~>~0.05).

DISCUSSION: Living in regions with higher toxicity-weighted concentrations was associated with higher odds of prevalent dementia and a higher risk of incident vascular dementia in this large, community-based cohort of older adults. These findings support the need for additional studies to examine whether toxic chemical emissions from industrial and federal facilities may be a modifiable target for dementia prevention.

}, keywords = {Aged, Aged, 80 and over, Air Pollutants, Air Pollution, Dementia, Environmental Exposure, Female, Humans, Male, Risk Factors}, issn = {1879-1026}, doi = {10.1016/j.scitotenv.2024.173706}, author = {Crane, Breanna M and Moored, Kyle D and Donahue, Patrick T and Corrigan, Anne E and Curriero, Frank C and Shields, Timothy M and Desjardins, Michael R and Richards, Emily A and Rosso, Andrea L and Lovasi, Gina S and Odden, Michelle C and Lopez, Oscar L and Biggs, Mary Lou and Newman, Anne B and Andrews, Ryan M and Carlson, Michelle C} }