03477nas a2200385 4500008004100000022001400041245014400055210006900199260001600268300001100284490000800295520234400303653000902647653002102656653002402677653001902701653002802720653001102748653001102759653000902770653002902779653001502808653001702823653001802840100002402858700002202882700002102904700002102925700002302946700002202969700002502991700002003016700002003036856003503056 2004 eng d a1539-370400aCognitive impairment and decline are associated with carotid artery disease in patients without clinically evident cerebrovascular disease.0 aCognitive impairment and decline are associated with carotid art c2004 Feb 17 a237-470 v1403 a

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.

10aAged10aCarotid Stenosis10aCognition Disorders10aCohort Studies10aCross-Sectional Studies10aFemale10aHumans10aMale10aNeuropsychological Tests10aOdds Ratio10aRisk Factors10aTunica Intima1 aJohnston, Claiborne1 aO'Meara, Ellen, S1 aManolio, Teri, A1 aLefkowitz, David1 aO'Leary, Daniel, H1 aGoldstein, Steven1 aCarlson, Michelle, C1 aFried, Linda, P1 aLongstreth, W T uhttps://chs-nhlbi.org/node/76602286nas a2200313 4500008004100000022001400041245012100055210006900176260001600245300001200261490000800273520139100281653000901672653001301681653001101694653001101705653001401716653000901730653001701739653002801756653002201784100002301806700002401829700001901853700002501872700002101897700001801918856003601936 2010 eng d a1476-625600aSecondhand smoke, vascular disease, and dementia incidence: findings from the cardiovascular health cognition study.0 aSecondhand smoke vascular disease and dementia incidence finding c2010 Feb 01 a292-3020 v1713 a

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.

10aAged10aDementia10aFemale10aHumans10aIncidence10aMale10aRisk Factors10aTobacco Smoke Pollution10aVascular Diseases1 aBarnes, Deborah, E1 aHaight, Thaddeus, J1 aMehta, Kala, M1 aCarlson, Michelle, C1 aKuller, Lewis, H1 aTager, Ira, B uhttps://chs-nhlbi.org/node/115702886nas a2200445 4500008004100000022001400041245008300055210006900138260001300207300001100220490000700231520166800238653001601906653000901922653002201931653001001953653004301963653001902006653001102025653000902036653002502045653001202070653002902082653001102111653001102122653000902133653000902142653003202151653001702183100002102200700002202221700002102243700002402264700002202288700002502310700002102335700002802356700002002384856003602404 2015 eng d a1758-535X00aMultisystem physiologic impairments and changes in gait speed of older adults.0 aMultisystem physiologic impairments and changes in gait speed of c2015 Mar a319-240 v703 a

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.

10aAge Factors10aAged10aAged, 80 and over10aBrain10aCardiovascular Physiological Phenomena10aCohort Studies10aFemale10aGait10aGeriatric Assessment10aGlucose10aHealth Status Indicators10aHumans10aKidney10aLung10aMale10aSensitivity and Specificity10aTime Factors1 aRosso, Andrea, L1 aSanders, Jason, L1 aArnold, Alice, M1 aBoudreau, Robert, M1 aHirsch, Calvin, H1 aCarlson, Michelle, C1 aRosano, Caterina1 aKritchevsky, Stephen, B1 aNewman, Anne, B uhttps://chs-nhlbi.org/node/659604434nas a2200361 4500008004100000022001400041245008300055210006900138260001600207300001300223490000600236520343700242653000903679653002203688653002203710653001403732653001903746653001103765653003103776653001103807653000903818653001703827100002303844700002203867700002703889700001403916700002503930700002003955700002203975700001703997700002204014856003604036 2023 eng d a2574-380500aCogDrisk, ANU-ADRI, CAIDE, and LIBRA Risk Scores for Estimating Dementia Risk.0 aCogDrisk ANUADRI CAIDE and LIBRA Risk Scores for Estimating Deme c2023 Aug 01 ae23314600 v63 a

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.

10aAged10aAged, 80 and over10aAlzheimer Disease10aAustralia10aCohort Studies10aFemale10aHeart Disease Risk Factors10aHumans10aMale10aRisk Factors1 aHuque, Md, Hamidul1 aKootar, Scherazad1 aEramudugolla, Ranmalee1 aHan, Duke1 aCarlson, Michelle, C1 aLopez, Oscar, L1 aBennett, David, A1 aPeters, Ruth1 aAnstey, Kaarin, J uhttps://chs-nhlbi.org/node/948003397nas a2200445 4500008004100000022001400041245013300055210006900188260001600257300001100273490000800284520211100292653000902403653002202412653001902434653001802453653001302471653002702484653001102511653001102522653000902533653001702542100002202559700002002581700002402601700002202625700002302647700002402670700002702694700002302721700002102744700002002765700002302785700002002808700002102828700002002849700002102869700002502890856003602915 2024 eng d a1879-102600aAssociations between toxicity-weighted concentrations and dementia risk: Results from the Cardiovascular Health Cognition Study.0 aAssociations between toxicityweighted concentrations and dementi c2024 Oct 01 a1737060 v9453 a

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' baseline census tract, averaged across 1988-1992, and log2-transformed. Dementia status was clinically adjudicated in 1998-1999 and categorized by subtype (Alzheimer'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's disease, or mixed dementia (p'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.

10aAged10aAged, 80 and over10aAir Pollutants10aAir Pollution10aDementia10aEnvironmental Exposure10aFemale10aHumans10aMale10aRisk Factors1 aCrane, Breanna, M1 aMoored, Kyle, D1 aDonahue, Patrick, T1 aCorrigan, Anne, E1 aCurriero, Frank, C1 aShields, Timothy, M1 aDesjardins, Michael, R1 aRichards, Emily, A1 aRosso, Andrea, L1 aLovasi, Gina, S1 aOdden, Michelle, C1 aLopez, Oscar, L1 aBiggs, Mary, Lou1 aNewman, Anne, B1 aAndrews, Ryan, M1 aCarlson, Michelle, C uhttps://chs-nhlbi.org/node/9737