Todd Beck

Elder Self-neglect and Abuse and Mortality Risk in a Community-Dwelling Population

CONTEXT Both elder self-neglect and abuse have become increasingly prominent public health issues. The association of either elder self-neglect or abuse with mortality remains unclear. OBJECTIVE To examine the relationship of elder self-neglect or abuse reported to social services agencies with all-cause mortality among a community-dwelling elderly population. DESIGN, SETTING, AND PARTICIPANTS Prospective, population-based cohort study (conducted from 1993 to 2005) of residents living in a geographically defined community of 3 adjacent neighborhoods in Chicago, Illinois, who were participating in the Chicago Health and Aging Project (CHAP; a longitudinal, population-based, epidemiological study of residents aged > or = 65 years). A subset of these participants had suspected elder self-neglect or abuse reported to social services agencies. MAIN OUTCOME MEASURES Mortality ascertained during follow-up and by use of the National Death Index. Cox proportional hazard models were used to assess independent associations of self-neglect or elder abuse reporting with the risk of all-cause mortality using time-varying covariate analyses. RESULTS Of 9318 CHAP participants, 1544 participants were reported for elder self-neglect and 113 participants were reported for elder abuse from 1993 to 2005. All CHAP participants were followed up for a median of 6.9 years (interquartile range, 7.4 years), during which 4306 deaths occurred. In multivariable analyses, reported elder self-neglect was associated with a significantly increased risk of 1-year mortality (hazard ratio [HR], 5.82; 95% confidence interval [CI], 5.20-6.51). Mortality risk was lower but still elevated after 1 year (HR, 1.88; 95% CI, 1.67-2.14). Reported elder abuse also was associated with significantly increased risk of overall mortality (HR, 1.39; 95% CI, 1.07-1.84). Confirmed elder self-neglect or abuse also was associated with mortality. Increased mortality risks associated with either elder self-neglect or abuse were not restricted to those with the lowest levels of cognitive or physical function. CONCLUSION Both elder self-neglect and abuse reported to social services agencies were associated with increased risk of mortality.

Influence of behavioral symptoms on rates of institutionalization for persons with Alzheimer's disease

BACKGROUND Recent studies indicate that behavioral symptoms may play a key role in decisions to institutionalize persons with Alzheimers disease (AD), but the specific types of behavior that contribute to this increased risk have not been reliably identified. The relationship between behavioral symptoms and time to institutionalization was evaluated in a 4-year longitudinal study. METHOD A total of 410 persons with the clinical diagnosis of AD completed annual clinical evaluations to assess cognitive impairment, functional limitations, delusions, hallucinations, depressive symptoms and physical aggression. Participation rates among survivors exceeded 90% for four follow-up evaluations with complete ascertainment of mortality and institutionalization. Time to institutionalization was evaluated using proportional hazards regression models in relation to time-varying clinical features. RESULTS In multivariate models, adjusted for demographic and social variables, four clinical features emerged as the predominant predictors of institutionalization: cognitive impairment level, physical aggression, hallucinations and depressive symptoms. These associations were virtually unchanged in analyses controlling for mortality. CONCLUSIONS Specific behavioral symptoms are important independent risk factors for institutionalization in persons with AD. Because behavioral symptoms are susceptible to therapy, efforts to modify or prevent these symptoms deserve careful consideration as a means to delay institutionalization for persons with this disease.

Mild cognitive impairment in different functional domains and incident Alzheimer’s disease

Background: Little is known about factors that predict transition from mild cognitive impairment to Alzheimer’s disease (AD). Objective: To examine the relation of impairment in different cognitive systems to risk of developing AD in persons with mild cognitive impairment. Methods: Participants are 218 older Catholic clergy members from the Religious Orders Study. At baseline, they met criteria for mild cognitive impairment based on a uniform clinical evaluation that included detailed cognitive testing. Evaluations were repeated annually for up to 10 years. Analyses were controlled for age, sex, and education. Results: Eighty two persons (37.6%) developed AD. In separate analyses, episodic memory, semantic memory, working memory, and perceptual speed, but not visuospatial ability, were associated with risk of AD, but when analysed together only episodic memory and perceptual speed were associated with AD incidence, with the effect for episodic memory especially strong. Overall, those with impaired episodic memory were more than twice as likely to develop AD as those with impairment in other cognitive domains (relative risk (RR) = 2.45; 95% confidence interval (CI): 1.53 to 3.92), and they experienced more rapid cognitive decline. Lower episodic memory performance was associated with increased risk of AD throughout the observation period, whereas impairment in other cognitive domains was primarily associated with risk during the following year but not thereafter. Conclusion: Among persons with mild cognitive impairment, episodic memory impairment is associated with a substantial and persistent elevation in risk of developing AD compared to impairment in other cognitive systems.

Terminal Cognitive Decline: Accelerated Loss of Cognition in the Last Years of Life

Objective: To test the hypothesis that rate of cognitive decline accelerates in the last years of life. Methods: Participants are 853 older persons without dementia at study onset. For up to 8 years, they underwent annual clinical evaluations that included a battery of 19 cognitive tests from which previously established composite measures of global cognition and specific cognitive domains were derived. In analyses, we used linear mixed-effects models that allowed rate of cognitive decline to change at a given point before death to estimate the onset of a terminal decline period and rate of cognitive decline before and after that point. In subsequent analyses, we tested potential modifiers of terminal decline. Results: There were 115 deaths. Those who died did not differ from survivors in their level of global cognitive function at study onset, but beginning a mean of 42 months before death, their rate of global cognitive decline sharply increased. The duration and rapidity of terminal decline in global cognition differed from person to person. Terminal cognitive decline was not modified by age, sex, education, or the presence of mild cognitive impairment, but it was not present in those with vascular disease (e.g., stroke and heart attack) or in those without at least one copy of the apolipoprotein E ϵ4 allele, suggesting that Alzheimer’s disease pathology may contribute to the phenomenon. Conclusions: In old age, cognitive decline markedly accelerates during the last 3 to 4 years of life, consistent with the terminal decline hypothesis. SD = standard deviation; SE = standard error.

The apolipoprotein E ϵ4 allele and incident Alzheimer’s disease in persons with mild cognitive impairment

Possession of one or more copies of the apolipoprotein E (APOE) ϵ4 allele is a known risk factor for Alzheimer’s disease (AD), but it is uncertain whether the ϵ4 allele is associated with disease incidence among persons with mild cognitive impairment (MCI). We addressed this issue with data from the Religious Orders Study. Participants were 181 older Catholic clergy members who met criteria for MCI based on a uniform structured clinical evaluation; 56 (30.9%) had at least one ϵ4 allele. Clinical evaluations, which included clinical classification of dementia and AD, were repeated annually. During a mean of 5.7 years of observation, 79 persons (43.6%) developed AD. In a proportional hazards model that controlled for age, sex, and education, possession of an ϵ4 allele was associated with a 93% increase in the risk of developing Alzheimer’s disease (95% CI: 1.02, 2.63). There was a marginally significant reduction in the effect of ϵ4 in older compared to younger participants (p = .053). The results suggest that possession of an ϵ4 allele does increase risk of AD in persons with MCI. The authors thank the hundreds of nuns, priests, and brothers from the following groups participating in the Religious Orders Study: archdiocesan priests, Chicago, IL, Dubuque, IA, and Milwaukee, WI, Benedictine monks, Lisle, IL, and Collegeville, MN, Benedictine Sisters, Erie, PA: Benedictine Sisters of the Sacred Heart, Lisle, IL, Capuchins, Appleton, WI, Christian Brothers, Chicago, IL, and Memphis TN, diocesan priests, Gary, IN, Dominicans, River Forest, IL, Felician Sisters, Chicago, IL, Franciscan Handmaids of Mary, New York NY; Franciscans Chicago, IL, Holy Spirit Missionary Sisters, Techny IL, Maryknolls, Los Altos, CA, and Maryknolls, NY, Norbertines, De Pere, WI, Oblate Sisters of Providence, Baltimore, MD, Passionists, Chicago, IL, Presentation Sisters, BVM, Dubuque, IA, Servites, Chicago, IL, Sinisinawa Dominican Sisters, Chicago, IL, and Sinsinawa WI, Sisters of Charity, BVM, Chicago, IL, and Dubuque IA, Sisters of the Holy Family, New Orleans, LA, Sisters of the Holy Family of Nazareth, Des Plaines, IL, Sisters of Mercy of the Americans, Chicago, IL, Aurora, IL, and Erie, PA, Sisters of St. Benedict, St. Cloud, MN and St. Joseph, MN, Sisters of St. Casimir Chicago, IL, Sisters of St. Francis of Mary Immaculate, Joliet, IL, Sisters of St. Joseph of La Grange, La Grange Park, IL, Society of Divine Word, Techny, IL, Trappists, Gethsemane, KY and Peosta, IA, and Wheaten Franciscan Sisters, Wheaten, IL. They also thank Julie Bach MSW, coordinator of the Religious Orders Study, Beth Howard, Coordinator of the Rush Alzheimer’s Disease Center Laboratory, and George Dombrowski MS and Greg Klein for data management. This research was supported by National Institute on Aging grants R01 AG1589, P30 AG10161, P01AG09466, P01AG14449

Psychosocial Distress and Stroke Risk in Older Adults

Background and Purpose— To investigate the association of psychosocial distress with risk of stroke mortality and incident stroke in older adults. Methods— Data were from the Chicago Health and Aging Project, a longitudinal population-based study conducted in 3 contiguous neighborhoods on the south side of Chicago, IL. Participants were community-dwelling black and non-Hispanic white adults, aged 65 years and older (n=4120 for stroke mortality; n=2649 for incident stroke). Psychosocial distress was an analytically derived composite measure of depressive symptoms, perceived stress, neuroticism, and life dissatisfaction. Cox proportional hazards models examined the association of distress with stroke mortality and incident stroke over 6 years of follow-up. Results— Stroke deaths (151) and 452 incident strokes were identified. Adjusting for age, race, and sex, the hazard ratio (HR) for each 1-SD increase in distress was 1.47 (95% confidence interval [CI]=1.28–1.70) for stroke mortality and 1.18 (95% CI=1.07–1.30) for incident stroke. Associations were reduced after adjustment for stroke risk factors and remained significant for stroke mortality (HR=1.29; 95% CI=1.10–1.52) but not for incident stroke (HR=1.09; 95% CI=0.98–1.21). Secondary analyses of stroke subtypes showed that distress was strongly related to incident hemorrhagic strokes (HR=1.70; 95% CI=1.28–2.25) but not ischemic strokes (HR=1.02; 95% CI=0.91–1.15) in fully adjusted models. Conclusions— Increasing levels of psychosocial distress are related to excess risk of both fatal and nonfatal stroke in older black and white adults. Additional research is needed to examine pathways linking psychosocial distress to cerebrovascular disease risk.

Change in Depressive Symptoms During the Prodromal Phase of Alzheimer Disease

CONTEXT Prospective studies have established an association between depressive symptoms and risk of dementia, but how depressive symptoms change during the evolution of dementia is uncertain. OBJECTIVE To test the hypothesis that depressive symptoms increase during the prodromal phase of Alzheimer disease (AD). DESIGN Prospective cohort study. PARTICIPANTS AND SETTING For up to 13 years, 917 older Catholic nuns, priests, and monks without dementia at study onset completed annual clinical evaluations that included administration of the 10-item Center for Epidemiologic Studies Depression Scale and clinical classification of mild cognitive impairment and AD. MAIN OUTCOME MEASURE Change in depressive symptoms reported on the Center for Epidemiologic Studies Depression Scale. RESULTS At baseline, participants reported a mean (SD) of 1.0 (1.5) depressive symptoms. Those who developed AD (n = 190) showed no increase in depressive symptoms before the diagnosis was made, and this finding was not modified by age, sex, education, memory complaints, vascular burden, or personality. There was no systematic change in depressive symptoms after the AD diagnosis, although symptoms tended to decrease in women relative to men and in those with a higher premorbid level of openness and a lower premorbid level of agreeableness. Among those without cognitive impairment at baseline, depressive symptoms did not increase in those who subsequently developed mild cognitive impairment. CONCLUSION We found no evidence of an increase in depressive symptoms during the prodromal phase of AD.

Perceived stress and change in cognitive function among adults 65 years and older.

Objective Exposure to acute and chronic stress can affect learning and memory, but most evidence comes from animal studies or clinical observations. Almost no population-based studies have investigated the relation of stress to cognition or changes in cognition over time. We examined whether higher levels of perceived stress were associated with accelerated decline in cognitive function in older blacks and whites from a community-based population sample. Methods Participants included 6207 black and white adults (65.7% black, 63.3% women) from the Chicago Health and Aging Project. Two to five in-home assessments were completed over an average of 6.8 years of follow-up and included sociodemographics, health behaviors, psychosocial measures, cognitive function tests, and health history. Perceived stress was measured by a six-item scale, and a composite measure of four tests of cognition was used to determine cognitive function at each assessment. Results Mixed-effects regression models showed that increasing levels of perceived stress were related to lower initial cognitive scores (B = −0.0379, standard error = 0.0025, p < .001) and a faster rate of cognitive decline (stress × time interaction: B = −0.0015, standard error = 0.0004, p < .001). Results were similar after adjusting for demographic variables, smoking, systolic blood pressure, body mass index, chronic medical conditions, and psychosocial factors and did not vary by race, sex, age, or education. Conclusions Increasing levels of stress are independently associated with accelerated declines in cognitive function in black and white adults 65 years and older.

The associations of gender, depression and elder mistreatment in a community-dwelling Chinese population: the modifying effect of social support.

The aims of this study are to: (1) examine the gender differences in the association of depression and elder mistreatment (EM) in a community-dwelling Chinese population; and (2) examine the potential differential modifying effect of greater social support on these associations. We conducted a cross-sectional study of 141 women and 270 men aged 60 years or greater who presented to an urban medical center. EM was assessed using the modified Vulnerability to Abuse Screening Scale (VASS) and depression was assessed using the Geriatric Depression Scale (GDS) and overall social support was measured using the Social Support Index (SSI). After adjusting for potential confounders, depression was associated with 447% increased risk for EM among men (odds ratio, OR = 4.47; 95% confidence intervals (CI) = 1.52-13.13) and 854% increased risk for EM among women (OR = 8.54; 95% CI = 2.85-25.57). After examining the effect of greater social support on depression (social support x depression), depression was no longer associated with increased risk for EM in men (parameter estimate = PE = 0.62 + or - 0.82 (+ or - S.E.M.) = 0.82, p = 0.454). However, among women, depression remained as a significant risk factor for EM (PE = 1.49 + or - 0.68, p = 0.029). Depression is significant risk factor for EM for both men and women. However, effect of greater overall social support may have higher protective effect in men than in women.

Neighborhood Cohesion Is Associated With Reduced Risk of Stroke Mortality

Background and Purpose— Greater social cohesion is related to lower rates of coronary heart disease, but its relation to stroke risk is unstudied. This study examined whether neighborhood social cohesion was protective against stroke mortality and incidence. Methods— Data come from 5789 participants (60% female; 62% black; mean age, 74.7 years) in a longitudinal study of chronic diseases in the elderly. Stroke mortality, ascertained through December 31, 2007, was verified through the National Death Index; 186 stroke deaths were identified in 11 years of follow-up. Stroke incidence was determined in a subset (N=3816) with linkage to Medicare claims files; 701 first-ever strokes were identified. Cohesion was measured by 6 items assessing frequency of contact and social interactions with neighbors; items were z-scored and averaged. Individual scores were averaged across 82 census block groups, forming a neighborhood-level measure of social cohesion. Marginal Cox proportional hazard models tested the association of neighborhood-level cohesion with stroke mortality and incidence. Results— Each 1-point increase in cohesion related to a 53% reduced risk of stroke mortality (hazard ratio, 0.47; 95% CI, 0.24 to 0.90), adjusting for relevant covariates, including sociodemographics, known stroke risk factors, and neighborhood-level socioeconomic status. A race×cohesion interaction (P=0.04) revealed cohesion was protective in whites (hazard ratio, 0.34; 95% CI, 0.17 to 0.67) but not blacks (hazard ratio, 1.17; 95% CI, 0.35 to 3.86). Cohesion was unrelated to stroke incidence (P>0.5). Conclusions— Neighborhood-level social cohesion was independently protective against stroke mortality. Research is needed to further examine observed race differences and pathways by which cohesion is health-protective.