Introduction : Cognitive impairment and anxiety disorders are the two most common psychiatric disorders in later life. These problems commonly co-occur and are associated with a range of negative outcomes such as increased functional impairment, greater healthcare utilization, and elevated risk of nursing home placement. Little research has examined the stability of genetic influences on anxiety symptoms in older adults. Similarly, the temporal dynamics of the relationship between cognitive performance and anxiety as well as the extent to which shared genetic factors explain this association is unclear. The specific goals of this dissertation were to (1) explore the stability of genetic and environmental influences on anxiety in older adulthood, (2) explore the extent to which genetic factors influencing anxiety are also influencing cognitive performance, (3) determine the temporal dynamics of this phenotypic association, and (4) examine the extent to which genetic and environmental factors were driving this association over time. Design : We examined data from the Swedish Adoption/Twin Study of Aging (SATSA). Between the years 1984 - 2007, 2,018 participants aged 31-98 years completed as many as 7 assessments which included measures of anxiety and cognitive performance. For aim 1, genetic simplex models were fit to examine the stability of genetic and environmental influences on anxiety later in life. For the second aim bivariate Cholesky decompositions were conducted to examine the extent to which shared genetic influences explained the association between anxiety and cognitive performance. For aim 3 we examined the temporal dynamics of the association between anxiety and cognitive performance by fitting bivariate dual change score models (DCSM). For the last aim biometric DCSM models were estimated to examine the temporal dynamics of genetic and environmental contributions. Results : New genetic contributions to the etiology of anxiety were found beginning at the ages 60-64. New significant unique environmental factors contributed to anxiety symptoms starting after age 70. For aim 2, in males anxiety was associated with worse nonverbal memory, attention, working memory, and aspects of spatial performance. Anxiety was only associated with worse visuospatial performance and picture memory in females. For males, shared genetic factors were mostly explaining this association. For females unique environmental factors were explaining this association. When examining this association over time, across all cognitive tests worse cognitive performance was a leading indicator of change in anxiety. Anxiety was not associated with subsequent changes in cognitive performance. The biometric models suggested that genetic factors contributing to variance in processing speed and attention were driving variation in anxiety over time. Unique environmental contributions to spatial abilities were driving subsequent variation in anxiety. Conclusions : The findings from these four studies deepen our understanding of the etiology of late life anxiety and its association with cognitive performance. This information can help to identify older adults at risk for the development of anxiety. The findings from this study also may inform intervention and prevention efforts for older adults experiencing cognitive decline and anxiety

Introduction

We asked whether anxiety is associated with prospective risk of dementia, and the extent to which genetic influences mediate this association.

Methods

Nondemented twins (n = 1082) from the Swedish Adoption Twin Study of Aging completed an assessment of anxiety symptoms in 1984 and were followed for 28 years.

Results

Baseline anxiety score, independent of depressive symptoms, was significantly associated with incident dementia over follow-up (hazard ratio [HR] = 1.04; 95% confidence interval [CI] = 1.01-1.06). There was 48% increased risk of becoming demented for those who had experienced high anxiety at any time compared with those who had not. In co-twin analyses, the association between anxiety symptoms and dementia was greater for dizygotic (HR = 1.11; 95% CI = 1.02-1.20) compared with monozygotic twins (HR = 1.06; 95% CI = 0.95-1.20), indicating genetic mediation.

Discussion

Anxiety symptoms were associated with increased risk of dementia. Genetic factors common to dementia and anxiety partially mediated this association.

Cognitive decline and anxiety symptoms commonly co-occur in later life, but the temporal order of changes on these two attributes is unclear. Specifically, it is unknown if greater anxiety leads to subsequent declines in cognitive performance or if worse cognitive performance leads to increased anxiety. In this study, we sought to elucidate the temporal dynamics between anxiety symptoms and cognitive performance across old age-that is, the extent to which level and change in one variable influence subsequent changes in a second variable. We examined data from 721 nondemented participants from the Swedish Adoption/Twin Study of Aging. Participants completed as many as eight assessments of cognitive performance and anxiety over a 26-year period. Bivariate dual-change score models were fit to examine the dynamic association between anxiety and cognitive performance. Bidirectional associations between anxiety and cognitive performance were found among measures of processing speed, attention, and memory but not visuospatial abilities. Higher anxiety was associated with greater declines in processing speed over the duration of 6 years and worsening attention over a span of 3 years. The reverse direction was also significant in that slower processing speed, worse attention, and poorer nonverbal and working memory performance were associated with larger increases in anxiety 3 years later. These findings highlight that in cognitively intact older adults, the association between anxiety and worse cognitive performance is bidirectional and complex. (PsycINFO Database Record

Anxiety symptoms are common in later life and are associated with diverse adverse health outcomes. Little is known about how genetic and environmental influences on anxiety symptoms might vary across older adulthood. The purpose of this study was to explore change and stability of contributions to anxiety symptoms across older adulthood. We examined data from the Swedish Adoption/Twin Study of Aging (SATSA). Between the years 1984 and 2010, 2021 participants (including 753 complete twin pairs) completed up to seven assessments containing two measures of anxiety symptoms. Longitudinal genetic simplex models were fit to examine the stability and change in genetic and environmental influences. Amplification of genetic factors at ages 75-80 suggests tentative new genetic contributions to anxiety symptoms. These findings suggest that the heritability of anxiety symptoms may increase later in life. Physiological factors associated with aging are discussed as potential factors explaining this increase.

Objectives

The effect of fear of falling (FoF) on recovery 1 year after hip fracture is not well known. Furthermore, the potential influence of premorbid function has not been explored. We aimed to describe rates of FoF after hip fracture, to assess the association of FoF with functional recovery 1 year post-fracture, and to evaluate the potential moderating effect of premorbid function on the relationship between FoF and functional recovery.

Design

Secondary analysis of data from a prospective, longitudinal observational study to assess genetic factors influencing functional and psychological outcomes after hip fracture over 52 weeks.

Setting

Eight area hospitals in St. Louis, MO.

Participants

241 cognitively intact individuals 60 years of age or older requiring surgical repair for hip fracture.

Measurements

Fear of falling was measured by the short Falls Efficacy Scale-International 4 and 12 weeks post-fracture. The primary outcome was probability of full recovery 52 weeks post-fracture assessed with the Functional Recovery Score.

Results

High rates of FoF were seen at 4 (60.5%) and 12 weeks (47.0%) post-fracture. Week 12 FoF was associated with lower odds of recovery for those with high function pre-fracture (odds ratio [OR]: 0.82, 95% confidence interval [CI]: 0.72, 0.93), but not for those with impaired activities of daily living performance (OR: 1.04, 95% CI: 0.91, 1.19).

Conclusions

Fear of falling is common after hip fracture and is associated with poorer functional recovery 1 year after fracture, particularly in patients with high premorbid function. Fear of falling is a modifiable problem that represents a potential target for interventions to improve functional outcomes after hip fracture.

Objective

Childhood trauma is common and associated with both worse cognitive performance and disruption to the hypothalamic-pituitary-adrenal axis in younger adults. The extent to which these associations persist into older adulthood remains unknown. The aim of this study was to investigate self-reported childhood trauma in relation to cognitive performance, and the extent to which cortisol explained this association, in 2 independent samples of older adults.

Methods

In this cross-sectional study, participants in the discovery sample (N = 76) consisted of older adults with a DSM-IV diagnosis of generalized anxiety disorder (N = 57) and age-equated psychiatrically healthy comparison subjects (N = 19) who were referred largely through primary care clinics between 2004-2006. The replication sample (N = 48) consisted of older adults with DSM-IV anxiety or depressive disorders recruited between 2012-2013. Participants were administered the Early Trauma Inventory Self-Report-Short Form and a neuropsychological assessment (primary outcome).

Results

Across both samples, childhood trauma was significantly associated with worse performance on measures of processing speed, attention, and executive functioning. The effect of trauma exposure was stronger when general, physical, and sexual traumatic events were examined specifically (all P < .05). Childhood trauma was not associated with cortisol levels, and cortisol did not explain the association between trauma and cognitive functioning.

Conclusions

Self-reported traumatic events experienced in childhood are associated with poorer cognitive performance in anxious and depressed older adults. Findings demonstrate a deleterious impact of childhood trauma on brain health in old age.

Objective

Fear of falling is an important problem among older adults, even those with relatively low rates of objective fall risk, who are often overlooked as targets for intervention.

Method

We developed and pilot tested a new intervention, Activity, Balance, Learning, and Exposure (ABLE), in a sample of 10 older adults with excessive fear of falling. The ABLE intervention integrates exposure therapy and cognitive restructuring with a home safety evaluation and an exercise program and is conducted in the home. In this pilot project, ABLE was jointly conducted by a physical therapist and a psychologist with expertise in geriatric anxiety disorders.

Results

The intervention was feasible and acceptable and resulted in decreases in fear and activity avoidance for most participants. One participant experienced an injurious fall.

Discussion

We learned a number of important lessons resulting in modifications to the inclusion criteria, assessments, and intervention over the course of this pilot study. Results suggest that ABLE has promise for treating excessive fear of falling in the elderly and support testing the intervention in a larger randomized trial. Copyright © 2016 John Wiley & Sons, Ltd.

OBJECTIVES:To evaluate the safety and acceptability of a novel 8-week intervention integrating exercise, exposure therapy, cognitive restructuring, and a home safety evaluation, conducted by a physical therapist, in reducing fear of falling and activity avoidance. To collect preliminary evidence of efficacy. DESIGN:Randomized pilot study comparing the intervention to time- and attention-equivalent fall prevention education. SETTING:Participants' homes. PARTICIPANTS:42 older adults with disproportionate fear of falling (high fear, low to moderate objective fall risk). MEASUREMENTS:Falls Efficacy Scale-International, modified Activity Card Sort, satisfaction, falls. RESULTS:Relative to education, the intervention reduced fear of falling (d = 1.23) and activity avoidance (d = 1.02) at 8 weeks, but effects eroded over a 6-month follow-up period. The intervention did not increase falls, and participants rated the exercise, exposure therapy, and non-specific elements as most helpful. CONCLUSIONS:An integration of exercise and exposure therapy may help older adults with disproportionate fear of falling, but modifications to the intervention or its duration may be needed to maintain participants' gains.

Background

Although fear of falling is prevalent among older adults recovering from hip fracture, current instruments are inadequate due to focus on specific situations and measurement of self-efficacy rather than fear.

Methods

The authors revised and tested a form of the Fear of Falling Questionnaire with three groups of older adults: 405 recovering from hip fracture, 89 healthy community dwelling, and 42 with severe fear of falling. Test-retest reliability was evaluated in a subsample of 16 hip fracture patients. Internal consistency was compared across all groups. Construct validity was established through factor analysis, convergent validity with a measure of fall-related self-efficacy, and discriminant validity with measures of depression and affect.

Results

A revised two-factor, six-item scale appears to have adequate psychometric properties. Scores were lower in the healthy comparison group relative to the hip fracture and fear of falling groups. Cronbach's α ranged from 0.72-0.83, with test-retest reliability of 0.82. Correlations with a measure of fall-related self-efficacy were moderate for the hip fracture group (0.42) and high with the healthy comparison (0.68) and fear of falling (0.70) groups. Correlations with depression and negative and positive affect were low to moderate.

Conclusions

The Fear of Falling Questionnaire - Revised shows promise as a self-report measure of fear of falling, and is one of the first to be tested in older adults recovering from hip fracture. Advantages are that it is global rather than situation-specific and measures fear rather than self-efficacy. Future research on this scale is recommended in other older adult samples for whom fear of falling is relevant.

Background

Emerging data suggests PM_2.5 (particulate matter with aerodynamic diameter <2.5 μm) may be associated with both earlier declines in episodic memory (EM) and increased depressive symptoms in older adults. Although late-life depressive symptoms are associated with EM, no longitudinal studies have examined the inter-relationship among PM_2.5, depressive symptoms and EM.

Methods

Older women (n = 2,202; aged 67-83 in 1999) enrolled in the Women's Health Initiative Study of Cognitive Aging completed up to eight annual assessments of depressive symptoms (15-item Geriatric Depression Scale) and EM (California Verbal Learning Test). A nationwide spatiotemporal model (1999-2010) was used to estimate ambient PM_2.5 exposure at residential locations. Univariate and bivariate structural equation models (SEMs) for latent-change scores were used to examine how 3-year average PM_2.5 preceding each assessment affects the temporal dynamics and bidirectional relations of annual changes in depressive symptoms and EM.

Results

In univariate SEMs, one inter-quartile (4.04 μg/m³) increment of 3-year PM_2.5 was significantly (p < 0.05) associated with accelerated declines in verbal learning (List A trials 1-3: β = -1.48) and free-recall memory (short-delay: β = -1.43; long-delay: β = -1.11), but not with change in depressive symptoms (β = 0.12; p = 0.71). In bivariate SEMs, significant associations were observed between PM_2.5 and accelerated declines in EM measures (β = -1.44 to -0.99; p < 0.05) and between EM performance and changes in depressive symptoms (β = -0.08 to -0.05; p < 0.05), with significant indirect PM_2.5 effects on changes in depressive symptoms (β = 0.08-0.10; p < 0.05). These findings were robust with adjustment for multiple demographic, lifestyle, and clinical factors, and remained after excluding subjects with dementia or mild cognitive impairment. No associations were found between PM_2.5 and change in depressive symptoms or depressive symptoms and subsequent EM decline.

Conclusions

Findings suggest that PM_2.5 neurotoxicity may damage brain areas implicated in EM, followed by manifestation of depressive symptoms. Our data did not support depressive symptoms as the neuropsychological mediator of accelerated brain aging associated with PM_2.5 exposure.