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.