Insomnia, cognition, aging: genetic and environmental influences

• Main Author: Genderson, Margo R
• Language: en_US
• Published: Boston University 2015
• Online Access: https://hdl.handle.net/2144/12759

Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at [e-mail]. Thank you. === Studying insomnia in aging populations is critical since the risk of insomnia increases with age, and insomnia is associated with numerous negative outcomes, such as cognitive impairments and co-occurring psychiatric disorders. The Vietnam Era Twin Study of Aging (VETSA) is a longitudinal study that investigates the relative contributions of genes and the environment to age-related changes in a broad range of characteristics. This thesis examined VETSA participants (n=1237; mean age=55.6) and utilized classic twin analyses, neuropsychological assessments, hormone, genotype, and structural MRI data to explore the etiology of insomnia, the relationship between insomnia and depression, and the mechanisms through which insomnia may influence cognitive decline. Results demonstrate that genetic factors are responsible for approximately 34% of the variation in individual differences in insomnia while non-shared environmental influences are responsible for the remaining 66%; shared family environmental influences are negligible. This study was the first investigation of the extent to which symptoms of insomnia and depression share a single genetic liability or independent liabilities, as these disorders often co-occur. Results demonstrate that much of the genetic influence on insomnia is also associated with depression, suggesting that the comorbidity between these disorders reflects shared genetic effects. There is an association between insomnia and poorer performance on tests of general cognitive ability, visual spatial processing and memory, short term memory, and working memory. After adjusting for depression, insomnia was significantly related to visual spatial processing and memory, suggesting that treating insomnia might be a successful intervention for individuals who demonstrate visual spatial memory and processing impairments. To explore mechanisms through which insomnia influences cognitive decline, cortisol, hippocampal volume, and the apoE genotype were examined. Insomnia was significantly related to smaller hippocampal volume; there was no association between insomnia and cortisol levels. ApoE genotype is related to deficits in recovering from neuronal insult, but insomnia did not differentially impact cognition based on apoE genotype. However, trends towards interactions were observed, particularly on memory domains. These findings have implications for the treatment of insomnia and depression and may inform prevention and intervention techniques aimed at cognitive preservation, which is of central importance in successful aging.