An integrated neurovascular investigation of cognitive aging

Age-related declines in cognition are associated with widespread structural and functional brain changes, including changes in resting state functional connectivity (rsFC) and gray and white matter status. In addition, research has demonstrated that individual variance in cognitive aging is associated with cardiovascular health. In this dissertation, I integrate these factors into a cascade model and show how they might jointly and hierarchically account for individual differences in cognitive aging. The aim here is to have a framework that provides a starting point from which mechanistic pathways can be revealed and tested, ultimately advancing our knowledge for preventing or reducing age- related cognitive decline. In Chapter 1, I first review the factors that promote healthy cognitive aging and discuss the motivation for the focus on rsFC in later chapters. In Chapter 2, I introduce a cascade framework for cognitive aging that integrates the factors important for healthy brain health in aging. The results demonstrate for the first time that optically-measured cerebral arterial elasticity is strongly associated with segregation measures, and replicate previous findings of strong relationships between brain structure, brain function and cognition. In addition, the pattern of associations between these different factors is consistent with a hierarchical cascade framework linking them, suggesting that preventing or slowing age-related changes in one or more of these factors may induce a neurophysiological cascade beneficial for preserving cognition in aging. Extending these findings, Chapter 3 demonstrates that the results in Chapter 2 are not limited to parcellations derived from young-adult populations and can be extended to age-cohort- based parcellations. In Chapter 4, the main rsFC measure used in this dissertation– segregation – is investigated. Specifically, while network segregation is without doubt important as an index of brain health and cognitive function, the age-related changes in its topography has not been fully explored in previous studies due to various methodological constraints. In this chapter, I employ a distribution-based analysis to examine how decreased segregation is topographically changed with aging, manifesting in age-related cognitive declines. The results show that connectivity between networks is in fact systematically increased during aging, and that age-related decreases in segregation as a result of age-related adjustments in connectivity between networks are not simply the result of increased neural noise. Finally, Chapter 5 summarizes the results of previous chapters and discusses implications and future directions for the work in this dissertation. Overall, the research here demonstrates that individual variations in cognitive aging are connected to neurovascular factors in a cascade fashion, and implicates how we might optimize future interventions aimed at mitigating cognitive aging. Further, it extends our current understanding of how age changes the modular organization of functional networks, allowing us greater insight into how cognitive aging might be affected. Taken together with research showing the intervention effects of exercise, the current research supports the importance and potential of a healthy and active lifestyle for promoting healthy cognitive aging.

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Psychology

Grantor

University of Illinois at Urbana-Champaign

Year dc:date

2020

Author dc:creator

• Kong, Tania Suet Ling

Contributors dc:contributor

• Gratton, Gabriele
• Fabiani, Monica
• Barbey, Aron
• Sutton, Brad
• Sadaghiani, Sepideh

• Aging
• Resting state functional connectivity (rsFC)
• Cerebrovascular health
• Optical brain arterial pulse (pulse-DOT)
• White matter signal abnormalities (WMSAs)
• Cortical thickness

Statement dc:rights

• Copyright 2019 Tania Kong

Language dc:language

en

Handle dc:identifier

http://hdl.handle.net/2142/106331

OAI identifier oai:identifier

oai:www.ideals.illinois.edu:2142/106331