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Effects of Carotid Intima-Media Thickness and Infections on Cognition
Effects of Carotid Intima-Media Thickness and Infections on Cognition
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20250211152939
- ISBN
- 9798384493112
- DDC
- 614.4
- 서명/저자
- Effects of Carotid Intima-Media Thickness and Infections on Cognition
- 발행사항
- [Sl] : Columbia University, 2024
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2024
- 형태사항
- 232 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-04, Section: B.
- 주기사항
- Advisor: Factor-Litvak, Pam.
- 학위논문주기
- Thesis (Ph.D.)--Columbia University, 2024.
- 초록/해제
- 요약Carotid intima-media thickness (IMT) is a measure of atherosclerosis. A large carotid IMT may be indicative of an impaired blood-brain barrier, providing a pathway for infections and inflammation to more readily enter the brain to contribute to neuronal damage as proposed by the 'microbial hypothesis'. However, no consensus exists regarding the effects of carotid IMT and infections on cognitive decline. Therefore, the goal of my dissertation was to investigate the potential mechanisms proposed by the 'microbial hypothesis' that may result in the outcome of cognitive decline. This goal was accomplished through investigating three specific aims. First, I conducted a scoping review to examine and synthesize existing literature assessing the effects of either carotid IMT or infections on the outcome of change in cognition over at least two years. Secondly, I empirically assessed the association between mid-life carotid IMT and late-life cognitive function at baseline and over time in a well characterized cohort. Finally, in the same cohort, I examined the association between mid- to late-life hospitalized infections and late-life cognitive function at baseline and change over time. Studies included in the scoping review moderately supported an association between carotid IMT and decline in global cognition, though evidence for an association between infections and cognitive decline is lacking. Infections most commonly were identified using antibodies, which are representative of past infections and may explain null findings. When examining carotid IMT empirically, I found no association between mid-life carotid IMT on 6-year change in late-life global cognitive function, however there was a significant association between greater carotid IMT and decreasing executive function scores over time. In a secondary analysis, I was able to expand follow-up time for global cognition up to 21 years, beginning in mid-life immediately following last carotid IMT measurement and found a significant association with change over time with this approach. This may support the need for interventions for reducing or preventing atherosclerosis earlier in the life course to prevent cognitive decline and potentially halt progression to dementia. In the same cohort, I found no significant associations between mid- to late-life hospitalized infections and 6-year change in late-life cognition for global cognition or domains. However, a history of having a hospitalized infection was significantly associated with baseline global cognition and baseline scores for language and executive function, but not memory. This may support theories that infections may result in faster rates of decline immediately following infections while then returning to normal rates in later life, however further examination of trajectories immediately after infections is needed. Results from this dissertation do not directly support the 'microbial hypothesis', however, they do provide insight that may be applicable to future studies examining these relationships.
- 일반주제명
- Epidemiology
- 일반주제명
- Neurosciences
- 일반주제명
- Cognitive psychology
- 키워드
- Atherosclerosis
- 키워드
- Cognition
- 키워드
- Infections
- 기타저자
- Columbia University Epidemiology
- 기본자료저록
- Dissertations Abstracts International. 86-04B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■00520250211152939
■006m o d
■007cr#unu||||||||
■020 ▼a9798384493112
■035 ▼a(MiAaPQ)AAI31564679
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a614.4
■1001 ▼aVollmer, Brandi L.
■24510▼aEffects of Carotid Intima-Media Thickness and Infections on Cognition
■260 ▼a[Sl]▼bColumbia University▼c2024
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2024
■300 ▼a232 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-04, Section: B.
■500 ▼aAdvisor: Factor-Litvak, Pam.
■5021 ▼aThesis (Ph.D.)--Columbia University, 2024.
■520 ▼aCarotid intima-media thickness (IMT) is a measure of atherosclerosis. A large carotid IMT may be indicative of an impaired blood-brain barrier, providing a pathway for infections and inflammation to more readily enter the brain to contribute to neuronal damage as proposed by the 'microbial hypothesis'. However, no consensus exists regarding the effects of carotid IMT and infections on cognitive decline. Therefore, the goal of my dissertation was to investigate the potential mechanisms proposed by the 'microbial hypothesis' that may result in the outcome of cognitive decline. This goal was accomplished through investigating three specific aims. First, I conducted a scoping review to examine and synthesize existing literature assessing the effects of either carotid IMT or infections on the outcome of change in cognition over at least two years. Secondly, I empirically assessed the association between mid-life carotid IMT and late-life cognitive function at baseline and over time in a well characterized cohort. Finally, in the same cohort, I examined the association between mid- to late-life hospitalized infections and late-life cognitive function at baseline and change over time. Studies included in the scoping review moderately supported an association between carotid IMT and decline in global cognition, though evidence for an association between infections and cognitive decline is lacking. Infections most commonly were identified using antibodies, which are representative of past infections and may explain null findings. When examining carotid IMT empirically, I found no association between mid-life carotid IMT on 6-year change in late-life global cognitive function, however there was a significant association between greater carotid IMT and decreasing executive function scores over time. In a secondary analysis, I was able to expand follow-up time for global cognition up to 21 years, beginning in mid-life immediately following last carotid IMT measurement and found a significant association with change over time with this approach. This may support the need for interventions for reducing or preventing atherosclerosis earlier in the life course to prevent cognitive decline and potentially halt progression to dementia. In the same cohort, I found no significant associations between mid- to late-life hospitalized infections and 6-year change in late-life cognition for global cognition or domains. However, a history of having a hospitalized infection was significantly associated with baseline global cognition and baseline scores for language and executive function, but not memory. This may support theories that infections may result in faster rates of decline immediately following infections while then returning to normal rates in later life, however further examination of trajectories immediately after infections is needed. Results from this dissertation do not directly support the 'microbial hypothesis', however, they do provide insight that may be applicable to future studies examining these relationships.
■590 ▼aSchool code: 0054.
■650 4▼aEpidemiology
■650 4▼aNeurosciences
■650 4▼aCognitive psychology
■653 ▼aAtherosclerosis
■653 ▼aCognition
■653 ▼aCognitive decline
■653 ▼aInfections
■690 ▼a0766
■690 ▼a0317
■690 ▼a0633
■71020▼aColumbia University▼bEpidemiology.
■7730 ▼tDissertations Abstracts International▼g86-04B.
■790 ▼a0054
■791 ▼aPh.D.
■792 ▼a2024
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17164254▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.


