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Effects of Carotid Intima-Media Thickness and Infections on Cognition
Effects of Carotid Intima-Media Thickness and Infections on Cognition
Effects of Carotid Intima-Media Thickness and Infections on Cognition

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자료유형  
 학위논문 서양
최종처리일시  
20250211152939
ISBN  
9798384493112
DDC  
614.4
저자명  
Vollmer, Brandi L.
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  
Cognitive decline
키워드  
Infections
기타저자  
Columbia University Epidemiology
기본자료저록  
Dissertations Abstracts International. 86-04B.
전자적 위치 및 접속  
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MARC

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■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.

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