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Hyperhomocysteinemia as an early modifiable biomarker of age-related cognitive decline and risk of Alzheimer disease
Descriptive
TitleInfo
Title
Hyperhomocysteinemia as an early modifiable biomarker of age-related cognitive decline and risk of Alzheimer disease
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Ferguson
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Keelin
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Keelin Ferguson
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author
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Miller
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Joshua
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Joshua Miller
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Advisory Committee
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chair
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Miller
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Joshua
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Joshua Miller
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Advisory Committee
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member
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Hoffman
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Daniel
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Daniel Hoffman
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Advisory Committee
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(authority = local)
member
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Shapses
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Sue
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Sue Shapses
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Advisory Committee
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member
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Rutgers University
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degree grantor
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School of Graduate Studies
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theses
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2023
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2023-01
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English
Abstract
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Statement of Problem: Studies have demonstrated associations between elevated plasma homocysteine and cognitive impairment, Alzheimer’s disease, and dementia. This study sought to explore the relationship between elevated plasma homocysteine, regional brain volumes, and cognitive function in older adults with no overt cognitive impairment and the potential of elevated homocysteine to serve as an early modifiable biomarker for age-related neurodegeneration and cognitive decline. Objective: We evaluated the relationship between plasma homocysteine, regional brain volumes, and cognitive function in older adults with no cognitive impairment (age 69-90 y; N=243, 129 women, 114 men).
Methods: Blood samples were collected to determine concentration of plasma total homocysteine, RBC folate, serum vitamin B12 and serum creatinine. Cognitive function tests included assessment of global cognitive function, processing speed, verbal memory, and executive function. Regional brain volume scans were conducted using MRI imaging analyzed by Freesurfer. Associations between plasma homocysteine, cognitive function and regional brain volumes were assessed using multiple regression analysis with control for age, sex, education, RBC folate, vitamin B12 and serum creatinine.
Results: Homocysteine was inversely correlated with 12 of 15 regional brain volumes (P<0.05) after adjusting for demographic and biochemical variables. Homocysteine was inversely correlated with 3 of the 12 cognitive function tests (P<0.05) after adjusting for demographic and biochemical variables. The three cognitive function tests that were significantly associated with homocysteine were tests of executive functions.
Conclusions: Elevated homocysteine can serve as an early modifiable risk factor for impaired cognitive function and neurodegeneration in healthy adults without overt clinical cognitive impairment. Further research is needed to confirm if lowering homocysteine with B vitamin supplements will slow the progression of neurodegeneration and cognitive decline in older adults.
Methods: Blood samples were collected to determine concentration of plasma total homocysteine, RBC folate, serum vitamin B12 and serum creatinine. Cognitive function tests included assessment of global cognitive function, processing speed, verbal memory, and executive function. Regional brain volume scans were conducted using MRI imaging analyzed by Freesurfer. Associations between plasma homocysteine, cognitive function and regional brain volumes were assessed using multiple regression analysis with control for age, sex, education, RBC folate, vitamin B12 and serum creatinine.
Results: Homocysteine was inversely correlated with 12 of 15 regional brain volumes (P<0.05) after adjusting for demographic and biochemical variables. Homocysteine was inversely correlated with 3 of the 12 cognitive function tests (P<0.05) after adjusting for demographic and biochemical variables. The three cognitive function tests that were significantly associated with homocysteine were tests of executive functions.
Conclusions: Elevated homocysteine can serve as an early modifiable risk factor for impaired cognitive function and neurodegeneration in healthy adults without overt clinical cognitive impairment. Further research is needed to confirm if lowering homocysteine with B vitamin supplements will slow the progression of neurodegeneration and cognitive decline in older adults.
Subject
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Topic
Nutrition
Subject
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Topic
Alzheimer disease
Subject
(authority = local)
Topic
Cognitive decline
Subject
(authority = local)
Topic
Folate
Subject
(authority = local)
Topic
Homocysteine
Subject
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Topic
Vitamin B12
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Rutgers University Electronic Theses and Dissertations
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http://dissertations.umi.com/gsnb.rutgers:12296
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41 pages
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M.S.
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Includes bibliographical references
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School of Graduate Studies Electronic Theses and Dissertations
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rucore10001600001
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NjNbRU
Identifier
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doi:10.7282/t3-6aaa-de09
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Rights
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The author owns the copyright to this work.
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Ferguson
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Keelin
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Permission or license
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2023-02-23T12:40:49
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Keelin Ferguson
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Rutgers University. School of Graduate Studies
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Author Agreement License
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I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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2022-12-21T16:15:54
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2022-12-21T16:15:54
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