Linking levels of the antioxidant SOD-1, brain vascular damage, and cognitive performance across the Alzheimer’s disease spectrum

dc.contributor.advisor Willette, Auriel
dc.contributor.author Anton, Faith
dc.contributor.department Department of Food Science and Human Nutrition (HSS)
dc.date.accessioned 2024-05-08T18:11:22Z
dc.date.available 2024-05-08T18:11:22Z
dc.date.issued 2021-05
dc.description.abstract Copper/zinc superoxide dismutase 1 (SOD-1) is an antioxidant enzyme which may preserve cognition in Alzheimer’s disease (AD). Specifically, SOD-1 may degrade harmful free radicals that damage brain tissue and cause lesions. It is unknown if SOD-1 may act as an early warning sign for AD-related brain atrophy. This project primarily investigated if cerebrospinal fluid (CSF) levels of SOD-1 GDGY8 peptide could predict such atrophy. Data were downloaded from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), which included older adult participants classified as cognitively unimpaired or having mild cognitive impairment (MCI). Using SPSS, linear mixed models tested CSF SOD-1 relationships with: 1) total lesion load; and 2) performance on several cognitive measures (language, visuospatial, the functional assessment questionnaire). Interactions between SOD-1 and diagnosis category or Apolipoprotein E (APOE) status (a genetic risk factor for AD) were also examined. Main effects were not observed for SOD-1. Interactions with APOE and clinical category, however, indicated that higher SOD-1 levels were related to fewer lesions and better cognition in non-risk participants, but the opposite for adults with genetic risk or MCI. These results suggest that SOD-1 may dynamically track the degree of AD pathology before AD diagnosis occurs.
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/Ewpa8Abv
dc.relation.ispartofseries Honors Projects and Posters
dc.subject.disciplines DegreeDisciplines::Life Sciences::Kinesiology
dc.title Linking levels of the antioxidant SOD-1, brain vascular damage, and cognitive performance across the Alzheimer’s disease spectrum
dc.type Presentation
dspace.entity.type Publication
relation.isOrgUnitOfPublication 95fe1086-c07b-408b-a017-f17053e4bfbf
relation.isSeriesOfPublication 78a1cb49-0dee-4c38-97a8-c1fd0b7a74ea
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