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Integrative blood-based characterization of oxidative mitochondrial DNA damage variants implicates Mexican American's metabolic risk for developing Alzheimer's disease. | LitMetric

AI Article Synopsis

  • Alzheimer's Disease (AD) is a major cause of death in the US, especially impacting vulnerable groups like the Hispanic/Latino population due to health disparities.
  • The study explores how oxidative stress indicated by 8-oxo-guanine (8oxoG) in blood samples relates to age, sex, education, and AD risk among Mexican American and non-Hispanic White participants.
  • Findings show that Mexican Americans exhibit higher levels of mitochondrial DNA oxidative damage, which may increase their susceptibility to AD and highlight racial/ethnic differences in metabolic health.

Article Abstract

Alzheimer's Disease (AD) continues to be a leading cause of death in the US. As the US aging population (ages 65 +) expands, the impact will disproportionately affect vulnerable populations, e.g., Hispanic/Latino population, due to their AD-related health disparities. Age-related regression in mitochondrial activity and ethnic-specific differences in metabolic burden could potentially explain in part the racial/ethnic distinctions in etiology that exist for AD. Oxidation of guanine (G) to 8-oxo-guanine (8oxoG) is a prevalent lesion and an indicator of oxidative stress and mitochondrial dysfunction. Damaged mtDNA (8oxoG) can serve as an important marker of age-related systemic metabolic dysfunction and upon release into peripheral circulation may exacerbate pathophysiology contributing to AD development and/or progression. Analyzing blood samples from Mexican American (MA) and non-Hispanic White (NHW) participants enrolled in the Texas Alzheimer's Research & Care Consortium, we used blood-based measurements of 8oxoG from both buffy coat PBMCs and plasma to determine associations with population, sex, type-2 diabetes, and AD risk. Our results show that 8oxoG levels in both buffy coat and plasma were significantly associated with population, sex, years of education, and reveal a potential association with AD. Furthermore, MAs are significantly burdened by mtDNA oxidative damage in both blood fractions, which may contribute to their metabolic vulnerability to developing AD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10484983PMC
http://dx.doi.org/10.1038/s41598-023-41190-6DOI Listing

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