Cerebrospinal fluid levels of 8‐isoprostane, a marker of oxidative stress, are elevated in patients with Alzheimer's disease compared to healthy subjects: Does the malfunction in the cell's powerhouse lead to Alzheimer's disease?. (31st December 2021)

• Record Type: Journal Article
• Authors: Jensen, Camilla Steen; Kellberg, Amanda Oliva; Hasselbalch, Steen Gregers; Simonsen, Anja Hviid
• Is Part Of: Alzheimer's & dementia. Volume 17(2021)Supplement 5
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-12-31
• Subjects: Alzheimer's disease -- Periodicals; Alzheimer Disease -- Periodicals; Dementia -- Periodicals; Démence; Maladie d'Alzheimer; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.83
• DOI: 10.1002/alz.052071
• Languages: English
• ISSNs: 1552-5260

Abstract

Abstract: Background: Oxidative stress may play an important role in the pathology of Alzheimer's disease (AD). 8‐Isoprostane is a prostaglandin (PG)‐F2‐like compound belonging to the F2 Isoprostane class that is produced in vivo by the free radical‐catalyzed peroxidation of cells membrane arachidonic acid. 8‐Isoprostane is a biomarker of oxidative stress, and could possibly be a surrogate marker of the mitochondrial health in AD. Method: We measured concentrations of cerebrospinal fluid (CSF) 8‐isoprostane from 113 subjects ranging from healthy subjects (HS, n=25), to Mild Cognitive Impairment with positive AD biomarkers (MCI+, n=16), AD( n=40), and non‐AD dementia (non‐AD, n=32). Analysis was done using 8‐isoprostane Enzyme‐linked immunosorbent assay from Cayman Chemicals (Cayman Chemicals, MI, USA). Result: Patient characteristics can be seen in Table 1. Analyzing the CSF levels of 8‐isoprostane, a significant difference between 8‐isoprostane concentrations among the groups (ANOVA) was found. Post‐hoc test (t‐test) revealed a difference between the HS and AD groups (Figure 1). Conclusion: In conclusion 8‐isoprostane may be a good surrogate marker of cellular oxidative stress and may be used to evaluate mitochondria's role in AD pathology in vivo.