Inability of plasma and urine F2A-isoprostane levels to differentiate mild cognitive impairment from Alzheimer's disease.
BACKGROUND: Oxidative stress has been implicated in the pathogenesis of Alzheimer's disease (AD). The pathobiological changes related to AD occur long before the overt clinical symptoms. The plasma lipid peroxidation enzyme F2-isoprostane has been suggested as a biomarker to detect the progression from mild cognitive impairment (MCI) to AD. OBJECTIVE: To test whether plasma and urine F2-isoprostane was diagnostic for dementia in living people. METHODS: Plasma and urine were collected from 222 Religious Orders Study participants with a clinical diagnosis of no cognitive impairment, MCI or AD at time of fluid collection. Isoprostane levels were determined using gas chromatography/mass spectroscopy. RESULTS: Plasma and urine F2-isoprostane levels did not differ between the three clinical groups. Postmortem neuropathologic diagnosis of subjects who died during the course of the study was not associated with baseline blood or plasma F2-isoprostane levels. CONCLUSIONS: In living people, plasma or urine isoprostane levels were not sensitive enough to discriminate between individuals with a clinical diagnosis of no cognitive impairment, MCI or AD.[1]References
- Inability of plasma and urine F2A-isoprostane levels to differentiate mild cognitive impairment from Alzheimer's disease. Mufson, E.J., Leurgans, S. Neurodegener. Dis (2010) [Pubmed]
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