Carbonyl Proteins as a Clinical Marker in Alzheimer's Disease and its Relation to Tryptophan Degradation and Immune Activation
Greilberger, J.; Fuchs, D.; Leblhuber, F.; Greilberger, M.; Wintersteiger, R.; Tafeit, E.
Clinical Laboratory 56(9-10): 441-448
2010
ISSN/ISBN: 1433-6510 PMID: 21086789 Document Number: 11301
Background: The question arises whether oxidative stress is connected with systemic immune activation in Alzheimer's disease (AD) and mild cognitive impairment (MCI). During immune response interferon-gamma stimulates the kynurenine (Kyn) pathway, a major route of L-tryptophan (Trp) degradation. Methods: Plasma Kyn, Trp and the Kyn to Trp ratio (Kyn/Trp), carbonyl proteins (CP) as oxidative stress parameter and homocysteine, neopterin, folate and vitamin B12 were measured from patients with AD and MCI (n = 16: 6 females and 4 males with AD, 3 females and 3 males with MCI; 63.3 ± 13.7 years), and an age matched healthy control group (n = 15: 11 females and 4 males; 62.8 ± 3.6 years). We correlated the oxidative stress parameter CP with the degradation of Trp creating a new quotient CP/Trp and calculated the sensitivity, specificity, and cut-off values for CP, Trp, CP/Trp, and Kyn/Trp using discriminate analysis. Results: CP was significantly higher in AD/MCI (930 ± 265 pmol/mg; p Conclusions: These preliminary results support the hypothesis that oxidative damage to proteins is directly connected with Trp degradation and Kyn pathway in the systemic immune activation.
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