Affiliations: [a] Laboratory of Neurochemistry, Neurology Department, Coimbra University Hospital, Coimbra, Portugal | [b] Neurology Department, Coimbra University Hospital, Coimbra, Portugal | [c] Center for Neuroscience and Cell Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Correspondence:
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Correspondence to: Inês Baldeiras, Laboratory of Neurochemistry, Neurology Department, Hospitais da Universidade de Coimbra, Praceta Mota Pinto, 3000 Coimbra, Portugal. Tel.: +351 239 400448; Fax: +351 239 822637; E-mail: ines.baldeiras@sapo.pt.
Abstract: Recent studies show that most of the oxidative changes found in Alzheimer's disease (AD) are already present in mild cognitive impairment (MCI) patients. The question arises as to whether oxidative stress has a role in the progression of MCI to AD. We conducted a longitudinal study on 70 MCI patients, and the peripheral blood levels of a broad spectrum of non-enzymatic and enzymatic antioxidant defenses, as well as lipid and protein oxidation markers and nitrogen oxidative species were determined. At baseline, there were no differences in any of the indexes of oxidative damage between stable MCI patients (MCI-MCI) and patients that progressed to AD (MCI-AD). Cellular levels of lipid peroxidation markers increased in both groups and this was accompained in MCI-AD, but not in MCI-MCI patients, by a significant decrease in cellular antioxidant defenses (oxidyzed/reduced glutathione ratio and vitamin E). Among MCI-AD patients, the longitudinal decrease in cellular vitamin E was associated with the deterioration in cognitive performance. These results suggest that accumulation of oxidative damage may start in pre-symptomatic phases of AD pathology and that progression to AD might be related to depletion of antioxidant defenses.
