Oxidative imbalance in patients with mild cognitive impairment and Alzheimer's disease

Increasing evidence supports a role of oxidative imbalance, characterized by impaired antioxidant enzymatic activity and increased reactive oxygen species (ROS) production, in mild cognitive impairment (MCI) and Alzheimer's disease (AD) pathogenesis. Hyperhomocysteinemia, another risk factor fo...

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Published in:Neurobiology of aging Vol. 27; no. 2; pp. 262 - 269
Main Authors: Guidi, Ilaria, Galimberti, Daniela, Lonati, Silvia, Novembrino, Cristina, Bamonti, Fabrizia, Tiriticco, Marco, Fenoglio, Chiara, Venturelli, Eliana, Baron, Pierluigi, Bresolin, Nereo, Scarpini, Elio
Format: Journal Article
Language:English
Published: London Elsevier Inc 01-02-2006
Elsevier Science
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Summary:Increasing evidence supports a role of oxidative imbalance, characterized by impaired antioxidant enzymatic activity and increased reactive oxygen species (ROS) production, in mild cognitive impairment (MCI) and Alzheimer's disease (AD) pathogenesis. Hyperhomocysteinemia, another risk factor for AD, also contributes to oxidative damage. Plasma total homocysteine (tHcy) and ROS levels, and total antioxidant capacity (TAC) were determined in 71 AD, 36 MCI and 28 vascular dementia (VaD) patients as well as in 44 age-matched controls. tHcy levels were significantly increased in patients with AD and VaD an a trend towards an increase in multiple domain MCI was observed. TAC was significantly decreased in AD as well as MCI, but not in VaD patients. In AD patients, a negative correlation was found between TAC and disease duration. ROS levels did not differ among groups, but were correlated with age. In conclusion, a pattern characterized by increased tHcy levels and decreased TAC is present in AD as well as MCI patients. While increased tHcy levels were also found in VaD, TAC modifications occur specifically in AD. ROS levels appear to be correlated with age rather than with a specific dementing disorder, thus leading to the hypothesis that oxidative imbalance observed in AD could be due to a decreased TAC.
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ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2005.01.001