Apocynin administration does not improve behavioral and neuropathological deficits in a transgenic mouse model of Alzheimer's disease

NEUROSCIENCE LETTERS

卷:492

Article

Dumont, Magali¹  Stack, Cliona¹  Elipenhali, Ceyhan¹  Calingasan, Noel Y.¹  Wille, Elizabeth¹  Beal, M. Flint¹ 

[1] Weill Cornell Med Coll, Dept Neurol & Neurosci, New York, NY 10065 USA

关键词: Alzheimer's disease;    Apocynin;    NADPH oxidase;    Amyloid plaques;    Oxidative stress;   

DOI  :  10.1016/j.neulet.2011.01.077

来源: Elsevier

【 摘 要 】

In addition to mitochondria, NADPH oxidase (NOX) is a source of oxidative stress, which can induce oxidative damage in Alzheimer's disease (AD). For this reason, several groups have investigated the effect of its inhibition. In AD mice, NADPH oxidase 2 (NOX2) deficiency improved behavior and cerebrovascular function, and reduced oxidative stress. In our study, we administered the NOX inhibitor apocynin to Tg19959 mice, and found that it did not improve cognitive and synaptic deficits, and did not decrease amyloid deposition, microgliosis and hyperphosphorylated tau. However, apocynin reduced carbonyl levels in the cerebral cortex but not the hippocampus, which may have not been sufficient to ameliorate symptoms. Also, the reduction of NOX-mediated oxidative stress may not be sufficient to prevent AD, since other sources of reactive oxygen species such as mitochondria may be more important. Published by Elsevier Ireland Ltd.

【 授权许可】

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