دورية أكاديمية

Tocovid Attenuated Oxidative Stress and Cognitive Decline by Inhibiting Amyloid-β-Induced NOX2 Activation in Alzheimer's Disease Mice.

التفاصيل البيبلوغرافية
العنوان: Tocovid Attenuated Oxidative Stress and Cognitive Decline by Inhibiting Amyloid-β-Induced NOX2 Activation in Alzheimer's Disease Mice.
المؤلفون: Bian, Zhihong, Yu, Haibo, Hu, Xinran, Bian, Yuting, Sun, Hongming, Tadokoro, Koh, Takemoto, Mami, Yunoki, Taijun, Nakano, Yumiko, Fukui, Yusuke, Morihara, Ryuta, Abe, Koji, Yamashita, Toru
المصدر: Journal of Alzheimer's Disease; 2024 Supplement, Vol. 99, pS23-S33, 11p
مصطلحات موضوعية: ALZHEIMER'S disease, OXIDATIVE stress, COGNITION disorders, TRANSGENIC mice, NADPH oxidase
مستخلص: Background: NADPH oxidase 2 (NOX2) is an important source of reactive oxygen species (ROS). Activated NOX2 may contribute to Alzheimer's disease (AD). Our previous studies showed that a novel vitamin E mixture, Tocovid, had potential neuroprotective effects in a stroke mice model and an AD cell model. Objective: The aim of this study was two-fold: to assess whether long-term Tocovid treatment can regulate NOX2, and the therapeutic effects of long-term administration of Tocovid to an AD mice model. Methods: Therapeutic effects of long-term administration of Tocovid (200 mg/kg /day) on an Aβ-overexpressed transgenic AD mice model (APP23, n = 8) was investigated. The therapeutic effect of Tocovid in 16-month-old mice compared with the no-treatment APP23 group (n = 9) was assessed. Results: Tocovid treatment strongly improved motor and memory deficits of APP23 mice by attenuating NOX2 expression, oxidative stress, neuroinflammation, neurovascular unit dysfunction, synaptic alteration, and Aβ deposition after 16 months. Conclusion: These findings suggest that NOX2 is a potential target in AD pathology. Long-term administration of Tocovid may be a promising candidate for AD treatment. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:13872877
DOI:10.3233/JAD-220761