Allicin ameliorates cognitive impairment in APP/PS1 mice via Suppressing oxidative stress by Blocking JNK Signaling Pathways. (February 2018)

• Record Type: Journal Article
• Authors: Zhang, Hao; Wang, Ping; Xue, Yixue; Liu, Libo; Li, Zhen; Liu, Yunhui
• Is Part Of: Tissue & cell. Volume 50(2018)
• Page Start: 89
• Page End: 95
• Publication Date: 2018-02
• Subjects: Allicin -- Alzheimer's disease -- APP (amyloid precursor protein)/PS1 (presenilin 1) mouse; Cytology -- Periodicals; 571.5
• DOI: 10.1016/j.tice.2017.11.002
• Languages: English
• ISSNs: 0040-8166

Abstract

Graphical abstract: Highlights: Allicin improves the cognitive function in AD mouse model. Allicin reduces the expression levels of Aβ by reducing APP lyases in AD mouse model. Allicin decreases oxidative stress and improves mitochondrial dysfunction by JNK/c-jun in AD mouse model. Abstract: In middle and old age, Alzheimer's disease (AD) is a progressive neurodegenerative disorder of brain. As an increasingly aging population, AD represents a huge burden for the patients' family and the country. However, current therapeutical strategies have shown limited effectiveness. Allicin, which is the main composition of garlic, was reported to prevent the learning and memory impairment of AD mouse model. As the mechanism is not clear, in this study, we used the APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice, which express human mutant APP and PS1, to determine the protective effect of allicin on neurons. AD involves a broad range of clinical, cellular, and biochemical manifestations. This has led to many views of AD, e.g. the amyloid, presenilin, oxidative stress, and mitochondrial dysfunction. We confirmed that allicin improves the cognitive function of APP/PS1 double transgenic mice by reducing the expression levels of Aβ, oxidative stress, and improving mitochondrial dysfunction. Application of behavioral, morphological and molecular biology, and other means were conducted to investigate the effect of allicin, which provide an experimental basis for the reliable application of allicin in the treatment of neurodegenerative diseases.