期刊
MOLECULAR NEURODEGENERATION
卷 3, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1750-1326-3-9
关键词
-
资金
- CONICYT through a Base Center for Excellence in Science and Technology [13980001]
- Millennium Institute for Fundamental and Applied and Biology (MIFAB)
- DIPUC
Recent evidence supports a neuroprotective role for Wnt signaling in neurodegenerative disorders such as Alzheimer's Disease (AD). In fact, a relationship between amyloid-beta-peptide (A beta)-induced neurotoxicity and a decrease in the cytoplasmic levels of beta-catenin has been observed. Apparently A beta binds to the extracellular cysteine-rich domain of the Frizzled receptor (Fz) inhibiting Wnt/beta-catenin signaling. Cross-talk with other signaling cascades that regulate Wnt/beta-catenin signaling, including the activation of M-1 muscarinic receptor and PKC, the use of Ibuprofen-ChE bi-functional compounds, PPAR alpha, gamma agonists, nicotine and some antioxidants, results in neuroprotection against A beta. These studies indicate that a sustained loss of Wnt signaling function may be involved in the A beta-dependent neurodegeneration observed in Alzheimer's brain. In conclusion the activation of the Wnt signaling pathway could be proposed as a therapeutic target for the treatment of AD.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据