A Butyrolactone Derivative 3BDO Alleviates Memory Deficits and Reduces Amyloid-beta Deposition in an A beta PP/PS1 Transgenic Mouse Model

作者：Wei LiFei; Yang Hui; Xie ZhaoHong; Yang ShaoNan; Yang HongNa; Zhao CuiPing; Wang Ping; Xu ShunLiang; Miao JunYing; Zhao BaoXiang; Bi JianZhong^*

来源：Journal of Alzheimer's Disease, 2012, 30(3): 531-543.

DOI：10.3233/JAD-2012-111985

• A beta PP/PS1 mouse
• Alzheimer's disease
• amyloid-beta peptides
• autophagy
• insulin-degrading enzyme
• neprilysin

Excessive extracellular deposition of amyloid- peptide (A beta) in the brain is the pathological hallmark of Alzheimer's disease (AD). Cumulative evidence indicates that autophagy is involved in the metabolism of A beta and pathogenesis of AD. However, the molecular mechanism underlying the pathogenesis of AD is not yet well defined, and there has been no effective treatment for AD. We recently found that long-term treatment with a butyrolactone derivative 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3 H)-one (3BDO) increased levels of insulin-degrading enzyme and neprilysin, suppressed autophagy via an mTOR pathway, lowered levels of A beta, and prevented AD-like cognitive deficits in the A beta PP/PS1 double transgenic mouse model. Therefore, our findings suggest that 3BDO may be beneficial in the prevention and treatment of AD.

• 出版日期2012
• 单位山东大学