Affiliations: [a] Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China | [b] Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, Institute of Developmental Biology, School of Life Science, Shandong University, Jinan, China | [c] Institute of Organic Chemistry, School of Chemistry and Chemical Engineering, Shandong University, Jinan, China
Correspondence:
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Correspondence to: BaoXiang Zhao, Institute of Organic Chemistry, School of Chemistry and Chemical Engineering, Shandong University, Jinan 250100, China. Tel.: +86 531 88366425; Fax: +86 531 88564464; E-mail: [email protected] and JianZhong Bi, Department of Neural Medicine, Second Hospital of Shandong University, Jinan 250033, China. Tel.: +86 531 85875006; Fax: +86 531 88962544; E-mail: [email protected].
Abstract: Excessive extracellular deposition of amyloid- peptide (Aβ) in the brain is the pathological hallmark of Alzheimer's disease (AD). Cumulative evidence indicates that autophagy is involved in the metabolism of Aβ 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 Aβ, and prevented AD-like cognitive deficits in the AβPP/PS1 double transgenic mouse model. Therefore, our findings suggest that 3BDO may be beneficial in the prevention and treatment of AD.
