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A butyrolactone derivative 3BDO alleviates memory deficits and reduces amyloid-β deposition in an AβPP/PS1 transgenic mouse model.
J Alzheimers Dis. 2012; 30(3):531-43.JA

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.

Authors+Show Affiliations

Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22451314

Citation

Wei, LiFei, et al. "A Butyrolactone Derivative 3BDO Alleviates Memory Deficits and Reduces Amyloid-β Deposition in an AβPP/PS1 Transgenic Mouse Model." Journal of Alzheimer's Disease : JAD, vol. 30, no. 3, 2012, pp. 531-43.
Wei L, Yang H, Xie Z, et al. A butyrolactone derivative 3BDO alleviates memory deficits and reduces amyloid-β deposition in an AβPP/PS1 transgenic mouse model. J Alzheimers Dis. 2012;30(3):531-43.
Wei, L., Yang, H., Xie, Z., Yang, S., Yang, H., Zhao, C., Wang, P., Xu, S., Miao, J., Zhao, B., & Bi, J. (2012). A butyrolactone derivative 3BDO alleviates memory deficits and reduces amyloid-β deposition in an AβPP/PS1 transgenic mouse model. Journal of Alzheimer's Disease : JAD, 30(3), 531-43. https://doi.org/10.3233/JAD-2012-111985
Wei L, et al. A Butyrolactone Derivative 3BDO Alleviates Memory Deficits and Reduces Amyloid-β Deposition in an AβPP/PS1 Transgenic Mouse Model. J Alzheimers Dis. 2012;30(3):531-43. PubMed PMID: 22451314.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A butyrolactone derivative 3BDO alleviates memory deficits and reduces amyloid-β deposition in an AβPP/PS1 transgenic mouse model. AU - Wei,LiFei, AU - Yang,Hui, AU - Xie,ZhaoHong, AU - Yang,ShaoNan, AU - Yang,HongNa, AU - Zhao,CuiPing, AU - Wang,Ping, AU - Xu,ShunLiang, AU - Miao,JunYing, AU - Zhao,BaoXiang, AU - Bi,JianZhong, PY - 2012/3/28/entrez PY - 2012/3/28/pubmed PY - 2012/10/17/medline SP - 531 EP - 43 JF - Journal of Alzheimer's disease : JAD JO - J Alzheimers Dis VL - 30 IS - 3 N2 - 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. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/22451314/A_butyrolactone_derivative_3BDO_alleviates_memory_deficits_and_reduces_amyloid_��_deposition_in_an_A��PP/PS1_transgenic_mouse_model_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-2012-111985 DB - PRIME DP - Unbound Medicine ER -