3-benzyl-5-((2-nitrophenoxy)methyl)dihydrofuran-2(3h)-one and Alzheimer-Disease

3-benzyl-5-((2-nitrophenoxy)methyl)dihydrofuran-2(3h)-one has been researched along with Alzheimer-Disease* in 1 studies

Other Studies

1 other study(ies) available for 3-benzyl-5-((2-nitrophenoxy)methyl)dihydrofuran-2(3h)-one and Alzheimer-Disease

Article	Year
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, 2012, Volume: 30, Issue:3 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. Topics: 4-Butyrolactone; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Autophagy; Brain; Disease Models, Animal; Insulysin; Maze Learning; Memory Disorders; Mice; Mice, Transgenic; Neprilysin; Presenilin-1; Signal Transduction	2012

Article

Year

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, 2012, Volume: 30, Issue:3

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.

Topics: 4-Butyrolactone; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Autophagy; Brain; Disease Models, Animal; Insulysin; Maze Learning; Memory Disorders; Mice; Mice, Transgenic; Neprilysin; Presenilin-1; Signal Transduction

2012