Tripchlorolide Attenuates β-amyloid Generation via Suppressing PPARγ-Regulated BACE1 Activity in N2a/APP695 Cells-Reference-Cited by-同舟云学术

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Tripchlorolide Attenuates β-amyloid Generation via Suppressing PPARγ-Regulated BACE1 Activity in N2a/APP695 Cells

Published:2015-11-19 Issue:9 Volume:53 Page:6397-6406
ISSN:0893-7648
Container-title:Molecular Neurobiology
language:en
Short-container-title:Mol Neurobiol

Author:

Lin Nan,Chen Li-min,Pan Xiao-dong,Zhu Yuan-gui,Zhang Jing,Shi Yan-qing,Chen Xiao-chun

Funder

Major Project of Fujian Science and Technology Bureau

National Natural Science Grant of China

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Subject

Neuroscience (miscellaneous),Cellular and Molecular Neuroscience,Neurology

Link

http://link.springer.com/article/10.1007/s12035-015-9542-2/fulltext.html

Reference35 articles.

1. Cai H, Wang Y, McCarthy D, Wen H, Borchelt DR, Price DL, Wong PC (2001) BACE1 is the major beta-secretase for generation of Abeta peptides by neurons. Nat Neurosci 4(3):233–234. doi: 10.1038/85064

2. Hardy J, Selkoe DJ (2002) The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 297(5580):353–356. doi: 10.1126/science

3. Stockley JH, O’Neill C (2008) Understanding BACE1: essential protease for amyloid-beta production in Alzheimer’s disease. Cell Mol Life Sci 65(20):3265–3289. doi: 10.1007/s00018-008-8271-3

4. Luo Y, Bolon B, Kahn S, Bennett BD, Babu-Khan S, Denis P, Fan W, Kha H et al (2001) Mice deficient in BACE1, the Alzheimer’s beta-secretase, have normal phenotype and abolished beta-amyloid generation. Nat Neurosci 4(3):231–232. doi: 10.1038/85059

5. Ohno M, Sametsky EA, Younkin LH, Oakley H, Younkin SG, Citron M, Vassar R, Disterhoft JF (2004) BACE1 deficiency rescues memory deficits and cholinergic dysfunction in a mouse model of Alzheimer’s disease. Neuron 41(1):27–33

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