Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2005.03.074
Title: Alzheimer's disease: Channeling APP to non-amyloidogenic processing
Authors: Tang, B.L. 
Keywords: β-Amyloid
Alzheimer's disease
Non-steroidal anti-inflammatory drugs
Rho
Rho-associated protein kinase
Statins
Issue Date: 2005
Source: Tang, B.L. (2005). Alzheimer's disease: Channeling APP to non-amyloidogenic processing. Biochemical and Biophysical Research Communications 331 (2) : 375-378. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2005.03.074
Abstract: A good number of pharmacologic agents have over the years been touted as potentially beneficial in either preventing the onset or delay the progression of Alzheimer's disease. These include compounds such as non-steroidal anti-inflammatory drugs (NSAIDs) (HMG-CoA reductase inhibitors (statins)) and flavonoids. The underlying mechanisms for the beneficial effect of these agents are by and large attributed to their ability to reduce β-amyloid (Aβ) production and amyloid load in the brain, via inhibition of amyloidogenic γ-secretase activity. Recent reports have now provided mechanistic insights as to how non-amyloidogenic processing might also be enhanced by these seemingly unrelated treatments. Intriguingly, this appears to involve the inhibition of the activity of small GTPase Rho and its effector, the Rho-associated kinase, ROCK. Dietary caloric restriction (CR) also enhances non-amyloidogenic processing of APP, and this may be part of a more general anti-aging effect of CR mediated by gene expression changes downstream of the activity of the histone deacetylase SIRT1. © 2005 Elsevier Inc. All rights reserved.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/38365
ISSN: 0006291X
DOI: 10.1016/j.bbrc.2005.03.074
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