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Biotech / Medical : Biotech Valuation -- Ignore unavailable to you. Want to Upgrade?

To: Biomaven who wrote (39422)	11/29/2012 8:27:37 AM
From: Biotech Jim	Respond to of 52153

Peter- I had not seen the abstract that you posted, but will dig into it. Here is another paper that is of interest along the same lines, published in Neuron: JNK3 perpetuates metabolic stress induced by Aß peptides. Yoon SO, Park DJ, Ryu JC, Ozer HG, Tep C, Shin YJ, Lim TH, Pastorino L, Kunwar AJ, Walton JC, Nagahara AH, Lu KP, Nelson RJ, Tuszynski MH, Huang K. Source Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH 43210, USA. sung.yoon@osumc.edu Abstract Although Aß peptides are causative agents in Alzheimer's disease (AD), the underlying mechanisms are still elusive. We report that Aß42 induces a translational block by activating AMPK, thereby inhibiting the mTOR pathway. This translational block leads to widespread ER stress, which activates JNK3. JNK3 in turn phosphorylates APP at T668, thereby facilitating its endocytosis and subsequent processing. In support, pharmacologically blocking translation results in a significant increase in Aß42 in a JNK3-dependent manner. Thus, JNK3 activation, which is increased in human AD cases and a familial AD (FAD) mouse model, is integral to perpetuating Aß42 production. Concomitantly, deletion of JNK3 from FAD mice results in a dramatic reduction in Aß42 levels and overall plaque loads and increased neuronal number and improved cognition. This reveals AD as a metabolic disease that is under tight control by JNK3. Copyright © 2012 Elsevier Inc. All rights reserved. I have the pdf if anyone wants a copy - send me a PM. Jim