tomorrows news today, page-4

Stocky, just one more thing. I am not really qualified to quote on the findings of the Prana research and rely on peer group reviwed publications and posts like this one. This is in response to the Prana publication outlining the previously unknown function of APP. You will notice if you cross check that in those world top 100 from Neurology, that the late Mark Smith and George Perry rank 2 & 3 in one of those lists. I have posted this before, but take note of "the repairative pathway of Amyloid cannot be questioned" These guys are the very elite of AD researchers and to back Prana?Ls discovery in this unreserved manner speaks volumes to me. It may put to rest your concerns about the fact they are playing with iron levels.

"Comment by George Perry, Xiongwei Zhu, Akihiko Nunomura, Paula I. Moreira, Rudy J. Castellani, Mark A. Smith
Amyloid-?? Protein Precursor at the Center of Iron and Redox Homeostasis: The Amyloid Reparative Cascade Hypothesis
It is an overused statement that the brain is poorly protected from oxidative stress. That statement is now put to rest by the elegant and meticulous work of Ashley Bush and colleagues (Duce et al., 2010). Bush has shown the amyloid-?? protein precursor (A??PP) has ferroxidase activities comparable to ceruloplasmin or ferritin. Ferroxidase, by stabilizing Fe+3, is at the center of protecting cells from Fe+2/Fe+3 cycling, with consequent hydroxyl radical production. Additionally, ferroxidase activity is essential for iron transport and tissue response to injury. These findings explain why, in the face of increased oxidative damage and response, ceruloplasmin is not induced (Castellani et al., 1999). A??PP, therefore, represents a unique system, adapted to the brain, to cope with iron homeostasis. These results suggest that the iron deposits surrounding A?? deposits are due to ferroxidase activity rather than iron binding (Dong et al., 2003). It is not surprising that A??PP is a critical marker of axonal injury (Cochran et al., 1991) and repair, as both ceruloplasmin and ferritin play similar roles. When seen together with the antioxidant role of A?? through copper chelation (Hayashi et al., 2007), the reparative power of the amyloid pathway cannot be questioned (Rottkamp et al., 2001; Castellani et al., 2009). "

http://www.alzforum.org/new/detail.asp?id=1775

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