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The confirmation of Aβ phosphorylation in AD brains in this paper and the suggested contribution to AD pathology supports a role for phosphorylated Aβ.
After noting that phosphorylation defects were a major pathological feature of AD, I discovered that Aβ itself could be phosphorylated, and that the phosphorylated Aβ form was significantly more toxic to neuronal cells (Milton, 2001). I suggested that Aβ becomes phosphorylated inside the neuronal cells of AD patients (Milton, 2001; Milton, 2005a). This modification causes the compound to become highly toxic, killing neurons. As a result of the neuronal damage, Aβ plaques build up around the dead cells, which is a normal response to cell death. It is possible that not all Aβ-plaques are toxic, but that pAβ plays a direct role in the formation of the toxic species, which cause further neural degeneration.
The extracellular phosphorylation of Aβ documented here provides another source of the toxin and removes the necessity for cellular uptake prior to the phosphorylation of Aβ.
It should be noted that the phosphorylated...