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  1. These interesting papers by Tsai et al. and Moolman et al. further support the idea that neuronal processes are important sites of damage during AD pathogenesis. A major question, of course, is why are processes being damaged? Is there any damage prior to plaques? Both papers consider the possibility that increases in levels of soluble Aβ may be important. In addition, increasing evidence supports a role for intraneuronal Aβ accumulation in the degeneration of processes (for example, see Wirths et al., 2004, for a current review).