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  1. A large body of work has shown regression/decreased plastic capacity in dendrites in AD (Flood and Coleman, 1990; Buell and Coleman, 1979; de Ruiter et al., 1987; Braak et al., 1994). It has often been assumed that these dendritic deficits related to cytoskeletal disruption consequent to tau phosphorylation. More recent evidence links functional deficits to Aβ oligomers (e.g., Lesne et al., 2006) as well as Aβ itself (Kelly et al., 2005). The present paper reintroduces fibrillar Aβ, now as a culprit in dendritic regression. Do the many flavors of Aβ have different consequences? Or are we faced with a need to more completely specify the forms of Aβ that are producing effects determined by optimally sensitive methods?


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