It seems likely that the Alzheimer disease (AD)-related dendritic changes addressed in this article are induced by two principally different processes. One process is linked to the plastic response associated with deafferentation, that is, long-lasting transneuronally induced regressive changes in dendritic geometry and structure. The other process is associated with severe alterations of the dendritic- and perikaryal cytoskeleton as seen in neurons with the neurofibrillary pathology of AD, that is, the formation of paired helical filaments formed by hyperphosphorylated microtubule- associated protein tau. As the development of dendritic and cytoskeletal abnormalities are at least mediated by alterations in signal transduction, this article also reviews changes in signal pathways in AD. We also discuss transgenic approaches developed to model and understand cytoskeletal abnormalities.
ASJC Scopus subject areas