AD is a neurodegenerative disease of complex etiology (29, 30). The formation of neurofibrillary tangles (NFT), neuropil threads, and senile plaques have been implicated in the onset and development of the disease, but the relative causal weight of these and other factors in sporadic AD continues to be debated (30, 31). Although initiation and progression of AD may thus be multifactorial, it has been noted that incidence and regional distribution of NFT are most closely associated with the clinical manifestations of the disease (32, 33). NFT formation is the result of the accumulation of altered components of the neuronal cytoskeleton (34), and it has been suggested that “clogging” of neuronal processes and disruption of long-distance transport may underlie at least some of the cytopathological changes that characterize the disease (19).

We suggest that such cellular changes on…