Abstract
There is increasing evidence that cytoskeletal changes, in particular perturbation of the microtubule (MT) system, play a role in the pathogenesis of Alzheimer disease (AD). The reappearance of the cytoplasmic MT network following treatment with the MT disrupting agent colchicine was investigated in commercially available (Human Genetic Cell Repository, Camden, NJ) fibroblasts derived from 11 patients with familial AD and 11 controls. The AD cells revealed a significant delay in the reappearance of that network following release from treatment with colchicine. Further research with larger samples is needed to determine the sensitivity and specificity of this finding for AD as well as research into the underlying bases for the observed differences.
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