Neuronal polo-like kinase in Alzheimer disease indicates cell cycle changes

Peggy L.R. Harris, Xiongwei Zhu, Christina Pamies, Catherine Rottkamp, Hossein A. Ghanbari, Andrew McShea, Yang Feng, Douglas K. Ferris, Mark A. Smith

Research output: Contribution to journalArticle

42 Scopus citations

Abstract

Neurons of adults apparently lack the components necessary to complete the cell division process. Therefore, in Alzheimer disease, the increased expression of cell cycle-related proteins in degenerating neurons likely leads to an interrupted mitotic process associated with cytoskeletal abnormalities and, ultimately, neuronal degeneration. In this study, to further delineate the role of mitotic processes in the pathogenesis of Alzheimer disease, we undertook a study of polo-like kinase (Plk), a protein that plays a crucial role in the cell cycle. Our results show disease-related increases in Plk in susceptible hippocampal and cortical neurons in comparison to young or age-matched controls. An increase in neuronal Plk further implicates aberrations in cell cycle control in the pathogenesis of Alzheimer disease and provides a novel mechanistic basis for therapeutic intervention. Copyright (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)837-841
Number of pages5
JournalNeurobiology of Aging
Volume21
Issue number6
DOIs
StatePublished - Dec 28 2000
Externally publishedYes

Keywords

  • Alzheimer disease
  • Cell cycle
  • Cytoskeleton
  • Pathogenesis
  • Phosphorylation
  • Polo-like kinase
  • tau

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

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    Harris, P. L. R., Zhu, X., Pamies, C., Rottkamp, C., Ghanbari, H. A., McShea, A., Feng, Y., Ferris, D. K., & Smith, M. A. (2000). Neuronal polo-like kinase in Alzheimer disease indicates cell cycle changes. Neurobiology of Aging, 21(6), 837-841. https://doi.org/10.1016/S0197-4580(00)00218-9