Export file:

Format

  • RIS(for EndNote,Reference Manager,ProCite)
  • BibTex
  • Text

Content

  • Citation Only
  • Citation and Abstract

Alzheimer’s Disease: A short introduction to the calmodulin hypothesis

1 Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada M5S 3G5
2 Department of Biology, University of Toronto Mississauga, Mississauga, Ontario, Canada L5L 1C6

Special Issues: Alzheimer’s Disease

At the cellular level, Alzheimer’s disease (AD) is characterized by the presence of intracellular plaques containing amyloid beta (Aβ) protein and neurofibrillary tangles consisting of phospho-tau (p-tau). These biomarkers are considered to contribute, at least in part, to the neurodegenerative events of the disease. But the accumulation of plaques and tangles is widely considered to be a later event with other factors likely being the cause of the disease. Calcium dysregulation—the unregulated accumulation of calcium ions—in neurons is an early event that underlies neurodegeneration. In 2002, O’Day and Myre extended this “Calcium Hypothesis” to include calmodulin (CaM) the primary target of calcium, suggesting the “Calmodulin Hypothesis” as an updated alternative. Here we overview the central role of CaM in the formation of the classic hallmarks of AD: plaques and tangles. Then some insight into CaM’s binding to various risk factor proteins is given followed by a short summary of specific receptors and channels linked to the disease that are CaM binding proteins. Overall, this review emphasizes the diversity of Alzheimer’s-linked CaM-binding proteins validating the hypothesis that CaM operates critically at all stages of the disease and stands out as a potential primary target for future research.
  Figure/Table
  Supplementary
  Article Metrics
Download full text in PDF

Export Citation

Article outline

Copyright © AIMS Press All Rights Reserved