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Differential Expression of Kinases and Cell Cycle Proteins in EW

Author

Listed:
  • LFM Scinto

    (Cambridge Neuro diagnostics LTD, UK)

  • Changiz Geula

    (Northwestern University Medical School, USA)

Abstract

The Edinger-Westphal (EW) of the nucleus of cranial nerve III (NCNIII), in contrast to the somatic portion, is an early site of pathology and cell loss in Alzheimer’s disease (AD) and the aging brain. Cell loss in the EW accounts for the observed pupillary hypersensitivity in Alzheimer’s disease (AD) patients to challenge with dilute tropicamide that could potentially serve as a biomarker for AD. The remarkable specificity of pathophysiology and cell loss offers a possible heuristic model by which to study selective cell vulnerability. Neurochemical differences in the somatic and EW portions of the NCNIII may account for their differential vulnerability. The EW pathology consists of phosphorylated tau in oligomers, tangles and neurites. This suggests that neurochemicals shown to be critical to the metabolism and phosphorylation of tau may be differentially expressed at the protein level in these two cell groups. This study examined the cellular expression of Cdc2, Cdk5 kinases, the prolyl isomerase Pin 1 and mitotic phosphoepitopes visualized by MPM-2 using immunohistochemical methods. The results demonstrated that the expression of target neurochemicals differs in the EW as opposed to somatic cell groups and in AD patients versus controls. The variability in the expression of some of these proteins may account for the observed regionally specific pathophysiology and cell loss within the NCNIII and perhaps also other cell groups vulnerable in AD and ageing.

Suggested Citation

  • LFM Scinto & Changiz Geula, 2017. "Differential Expression of Kinases and Cell Cycle Proteins in EW," Open Access Journal of Neurology & Neurosurgery, Juniper Publishers Inc., vol. 2(5), pages 92-100, March.
  • Handle: RePEc:adp:joajnn:v:2:y:2017:i:5:p:92-100
    DOI: 10.19080/OAJNN.2017.02.555599
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    References listed on IDEAS

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    1. Michel Goedert, 1999. "Pinning down phosphorylated tau," Nature, Nature, vol. 399(6738), pages 739-740, June.
    2. Pei-Jung Lu & Gerburg Wulf & Xiao Zhen Zhou & Peter Davies & Kun Ping Lu, 1999. "The prolyl isomerase Pin1 restores the function of Alzheimer-associated phosphorylated tau protein," Nature, Nature, vol. 399(6738), pages 784-788, June.
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