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Cyclin Dependent Kinase 11, Neuroinflammation and Alzheimer's Disease: A Review | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

Cyclin Dependent Kinase 11, Neuroinflammation and Alzheimer's Disease: A Review

Vladan Bajic1*, Boban Stanojevic1, Lada Zivkovic2, Andrea Cabarkapa2, George Perry3, Thomas Arendt4 and Biljana Spremo-Potparevic2
1Laboratory for Radiobiology and Molecular Genetics, “Vinca” Institute of Nuclear Sciences, University of Belgrade, Belgrade, Serbia
2Institute of Physiology, Department of Biology, Faculty of Pharmacy, University of Belgrade, Serbia
3College of Sciences, University of Texas at San Antonio, San Antonio, Texas, USA
4Paul-Flechsig- Institute for Brain Research, University of Leipzig, School of medicine, Leipzig, Germany
Corresponding Author : Bajic Vladan, PhD
Professor of Research
Institute for Nuclear Research “Vinca”
Department of Radiobiology and Molecular Genetics
University of Belgrade, PO 080, Belgrade, Serbia
Tel: 381-113610314
Email: [email protected]
Received: February 10, 2015; Accepted: March 03, 2015; Published: March 10, 2015
Citation: Bajic V, Stanojevic B, Zivkovic L, Cabarkapa A, Perry G, et al. (2015) Cyclin Dependent Kinase 11, Neuroinflammation and Alzheimer's Disease: A Review. J Clin Cell Immunol 6:305. doi:10.4172/2155-9899.1000305
Copyright: © 2015 Bajic V et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Aging is the main risk factor for Alzheimer’s disease (AD). With aging, inflammation has been recognized as potential trigger for starting the neurodegenerative cascade leading to neuronal death. Before Aβ and tau accumulation, evidence has put alterations of the cell cycle at the core of these processes.
Still, a number of features of the cell cycle re-entry phenotype have remained elusive to the role of ectopic protein expression in the process of neuroinflammation and consequently neuronal cell death. Recently, a novel cyclin dependent kinase CDK11 has been found to be involved in astrocyte mediated inflammatory response and Alzheimer’s disease.
In this review, we aim to establish the missing part of the puzzle between neuroinflammation and APP / Aβ deregulation in AD by evaluating the role of a cyclin, CDK11.
CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.