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
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.