FTO Knockdown Decreases Phosphorylation of Tau in Neuronal Cells; A Potential Model Implicating the Association of FTO with Alzheimer 's Disease
Department of Biomedical Sciences, University of Illinois College of Medicine, Rockford, Illinois, USA
- Corresponding Author:
- Neelu Puri
Department of Biomedical Sciences
University of Illinois College of Medicine
1601 Parkview Avenue, Rockford
Illinois 61107, USA
E-mail: [email protected]
Received date: August 08, 2013; Accepted date: September 17, 2013; Published date: September 30, 2013
Citation: Pitman RT, Fong JT, Stone AL, Devito JT, Puri N (2013) FTO Knockdown Decreases Phosphorylation of Tau in Neuronal Cells; A Potential Model Implicating the Association of FTO with Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 3:125. doi: 10.4172/2161-0460.1000125
Copyright: © 2013 Pitman RT, 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.
Recent genetic studies identify variants within the Fat Mass and Obesity Associated gene (FTO) as important contributors to the development of obesity and suggest a potential link between obesity-associated FTO variants and Alzheimer’s disease (AD). The mechanisms of association regarding FTO and AD are currently unclear; however, obesity is thought to be a well known risk factor for AD. In Alzheimer’s disease hyperphosphorylation of the Tau protein at certain epitopes causes the formation of neurofibrillary tangles due to microtubule collapse. AMP-activated protein kinase (AMPk) is known to phosphorylate Tau, and previous studies have proposed a relationship between FTO knockdown and phosphorylated AMPk (pAMPk). In this study we show that siRNA mediated knockdown of FTO expression in SH-SY5Y neuroblastoma cells decreases Tau phosphorylation. This novel finding suggests the potential for a cellular mechanism that may link FTO function with the development of AD.