Review Article
Interaction between Amyloid Beta Toxicity and the PI3K Pathway in Alzheimer's Disease
Hojin Choi and Seong-Ho Koh*
Department of Neurology, Hanyang University Guri Hospital, Korea
- *Corresponding Author:
- Seong-Ho Koh
Department of Neurology, Hanyang University Guri Hospital
153, Gyeongchun-ro, Guri-si
Gyeonggi-do, 11923 Korea
Tel: +82-31-560-2260
E-mail: ksh213@hanyang.ac.kr
Received date: September 20, 2016; Accepted date: October 05, 2016; Published date: October 12, 2016
Citation: Choi H, Koh SH (2016) Interaction between Amyloid Beta Toxicity and the PI3K Pathway in Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 6:269. doi:10.4172/2161-0460.1000269
Copyright: © 2016 Choi H, 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.
Abstract
Alzheimer’s disease (AD) is the most common disease causing dementia. Amyloid beta (Aβ) is well known to play the most important roles in the pathogenesis. Aβ induces neuronal cell death and neuroinflammation. It has been published that Aβ affects numerous intracellular signaling pathways. The phosphatidylinositol-3-kinase (PI3K) pathway associated with neuronal cell survival and various neural stem cell functions. In this review, the interaction between Aβ and the PI3K pathway will be discussed.