Thannickal TC. Hypocretin (orexin) pathology in Alzheimer’s disease. World J Neurol 2015; 5(3): 64-67 [DOI: 10.5316/wjn.v5.i3.64]
Corresponding Author of This Article
Thomas C Thannickal, PhD, Associate Researcher, Veterans Administration Greater Los Angeles Healthcare System, Neurobiology Research (151A3), North Hills, 16111 Plummer St., CA 91343, United States. thomastc@ucla.edu
Research Domain of This Article
Neurosciences
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Neurol. Sep 28, 2015; 5(3): 64-67 Published online Sep 28, 2015. doi: 10.5316/wjn.v5.i3.64
Hypocretin (orexin) pathology in Alzheimer’s disease
Thomas C Thannickal
Thomas C Thannickal, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA 90025, United States
Thomas C Thannickal, Veterans Administration Greater Los Angeles Healthcare System, Neurobiology Research (151A3), North Hills, CA 91343, United States
Author contributions: Thannickal TC solely contributed to this work.
Conflict-of-interest statement: None.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Thomas C Thannickal, PhD, Associate Researcher, Veterans Administration Greater Los Angeles Healthcare System, Neurobiology Research (151A3), North Hills, 16111 Plummer St., CA 91343, United States. thomastc@ucla.edu
Telephone: +1-818-8917711 Fax: +1-818-8959575
Received: January 29, 2015 Peer-review started: January 30, 2015 First decision: April 27, 2015 Revised: June 4, 2015 Accepted: July 16, 2015 Article in press: July 17, 2015 Published online: September 28, 2015 Processing time: 244 Days and 3.5 Hours
Abstract
Alzheimer’s disease (AD) is a growing health problem. It has enormous public health impact. Sleep problems show an early component of this disease. Hypocretin has a major function in sleep-wake cycle. The total number of hypocretin neurons in the normal humans ranges from 51000-83000, located exclusively in the hypothalamus. Deficiency in hypocretins neurotransmission results in narcolepsy, Parkinson’s disease, and other neurological and psychological disorders. Cerebrospinal fluid (CSF) hypocretin levels were directly related with t-tau protein amount in AD. Increased hypocretin CSF in AD suggest that hypocretin is involved in the mechanism of AD pathology.
Core tip: Hypocretin plays an important role in the control of sleep-wake cycle. Increased hypocretin levels in Alzheimer’s disease patients suggest hypocretin system is involved during development of the disease symptoms.
