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©2013 Baishideng Publishing Group Co., Limited. All rights reserved.
A common genetic mechanism underlying susceptibility to posttraumatic stress disorder
Zhen He, Sherry A Ferguson, Merle G Paule, Division of Neurotoxicology, National Center for Toxicological Research, Food and Drug Administration, Jefferson, AR 72079-9502, United States
Zhen He, Li Cui, Bei He, Department of Neurology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, United States
Author contributions: He Z reviewed literature and designed the project, conducted laser-assisted microdissection (LAM) and microarray experiments, and wrote the manuscript; Cui L optimized the experimental protocols and performed single cell collection with LAM and microarray data analysis; He B settled down the RAN quality-assurance method in the lab, determined sample RNA amount and quality, and revised the manuscript; Ferguson SA re-reviewed literature and significantly edited the manuscript; Paule MG contributed to the conceptual design and significantly edited the manuscript.
Supported by In part by the Mayo Foundation, Mayo Clinic Jacksonville, Florida; National Center for Toxicological Research/FDA (Protocol P00710) to He Z; in part supported by a UAMS Hornick Award to Cui L
Correspondence to: Zhen He, MD, PhD, Division of Neurotoxicology, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, Arkansas 72079-9502, United States. zhen.he@fda.hhs.gov
Telephone: +1-870-5437053 Fax: +1-870-5437745
Received: June 13, 2013
Revised: July 27, 2013
Accepted: August 20, 2013
Published online: September 28, 2013
Revised: July 27, 2013
Accepted: August 20, 2013
Published online: September 28, 2013
Core Tip
Core tip: We propose that susceptibility to post-traumatic stress disorder (PTSD) may be determined, in part, by aberrant microtubule-associated protein tau expression in neurons of critical brain structures. We review several lines of evidence to support this novel hypothesis. In addition, we review types of PTSD, namely non-classical PTSD, induced by various medical conditions and address this issue of why non-classical PTSD can be reliably elicited. To verify our hypothesis, we propose to use animal models of PTSD combined with laser-assisted/capture microdissection and microarray analysis to examine gene expression changes in selected cellular elements in response to the occurrence of PTSD.