These authors contributed equally to this work.
Perinatal exposure to di-(2-ethylhexyl)-phthalate leads to cognitive dysfunction and phospho-tau level increase in aged rats
Version of Record online: 19 MAY 2012
Copyright © 2012 Wiley Periodicals, Inc.
Volume 29, Issue 5, pages 596–603, May 2014
How to Cite
Sun, W., Ban, J.-B., Zhang, N., Zu, Y.-K. and Sun, W.-X. (2014), Perinatal exposure to di-(2-ethylhexyl)-phthalate leads to cognitive dysfunction and phospho-tau level increase in aged rats. Environ. Toxicol., 29: 596–603. doi: 10.1002/tox.21785
- Issue online: 7 APR 2014
- Version of Record online: 19 MAY 2012
- Manuscript Accepted: 22 APR 2012
- Manuscript Revised: 12 APR 2012
- Manuscript Received: 10 JAN 2012
- National Natural Science Foundation of China. Grant Number: 30600485
- Alzheimer's disease;
Di-(2-ethylhexyl)-Phthalate (DEHP) can affect glucose and insulin homeostasis in periphery and lead to insulin resistance, especially exposure of DEHP during critical developmental period. Given the potential relationship between insulin resistance and pathogenesis of Alzheimer's disease (AD) in elderly life, we investigated the relationship between perinatal DEHP exposure and AD pathogenesis. Our results suggested that perinatal exposure to DEHP can affect the expression of insulin and insulin-Akt- GSK-3β signal pathway in hippocampus. Furthermore, impaired cognitive ability and increased level of phospho-Tau was observed in DEHP-exposed rat offspring (1.25 ± 0.11 vs. 0.47 ± 0.07, P < 0.05). The present study demonstrates that perinatal exposure to DEHP may be a potential risk factor for AD pathogenesis associated with insulin resistance and insulin metabolism disorder in the hippocampus. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 596–603, 2014.