Int. J. Mol. Sci. 2013, 14(10), 20037-20047; doi:10.3390/ijms141020037
Review

New Insights in the Pathogenesis of Multiple Sclerosis—Role of Acrolein in Neuronal and Myelin Damage

1,2email and 1,3,* email
1 Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA 2 Indiana University School of Medicine, Indianapolis, IN 46202, USA 3 Department of Basic Medical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA
* Author to whom correspondence should be addressed.
Received: 13 August 2013; in revised form: 17 September 2013 / Accepted: 18 September 2013 / Published: 9 October 2013
(This article belongs to the Special Issue Pathology and Treatment of Central Nervous System Diseases)
PDF Full-text Download PDF Full-Text [156 KB, Updated Version, uploaded 11 October 2013 17:43 CEST]
The original version is still available [184 KB, uploaded 9 October 2013 14:42 CEST]
Abstract: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) characterized by an inappropriate inflammatory reaction resulting in widespread myelin injury along white matter tracts. Neurological impairment as a result of the disease can be attributed to immune-mediated injury to myelin, axons and mitochondria, but the molecular mechanisms underlying the neuropathy remain incompletely understood. Incomplete mechanistic knowledge hinders the development of therapies capable of alleviating symptoms and slowing disease progression in the long-term. Recently, oxidative stress has been implicated as a key component of neural tissue damage prompting investigation of reactive oxygen species (ROS) scavengers as a potential therapeutic option. Despite the establishment of oxidative stress as a crucial process in MS development and progression, ROS scavengers have had limited success in animal studies which has prompted pursuit of an alternative target capable of curtailing oxidative stress. Acrolein, a toxic β-unsaturated aldehyde capable of initiating and perpetuating oxidative stress, has been suggested as a viable point of intervention to guide the development of new treatments. Sequestering acrolein using an FDA-approved compound, hydralazine, offers neuroprotection resulting in dampened symptom severity and slowed disease progression in experimental autoimmune encephalomyelitis (EAE) mice. These results provide promise for therapeutic development, indicating the possible utility of neutralizing acrolein to preserve and improve neurological function in MS patients.
Keywords: multiple sclerosis; acrolein; oxidative stress; autoimmune; neurodegeneration; demyelination; axonal injury; EAE; hydralazine

Article Statistics

Load and display the download statistics.

Citations to this Article

Cite This Article

MDPI and ACS Style

Tully, M.; Shi, R. New Insights in the Pathogenesis of Multiple Sclerosis—Role of Acrolein in Neuronal and Myelin Damage. Int. J. Mol. Sci. 2013, 14, 20037-20047.

AMA Style

Tully M, Shi R. New Insights in the Pathogenesis of Multiple Sclerosis—Role of Acrolein in Neuronal and Myelin Damage. International Journal of Molecular Sciences. 2013; 14(10):20037-20047.

Chicago/Turabian Style

Tully, Melissa; Shi, Riyi. 2013. "New Insights in the Pathogenesis of Multiple Sclerosis—Role of Acrolein in Neuronal and Myelin Damage." Int. J. Mol. Sci. 14, no. 10: 20037-20047.

Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert