Next Article in Journal
Norethindrone Acetate in the Medical Management of Adenomyosis
Next Article in Special Issue
Neurotransmitter CART as a New Therapeutic Candidate for Parkinson’s Disease
Previous Article in Journal
Intranasal Delivery of Camptothecin-Loaded Tat-Modified Nanomicells for Treatment of Intracranial Brain Tumors
Previous Article in Special Issue
Unlocking the Door to Neuronal Woes in Alzheimer’s Disease: Aβ and Mitochondrial Permeability Transition Pore
Pharmaceuticals 2012, 5(10), 1103-1119; doi:10.3390/ph5101103
Review

Mitochondria-Targeted Antioxidant SS31 Prevents Amyloid Beta-Induced Mitochondrial Abnormalities and Synaptic Degeneration in Alzheimer’s Disease

1,2,* , 1
 and 1
1 Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA 2 Center for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA
* Author to whom correspondence should be addressed.
Received: 5 September 2012 / Revised: 4 October 2012 / Accepted: 8 October 2012 / Published: 16 October 2012
(This article belongs to the Special Issue Mitochondrial Drugs for Neurodegenerative Diseases)
View Full-Text   |   Download PDF [460 KB, uploaded 16 October 2012]   |   Browse Figures

Abstract

In neuronal systems, the health and activity of mitochondria and synapses are tightly coupled. For this reason, it has been postulated that mitochondrial abnormalities may, at least in part, drive neurodegeneration in conditions such as Alzheimer’s disease (AD). Mounting evidence from multiple Alzheimer’s disease cell and mouse models and postmortem brains suggest that loss of mitochondrial integrity may be a key factor that mediates synaptic loss. Therefore, the prevention or rescue of mitochondrial dysfunction may help delay or altogether prevent AD-associated neurodegeneration. Since mitochondrial health is heavily dependent on antioxidant defenses, researchers have begun to explore the use of mitochondria-targeted antioxidants as therapeutic tools to prevent neurodegenerative diseases. This review will highlight advances made using a model mitochondria-targeted antioxidant peptide, SS31, as a potential treatment for AD.
Keywords: Alzheimer’s; SS31; mitochondria; antioxidant Alzheimer’ s; SS31; mitochondria; antioxidant
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Share & Cite This Article

Export to BibTeX |
EndNote


MDPI and ACS Style

Calkins, M.J.; Manczak, M.; Reddy, P.H. Mitochondria-Targeted Antioxidant SS31 Prevents Amyloid Beta-Induced Mitochondrial Abnormalities and Synaptic Degeneration in Alzheimer’s Disease. Pharmaceuticals 2012, 5, 1103-1119.

View more citation formats

Related Articles

Article Metrics

Comments

Citing Articles

[Return to top]
Pharmaceuticals EISSN 1424-8247 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert