AI Chat Paper
Note: Please note that the following content is generated by AMiner AI. SciOpen does not take any responsibility related to this content.
{{lang === 'zh_CN' ? '文章概述' : 'Summary'}}
{{lang === 'en_US' ? '中' : 'Eng'}}
Chat more with AI
PDF (941.9 KB)
Collect
Submit Manuscript AI Chat Paper
Show Outline
Outline
Show full outline
Hide outline
Outline
Show full outline
Hide outline
Review Article | Open Access

Mitochondria as a therapeutic target in Alzheimer’s disease

Jian Wang, Guo-Jun Chen( )
Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, 1 Youyi Road, Chongqing 400016, China

Peer review under responsibility of Chongqing Medical University.

Show Author Information

Abstract

Alzheimer’s disease (AD) remains the most common neurodegenerative disease characterized by β-amyloid protein (Aβ) deposition and memory loss. Studies have shown that mitochondrial dysfunction plays a crucial role in AD, which involves oxidative stress-induced respiratory chain dysfunction, loss of mitochondrial biogenesis, defects of mitochondrial dynamics and mtDNA mutations. Thus mitochondria might serve as drug therapy target for AD. In this article, we first briefly discussed mitochondrial theory in the development of AD, and then we summarized recent advances of mitochondrial abnormalities in AD pathology and introduced a series of drugs and techniques targeting mitochondria. We think that maintaining mitochondrial function may provide a new way of thinking in the treatment of AD.

References

【1】
【1】
 
 
Genes & Diseases
Pages 220-227

{{item.num}}

Comments on this article

Go to comment

< Back to all reports

Review Status: {{reviewData.commendedNum}} Commended , {{reviewData.revisionRequiredNum}} Revision Required , {{reviewData.notCommendedNum}} Not Commended Under Peer Review

Review Comment

Close
Close
Cite this article:
Wang J, Chen G-J. Mitochondria as a therapeutic target in Alzheimer’s disease. Genes & Diseases, 2016, 3(3): 220-227. https://doi.org/10.1016/j.gendis.2016.05.001

775

Views

6

Downloads

44

Crossref

N/A

Web of Science

43

Scopus

0

CSCD

Received: 24 April 2016
Accepted: 30 May 2016
Published: 16 June 2016
© 2016 Chongqing Medical University.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).