Cited by 100Mitochondrial Function and PathologyParkinson's Disease Mechanisms and TreatmentsNeurological Disorders and Treatments

Development of Mitochondria‐targeted Aromatic‐cationic Peptides for Neurodegenerative Diseases

Szeto, Hazel H.·2008·Annals of the New York Academy of Sciences

Abstract

Mitochondrial impairment and oxidative damage are intimately involved in the pathogenesis of neurodegenerative diseases. Which is the initiating event is probably irrelevant because each can set into motion a self‐sustaining and amplifying feed‐forward cycle between reactive oxygen species (ROS) generation and mitochondrial impairment. Recent approaches to the development of neuroprotective agents have therefore targeted mitochondria protection and/or reduction of oxidative stress. There are several hurdles in the quest for neuroprotective drugs. The difficulties include penetration of the blood–brain barrier and delivery of drugs to mitochondria. Here we describe a novel class of mitochondria‐targeted peptides that can promote mitochondrial function, reduce mitochondrial ROS generation, inhibit mitochondrial permeability transition, and prevent apoptosis and necrosis. These peptides can readily penetrate the blood–brain barrier and have demonstrated efficacy in animal models of Parkinson's disease and amyotrophic lateral sclerosis.

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Crossref · 10.1196/annals.1427.013

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Authors
Szeto, H. H.
Affiliations
Cornell University (US)
Corresponding author
Szeto, Hazel H.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2008-12
Volume
1147
Issue
1
Pages
112-121
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W2082966118
Cited by
100
References
66
Citations by year
2026: 2 · 2025: 3 · 2024: 6 · 2023: 3 · 2022: 7 · 2021: 4 · 2020: 5 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 7 · 2015: 3 · 2014: 8 · 2013: 10 · 2012: 4
FWCI
0.69
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Drug Abuse (P01DA008924)
  • National Institute of Neurological Disorders and Stroke (R21NS048295)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
mitochondria-targeted peptide, neurodegenerative diseases, neuroprotection, mitochondrial dysfunction, oxidative stress, reactive oxygen species, mitochondrial permeability transition, blood-brain barrier penetration, Parkinson's disease, amyotrophic lateral sclerosis, apoptosis, necrosis
MeSH terms
Adenosine Triphosphate, Animals, Cations, Humans, Mitochondria, Peptides, Reactive Oxygen Species, Oxidative Stress, Neurodegenerative Diseases, Models, Animal

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