NeuroMolecular Medicine

, Volume 10, Issue 4, pp 291–315 | Cite as

Mitochondrial Medicine for Aging and Neurodegenerative Diseases

  • P. Hemachandra ReddyEmail author
Review Paper


Mitochondria are key cytoplasmic organelles, responsible for generating cellular energy, regulating intracellular calcium levels, altering the reduction-oxidation potential of cells, and regulating cell death. Increasing evidence suggests that mitochondria play a central role in aging and in neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and Freidriech ataxia. Further, several lines of evidence suggest that mitochondrial dysfunction is an early event in most late-onset neurodegenerative diseases. Biochemical and animal model studies of inherited neurodegenerative diseases have revealed that mutant proteins of these diseases are associated with mitochondria. Mutant proteins are reported to block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins and disrupt the electron transport chain, induce free radicals, cause mitochondrial dysfunction, and, ultimately, damage neurons. This article discusses critical issues of mitochondria causing dysfunction in aging and neurodegenerative diseases, and discusses the potential of developing mitochondrial medicine, particularly mitochondrially targeted antioxidants, to treat aging and neurodegenerative diseases.


Amyloid beta Alzheimer's disease Amyotrophic lateral sclerosis Amyloid precursor protein Adenosine triphosphate Caloric restricted Electron transport chain FRDA Freidriech ataxia Hydrogen peroxide Huntington's disease Mitochondrial DNA Peroxisome proliferator activated receptor–coactivator Superoxide radical Oxidative phosphorylation Parkinson's disease Reactive oxygen species SS peptide 


Amyloid beta


Alzheimer’s disease


Amyotrophic lateral sclerosis


Amyloid precursor protein


Adenosine triphosphate


Caloric restricted


Electron transport chain


Freidriech ataxia


Hydrogen peroxide


Huntington’s disease


Mitochondrial DNA


Peroxisome proliferator-activated receptor- coactivator


Superoxide radical


Oxidative phosphorylation


Parkinson’s disease


Reactive oxygen species

SS peptide

Szeto-Schiller peptide



I sincerely thank Drs. Maria Manczak and Wei Zhao (postdoctoral scientists in the lab) for their technical assistance of MitoQ and SS-31 treatments of N2a cells. The research presented in this article was supported by grants from the American Federation for Aging Research, National Institutes of Health (AG028072 and AG026051), and KaloBios Pharmaceuticals, Inc.


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Copyright information

© Humana Press 2008

Authors and Affiliations

  1. 1.Neurogenetics Laboratory, Neurological Sciences InstituteOregon Health & Science UniversityBeavertonUSA

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