Cited by 230Mitochondrial Function and PathologyAutophagy in Disease and TherapyParkinson's Disease Mechanisms and Treatments

Mitochondrial Medicine for Aging and Neurodegenerative Diseases

Open access
Reddy, P. Hemachandra·2008·NeuroMolecular Medicine

Abstract

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.

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Crossref · 10.1007/s12017-008-8044-z

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  • While aberrant Aβ42 accumulation begins in endosomes, mitochondrial Aβ may be a critical contributor in the pathological cascade leading to neuronal dysfunction and pathology in AD.

    “Thus, while aberrant Aβ42 accumulation begins in endosomes, mitochondrial Aβ may be a critical contributor in the pathological cascade leading to neuronal dysfunction and pathology in AD [33, 103, 149].”

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Authors
Reddy, P. H.
Affiliations
Oregon Health & Science University (US)
Corresponding author
Reddy, P. Hemachandra
Venue
NeuroMolecular Medicine
Published
2008-06-20
Volume
10
Issue
4
Pages
291-315
ISSN
  • 1535-1084 (ISSN-L)
  • 1559-1174
OpenAlex
W2146282250
Cited by
230
References
223
Citations by year
2026: 8 · 2025: 6 · 2024: 13 · 2023: 11 · 2022: 15 · 2021: 29 · 2020: 13 · 2019: 11 · 2018: 13 · 2017: 11 · 2016: 14 · 2015: 8 · 2014: 13 · 2013: 13 · 2012: 8
FWCI
1.08
Type
journal article
Language
en
Open access
Locations
  • NeuroMolecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Aging (AG026051, R03AG026051, R01AG028072, AG028072)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
mitochondria, mitochondrial dysfunction, aging, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich's ataxia, electron transport chain, free radicals, mitochondrial protein transport, protein mutants, cell death
MeSH terms
Aging, Animals, Antioxidants, Energy Metabolism, Humans, Mitochondria, Nerve Tissue Proteins, Oxidative Stress, Neuroprotective Agents, Neurodegenerative Diseases, Mitochondrial Proteins, Mitochondrial Diseases

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