The DOI matches its Crossref record; 223 of the 224 references it cites were found in a registry or an index.
Mitochondrial Medicine for Aging and Neurodegenerative Diseases
Open accessAbstract
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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“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].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [149]
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Metadata
- 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
- PMC
- PMC3235551
- OpenAlex
- W2146282250
- Cited by
- 230
- References
- 224
- 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
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Clinical 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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