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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Citations
Cites
Items 201–223 of 223
Siler‐Marsiglio, K. I., Pan, Q., Paiva, M., Madorsky, I., Khurana, N. C., & Heaton, M. B. (2005) · Brain Research · doi:10.1016/j.brainres.2005.06.030 · Cited by 75
Reddy, P. H., & McWeeney, S. K. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.04.014 · Cited by 73
Self-citationMitochondrial DNA Mutations and Apoptosis in Mammalian Aging
Kujoth, G. C., Leeuwenburgh, C., & Prolla, T. A. (2006) · Cancer Research · doi:10.1158/0008-5472.can-05-4670 · Cited by 70
In vivo pharmacokinetics of selective mu-opioid peptide agonists.
Szeto, H. H., Lovelace, J. L., Fridland, G., Soong, Y., Fasolo, J., Wu, D., Desiderio, D. M., & Schiller, P. W. (2001) · PubMed · Cited by 70
Debra Boyd-kimball, A., Rukhsana Sultana, A., Abdul, H. M., & Butterfield, D. A. (2005) · Journal of Neuroscience Research · doi:10.1002/jnr.20394 · Cited by 66
Zhao, G., Wu, D., Soong, Y., Shimoyama, M., Berezowska, I., Schiller, P. W., & Szeto, H. H. (2002) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.302.1.188 · Cited by 65
Presenilin-1 is located in rat mitochondria
Ankarcrona, M., & Hultenby, K. R. (2002) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(02)00735-0 · Cited by 63
Ding, Q., Cecarini, V., & Keller, J. N. (2006) · Trends in Neurosciences · doi:10.1016/j.tins.2006.11.003 · Cited by 63
Iron dysregulation and Parkinson's disease
Andersen, J. K. (2005) · Journal of Alzheimer s Disease · doi:10.3233/jad-2004-6s602 · Cited by 62
Selective degeneration in YAC mouse models of Huntington disease
Raamsdonk, J. M. V., Warby, S. C., & Hayden, M. R. (2006) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2006.10.018 · Cited by 60
Iron Dysregulation in Friedreich Ataxia
Wilson, R. B. (2006) · Seminars in Pediatric Neurology · doi:10.1016/j.spen.2006.08.005 · Cited by 59
Fukui, H., & Moraes, C. T. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddm023 · Cited by 57
Debra Boyd-kimball, A., Rukhsana Sultana, A., Poon, H. F., Abdul, H. M., Lynn, B. C., Klein, J. B., & Butterfield, D. A. (2005) · Journal of Neuroscience Research · doi:10.1002/jnr.20393 · Cited by 50
In Vivo Pharmacokinetics of Selective μ-Opioid Peptide Agonists
Szeto, H. H., Lovelace, J. L., Fridland, G., Soong, Y., Fasolo, J., Wu, D., Desiderio, D. M., & Schiller, P. W. (2001) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)29351-4 · Cited by 49
Chan, S. L., Furukawa, K., & Mattson, M. P. (2002) · NeuroMolecular Medicine · doi:10.1385/nmm:2:2:167 · Cited by 45
Behbahani, H., Shabalina, I. G., Wiehager, B., Concha, H., Hultenby, K. R., Petrovič, N., Nedergaard, J., Winblad, B. G., Cowburn, R. F., & Ankarcrona, M. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20990 · Cited by 42
Erratum: Pathways towards and away from Alzheimer's disease (Nature (2004) 430 (631-639))
Mattson, M. P. (2004) · Nature · Cited by 38
Schultz, D. W., & Harrison, D. G. (2000) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.20.6.1412 · Cited by 29
Cytotoxic mechanisms by M239V presenilin 2, a little‐analyzed Alzheimer's disease‐causative mutant
Abe, Y., Hashimoto, Y., Tomita, Y., Terashita, K., Aiso, S., Tajima, H., Niikura, T., Matsuoka, M., & Nishimoto, I. (2004) · Journal of Neuroscience Research · doi:10.1002/jnr.20163 · Cited by 16
Sayer, J. A., Mańczak, M., Akileswaran, L., Reddy, P. H., & Coghlan, V. M. (2005) · NeuroMolecular Medicine · doi:10.1385/nmm:7:4:297 · Cited by 14
Self-citationGenetic Aberrancies and Neurodegenerative Disorders
(1999) · Advances in cell aging and gerontology · doi:10.1016/s1566-3124(08)x6002-x · Cited by 12
Increased activity of surviving locus ceruleus neurons in Alzheimer's disease
Moser (1999) · Pure Amsterdam UMC · doi:10.1002/1531-8249(199901)45:1
Khan (2000) · doi:10.1002/1531-8249(200008)48:2
Flagged first, then by citations
1 of the 224 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Bhatti, J. S., Bhatti, G. K., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.010 · Cited by 1,655
Self-citationMitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease
Misrani, A., Tabassum, S., & Yang, L. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.617588 · Cited by 654
Basic mechanisms of neurodegeneration: a critical update
Jellinger, K. A. (2010) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2010.01010.x · Cited by 640
McManus, M. J., Murphy, M. P., & Franklin, J. L. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.0552-11.2011 · Cited by 432
Reddy, P. H., Tripathi, R., Troung, Q., Tirumala, K., Reddy, T. P., Anekonda, V., Shirendeb, U. P., Calkins, M. J., Reddy, A. P., Mao, P., et al. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.10.011 · Cited by 394
Self-citation
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
