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Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer’s disease: Implications to mitochondria-targeted antioxidant therapeutics
Open accessAbstract
Synaptic pathology and mitochondrial oxidative damage are early events in Alzheimer's disease (AD) progression. Loss of synapses and synaptic damage are the best correlates of cognitive deficits found in AD patients. Recent research on amyloid beta (Aβ) and mitochondria in AD revealed that Aβ accumulates in synapses and synaptic mitochondria, leading to abnormal mitochondrial dynamics and synaptic degeneration in AD neurons. Further, recent studies using live-cell imaging and primary neurons from amyloid beta precursor protein (AβPP) transgenic mice revealed reduced mitochondrial mass, defective axonal transport of mitochondria and synaptic degeneration, indicating that Aβ is responsible for mitochondrial and synaptic deficiencies. Tremendous progress has been made in studying antioxidant approaches in mouse models of AD and clinical trials of AD patients. This article highlights the recent developments made in Aβ-induced abnormal mitochondrial dynamics, defective mitochondrial biogenesis, impaired axonal transport and synaptic deficiencies in AD. This article also focuses on mitochondrial approaches in treating AD, and also discusses latest research on mitochondria-targeted antioxidants in AD. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease.
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“However, oxidative stress, mitochondrial dysfunction, and glucose hypometabolism have been well documented in MCI and AD brain [8,53,74,75,76].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [53]
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“As mentioned above, the use of redox proteomics has led to the identification of oxidized proteins, as indexed by carbonylation, nitration, and modification with HNE, in both in vitro and in vivo models of AD in addition to MCI and AD brain.”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [53]
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“Compelling evidence links neurodegeneration to altered brain metabolism and mitochondrial dysfunction, both of which are early hallmarks of AD [21–28].”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [27]
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“Consistent with the hypothesis that both oxidative stress and mitochondrial dysfunction are early events in the progression of AD [12,35,53], many of the oxidized proteins identified are mitochondrial proteins involved in metabolism, protein synthesis and folding, ROS scavenging, transport, and apoptosis (Table 1).”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [53]
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“The presence of Aβ oligomers in mitochondrial membranes is consistent with Aβ-induced mitochondrial dysfunction occurring early in the disease progression timeline [34,53].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [53]
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Ciabattoni, G., Porreca, E., Febbo, C. D., Iorio, A. D., Paganelli, R., Bucciarelli, T., Pescara, L., Re, L. D., Giusti, C., Falco, A., et al. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.12.011 · Cited by 77
Drago, D., Cavaliere, A., Mascetra, N., Ciavardelli, D., Ilio, C. D., Zatta, P. F., & Sensi, S. L. (2008) · Rejuvenation Research · doi:10.1089/rej.2008.0761 · Cited by 74
Dinámica mitocondrial: un potencial nuevo blanco terapéutico para la insuficiencia cardiaca
Kuzmicic, J., del Campo, A., López‐Crisosto, C., Morales, P. E., Pennanen, C., Bravo, R., Hechenleitner, J., Zepeda, R. J., Castro, P., Verdejo, H., et al. (2011) · Revista Española de Cardiología · doi:10.1016/j.recesp.2011.05.018 · Cited by 70
Pham, D. Q., & Plakogiannis, R. (2005) · Annals of Pharmacotherapy · doi:10.1345/aph.1g271 · Cited by 70
Nuclear-encoded mitochondrial proteins and their role in cardioprotection
Boengler, K., Heusch, G., & Schulz, R. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2011.01.009 · Cited by 68
Calkins, M. J., & Reddy, P. H. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.04.006 · Cited by 65
Self-citationKrzywanski, D. M., Moellering, D. R., Fetterman, J. L., Dunham‐Snary, K. J., Sammy, M. J., & Ballinger, S. W. (2011) · Laboratory Investigation · doi:10.1038/labinvest.2011.95 · Cited by 60
Sensi, S. L., Rapposelli, I. G., Frazzini, V., & Mascetra, N. (2007) · Experimental Gerontology · doi:10.1016/j.exger.2007.10.018 · Cited by 49
The awakening of an advanced malignant cancer: An insult to the mitochondrial genome
Cook, C. C., & Higuchi, M. (2011) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2011.08.017 · Cited by 33
Schneider, L. S. S., Raman, R., Schmitt, F. A., Doody, R. S., Insel, P. S., Clark, C. M., Morris, J. C., Reisberg, ., Petersen, R. C., & Ferris, S. H. (2009) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0b013e31819cb760 · Cited by 26
Flagged first, then by citations
2 of the 104 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Tönnies, E., & Trushina, E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161088 · Cited by 1,750
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-citationAgeing and Parkinson's disease: Why is advancing age the biggest risk factor?
Reeve, A. K., Simcox, E. M., & Turnbull, D. M. (2014) · Ageing Research Reviews · doi:10.1016/j.arr.2014.01.004 · Cited by 1,013
Is Alzheimer’s disease a type 3 diabetes? A critical appraisal
Kandimalla, R., Thirumala, V., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.08.018 · Cited by 621
Self-citationHippocampus and its involvement in Alzheimer’s disease: a review
Rao, Y. L., Ganaraja, B., Murlimanju, B. V., Joy, T., Krıshnamurthy, A., & Agrawal, A. (2022) · 3 Biotech · doi:10.1007/s13205-022-03123-4 · Cited by 646
Metadata
- Authors
- 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., & Manczak, M.
- Affiliations
- Oregon National Primate Research Center (US)
- Corresponding author
- Reddy, P. Hemachandra
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2012-05
- Volume
- 1822
- Issue
- 5
- Pages
- 639-649
- ISSN
- 0925-4439 (ISSN-L)
- PMC
- PMC3272314
- OpenAlex
- W1996981671
- Cited by
- 394
- References
- 104
- Citations by year
- 2026: 29 · 2025: 17 · 2024: 22 · 2023: 27 · 2022: 30 · 2021: 38 · 2020: 29 · 2019: 30 · 2018: 26 · 2017: 36 · 2016: 31 · 2015: 19 · 2014: 31 · 2013: 18 · 2012: 10
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH
- Alzheimer Association
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, mitochondrial dynamics, synaptic degeneration, amyloid-beta, mitochondrial oxidative damage, mitochondrial biogenesis, mitochondria-targeted antioxidants, antioxidant therapeutics, synaptic mitochondria
- MeSH terms
- Alzheimer Disease, Animals, Antioxidants, Humans, Mice, Transgenic, Mitochondria, Synapses, Amyloid beta-Protein Precursor, Mice
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 ›
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