The DOI matches its Crossref record; 242 of the 243 references it cites were found in a registry or an index.
Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD) is a chronic neurodegenerative disorder, in which multiple risk factors converge. Despite the complexity of the etiology of the disease, synaptic failure is the pathological basis of cognitive impairment, the cardinal sign of AD. Decreased synaptic density, compromised synaptic transmission, and defected synaptic plasticity are hallmark synaptic pathologies accompanying AD. However, the mechanisms by which synapses are injured in AD-related conditions have not been fully elucidated. Mitochondria are a critical organelle in neurons. The pivotal role of mitochondria in supporting synaptic function and the concomitant occurrence of mitochondrial dysfunction with synaptic stress in postmortem AD brains as well as AD animal models seem to lend the credibility to the hypothesis that mitochondrial defects underlie synaptic failure in AD. This concept is further strengthened by the protective effect of mitochondrial medicine on synaptic function against the toxicity of amyloid-β, a key player in the pathogenesis of AD. In this review, we focus on the association between mitochondrial dysfunction and synaptic transmission deficits in AD. Impaired mitochondrial energy production, deregulated mitochondrial calcium handling, excess mitochondrial reactive oxygen species generation and release play a crucial role in mediating synaptic transmission deregulation in AD. The understanding of the role of mitochondrial dysfunction in synaptic stress may lead to novel therapeutic strategies for the treatment of AD through the protection of synaptic transmission by targeting to mitochondrial deficits.
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“Apart from this, Aβ induces hypersensitivity of NMDA receptors and also disrupts the regulatory control of NMDA activity causing excitotoxicity [12].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [12]
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Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
Lin, M. T., & Beal, M. F. (2006) · Nature · doi:10.1038/nature05292 · Cited by 6,455
Control of inositol 1,4,5-trisphosphate-induced Ca2+ release by cytosolic Ca2+
Bootman, M. D., Missiaen, L., Parys, J. B., SMEDT, H. D., & Casteels, R. (1995) · Biochemical Journal · doi:10.1042/bj3060445 · Cited by 5,131
Querfurth, H. W., & LaFerla, F. M. (2010) · New England Journal of Medicine · doi:10.1056/nejmra0909142 · Cited by 4,569
Alzheimer's Disease Is a Synaptic Failure
Selkoe, D. J. (2002) · Science · doi:10.1126/science.1074069 · Cited by 4,420
Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397
Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
Interplay between Cortical Spreading Depolarization and Seizures
Kramer, D. R., Fujii, T., Ohiorhenuan, I. E., & Liu, C. Y. (2017) · Stereotactic and Functional Neurosurgery · doi:10.1159/000452841 · Cited by 3,721
An Energy Budget for Signaling in the Grey Matter of the Brain
Attwell, D., & Laughlin, S. B. (2001) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1097/00004647-200110000-00001 · Cited by 3,543
Seth, R. B., Sun, L., Ea, C.-K., & Chen, Z. J. (2005) · Cell · doi:10.1016/j.cell.2005.08.012 · Cited by 3,329
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Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
Zhang, Y., Chen, H., Li, R., Sterling, K., & Song, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01484-7 · Cited by 988
“Mitochondria are essential for the glutamate synthesis, synaptic transmission and calcium regulation.(193,194) Disrupted energy metabolism has been found in early AD and precedes the disease development, suggesting the core role of mitochondria dysfunction in Alzheimer’s pathogenesis.”
BackgroundRecent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease
Khan, S., Barve, K. H., & Kumar, M. S. (2020) · Current Neuropharmacology · doi:10.2174/1570159x18666200528142429 · Cited by 820
“Apart from this, Aβ induces hypersensitivity of NMDA receptors and also disrupts the regulatory control of NMDA activity causing excitotoxicity [12].”
BackgroundMitochondria: It is all about energy
Casanova, A., Wevers, A., Ledesma, S. N., & Pruimboom, L. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1114231 · Cited by 350
The Association of Tau With Mitochondrial Dysfunction in Alzheimer’s Disease
Cheng, Y., & Bai, F. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00163 · Cited by 239
Dysfunctional Mitochondria and Mitophagy as Drivers of Alzheimer’s Disease Pathogenesis
Chakravorty, A., Jetto, C. T., & Manjithaya, R. R. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00311 · Cited by 225
Metadata
- Authors
- Guo, L., Tian, J., & Du, H.
- Affiliations
- The University of Texas at Dallas (US)
- Shandong University (CN)
- Corresponding author
- Du, Heng
- Venue
- Journal of Alzheimer’s Disease
- Publisher
- SAGE Publications
- Published
- 2016-09-20
- Volume
- 57
- Issue
- 4
- Pages
- 1071-1086
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC5605817
- OpenAlex
- W2522744939
- Cited by
- 211
- References
- 243
- Citations by year
- 2026: 26 · 2025: 31 · 2024: 29 · 2023: 31 · 2022: 22 · 2021: 22 · 2020: 28 · 2019: 17 · 2018: 3 · 2017: 2
- FWCI
- 0.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R00AG037716, R01AG053588)
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, mitochondrial dysfunction
- MeSH terms
- Alzheimer Disease, Animals, Humans, Mitochondria, Synaptic Transmission, Mitochondrial Diseases
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