The DOI matches its Crossref record; 202 of the 202 references it cites were found in a registry or an index.
Calcium and neurodegeneration
Open accessAbstract
When properly controlled, Ca2+ fluxes across the plasma membrane and between intracellular compartments play critical roles in fundamental functions of neurons, including the regulation of neurite outgrowth and synaptogenesis, synaptic transmission and plasticity, and cell survival. During aging, and particularly in neurodegenerative disorders, cellular Ca2+-regulating systems are compromised resulting in synaptic dysfunction, impaired plasticity and neuronal degeneration. Oxidative stress, perturbed energy metabolism and aggregation of disease-related proteins (amyloid beta-peptide, alpha-synuclein, huntingtin, etc.) adversely affect Ca2+ homeostasis by mechanisms that have been elucidated recently. Alterations of Ca2+-regulating proteins in the plasma membrane (ligand- and voltage-gated Ca2+ channels, ion-motive ATPases, and glucose and glutamate transporters), endoplasmic reticulum (presenilin-1, Herp, and ryanodine and inositol triphosphate receptors), and mitochondria (electron transport chain proteins, Bcl-2 family members, and uncoupling proteins) are implicated in age-related neuronal dysfunction and disease. The adverse effects of aging on neuronal Ca2+ regulation are subject to modification by genetic (mutations in presenilins, alpha-synuclein, huntingtin, or Cu/Zn-superoxide dismutase; apolipoprotein E isotype, etc.) and environmental (dietary energy intake, exercise, exposure to toxins, etc.) factors that may cause or affect the risk of neurodegenerative disease. A better understanding of the cellular and molecular mechanisms that promote or prevent disturbances in cellular Ca2+ homeostasis during aging may lead to novel approaches for therapeutic intervention in neurological disorders such as Alzheimer's and Parkinson's diseases and stroke.
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“Excessive Ca2+ accumulation into mitochondria leads to decreased mitochondrial membrane potential and increased ROS production in the same AD mouse model [67,68,70].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [68]
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Cites
Pathways towards and Away from Alzheimer’s Disease
Mattson, M. P. (2004) · Nature · doi:10.1038/nature02621 · Cited by 3,052
Self-citationLipton, S. A., Choi, Y.-B., Pan, Z.-H., Lei, S. Z., Chen, H.-S. V., Sucher, N. J., Loscalzo, J., Singel, D. J., & Stamler, J. S. (1993) · Nature · doi:10.1038/364626a0 · Cited by 2,433
Impairment of the Ubiquitin-Proteasome System by Protein Aggregation
Bence, N., Sampat, R. M., & Kopito, R. R. (2001) · Science · doi:10.1126/science.292.5521.1552 · Cited by 2,209
Ankarcrona, M., Dypbukt, J. M., Bonfoco, E., Zhivotovsky, B., Orrenius, S., Lipton, S. A., & Nicotera, P. (1995) · Neuron · doi:10.1016/0896-6273(95)90186-8 · Cited by 1,884
Molecular Pathways of Neurodegeneration in Parkinson's Disease
Dawson, T. M., & Dawson, V. L. (2003) · Science · doi:10.1126/science.1087753 · Cited by 1,674
Mattson, M. P., Cheng, B., Davis, D. G., Bryant, K., Lieberburg, I. M., & Rydel, R. E. (1992) · Journal of Neuroscience · doi:10.1523/jneurosci.12-02-00376.1992 · Cited by 1,633
Self-citationClinical effects of Aβ immunization (AN1792) in patients with AD in an interrupted trial
Gilman, S., Koller, M., Black, R. S., Jenkins, L., Griffith, S. G., Fox, N. C., Eisner, L., Kirby, L., Rovira, M. B., Forette, F., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000159740.16984.3c · Cited by 1,329
MOLECULAR PATHOPHYSIOLOGY OF PARKINSON'S DISEASE
Moore, D. J., West, A. B., Dawson, V. L., & Dawson, T. M. (2005) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.28.061604.135718 · Cited by 1,304
Mitochondria and calcium: from cell signalling to cell death
Duchen, M. R. (2000) · The Journal of Physiology · doi:10.1111/j.1469-7793.2000.00057.x · Cited by 1,261
UNRAVELING THE MECHANISMS INVOLVED IN MOTOR NEURON DEGENERATION IN ALS
Bruijn, L. I., Miller, T. M., & Cleveland, D. W. (2004) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.27.070203.144244 · Cited by 1,185
Cited by
Sorted by citations
Hallmarks of neurodegenerative diseases
Wilson, D. M., Cookson, M. R., Van Den Bosch, L., Zetterberg, H., Holtzman, D. M., & Dewachter, I. (2023) · Cell · doi:10.1016/j.cell.2022.12.032 · Cited by 1,789
Zhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138
Lian, H., Yang, L., Cole, A., Sun, L., Chiang, A. C.-A., Fowler, S. W., Shim, D. J., Rodriguez-Rivera, J., Taglialatela, G., Jankowsky, J. L., et al. (2015) · Neuron · doi:10.1016/j.neuron.2014.11.018 · Cited by 697
Gandhi, S., Wood-Kaczmar, A., Yao, Z., Plun-Favreau, H., Deas, E., Klupsch, K., Downward, J., Latchman, D. S., Tabrizi, S. J., Wood, N. W., et al. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.02.013 · Cited by 682
Zempel, H., Thies, E., Mandelkow, E., & Mandelkow, E.-M. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.2357-10.2010 · Cited by 686
“, proteasome, mitochondria) and perturbation of calcium homeostasis (Mattson, 2007).”
Background
Metadata
- Authors
- Mattson, M. P.
- Affiliations
- National Institute on Aging (US)
- Corresponding author
- Mattson, Mark P.
- ORCID
- Mattson, Mark P.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2007-01-15
- Volume
- 6
- Issue
- 3
- Pages
- 337-350
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- OpenAlex
- W2110831253
- Cited by
- 751
- References
- 202
- Citations by year
- 2026: 14 · 2025: 27 · 2024: 30 · 2023: 29 · 2022: 41 · 2021: 32 · 2020: 25 · 2019: 36 · 2018: 31 · 2017: 33 · 2016: 34 · 2015: 30 · 2014: 35 · 2013: 50 · 2012: 55
- FWCI
- 4.62
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Aging Cell (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- calcium homeostasis, neurodegeneration, aging, calcium channels, voltage-gated calcium channels, presenilin 1, ryanodine receptor, IP3 receptor, mitochondrial calcium uptake, oxidative stress, energy metabolism, protein aggregation, amyloid-beta, alpha-synuclein, huntingtin, Cu/Zn superoxide dismutase, apolipoprotein E, synaptic dysfunction, neuroplasticity, Alzheimer's disease, Parkinson's disease, stroke, physical activity, diet
- MeSH terms
- Amyloid, Animals, Calcium, Endoplasmic Reticulum, Humans, Microscopy, Fluorescence, Models, Biological, Nerve Degeneration, Parkinson Disease, Apoptosis, Oxidative Stress, Neurodegenerative Diseases, Calcium Signaling, Presenilins
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