The DOI matches its Crossref record; 95 of the 96 references it cites were found in a registry or an index.
Protective effect of the energy precursor creatine against toxicity of glutamate and β-amyloid in rat hippocampal neurons
Abstract
The loss of ATP, which is needed for ionic homeostasis, is an early event in the neurotoxicity of glutamate and beta-amyloid (A(beta)). We hypothesize that cells supplemented with the precursor creatine make more phosphocreatine (PCr) and create larger energy reserves with consequent neuroprotection against stressors. In serum-free cultures, glutamate at 0.5-1 mM was toxic to embryonic hippocampal neurons. Creatine at >0.1 mM greatly reduced glutamate toxicity. Creatine (1 mM) could be added as late as 2 h after glutamate to achieve protection at 24 h. In association with neurotoxic protection by creatine during the first 4 h, PCr levels remained constant, and PCr/ATP ratios increased. Morphologically, creatine protected against glutamate-induced dendritic pruning. Toxicity in embryonic neurons exposed to A(beta) (25-35) for 48 h was partially prevented by creatine as well. During the first 6 h of treatment with A(beta) plus creatine, the molar ratio of PCr/ATP in neurons increased from 15 to 60. Neurons from adult rats were also partially protected from a 24-h exposure to A(beta) (25-35) by creatine, but protection was reduced in neurons from old animals. These results suggest that fortified energy reserves are able to protect neurons against important cytotoxic agents. The oral availability of creatine may benefit patients with neurodegenerative diseases.
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“In vitro, creatine elevates phosphocreatine and ATP levels11 and increases oxidative phosphorylation in synaptosomes and isolated brain mitochondria.12”
From Effects of creatine supplementation on memory in healthy individuals: a systematic review and meta-analysis of randomized controlled trials (2023) · cites this paper as [11]
In the citing paper
“These beneficial effects from creatine supplementation on memory performance may be related to creatine’s ability to influence brain bioenergetics.”
From Effects of creatine supplementation on memory in healthy individuals: a systematic review and meta-analysis of randomized controlled trials (2023) · cites this paper as [11]
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Cites
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Self-citationNeurotrophic and Neurotoxic Effects of Amyloid β Protein: Reversal by Tachykinin Neuropeptides
Yankner, B. A., Duffy, L. K., & Kirschner, D. A. (1990) · Science · doi:10.1126/science.2218531 · Cited by 1,975
Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state
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Mapping of metabolites in whole animals by 31P NMR using surface coils
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Transport of Energy in Muscle: The Phosphorylcreatine Shuttle
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Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis
Klivenyi, P., Ferrante, R. J., Matthews, R. T., Bogdanov, M. B., Klein, A. M., Andreassen, O. A., Mueller, G., Wermer, M., Kaddurah-Daouk, R., & Beal, M. F. (1999) · Nature Medicine · doi:10.1038/6568 · Cited by 682
Glutamate-induced neuron death requires mitochondrial calcium uptake
Stout, A. K., Raphael, H. M., Kanterewicz, B. I., Klann, E., & Reynolds, I. J. (1998) · Nature Neuroscience · doi:10.1038/1577 · Cited by 630
Research works printed but not linked: 1
- Brewer G.J., 1998, Protective effect of the energy precursor creatine against toxicity of glutamate and beta‐amyloid in rat hippocampal neurons., Soc. Neurosci. Abstr., 24, 1456
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The creatine kinase system and pleiotropic effects of creatine
Wallimann, T., Tokarska-Schlattner, M., & Schlattner, U. (2011) · Amino Acids · doi:10.1007/s00726-011-0877-3 · Cited by 797
Self-citationParsons, C. G., Stöffler, A., & Danysz, W. (2007) · Neuropharmacology · doi:10.1016/j.neuropharm.2007.07.013 · Cited by 724
Post-traumatic inflammation following spinal cord injury
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Mitochondria, Oxidative Damage, and Inflammation in Parkinson's Disease
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Metadata
- Authors
- Brewer, G. J., & Wallimann, T. W.
- Affiliations
- SIU Medicine (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2000-05
- Volume
- 74
- Issue
- 5
- Pages
- 1968-1978
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1971233715
- Cited by
- 230
- References
- 96
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 4 · 2023: 8 · 2022: 9 · 2021: 4 · 2020: 6 · 2019: 10 · 2018: 10 · 2017: 3 · 2016: 10 · 2015: 9 · 2014: 12 · 2013: 6 · 2012: 4
- FWCI
- 6.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01 AG 13435, R01AG013435)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- creatine, neuroprotection, glutamate excitotoxicity, amyloid-beta, hippocampal neurons, phosphocreatine, ATP depletion, energy reserves, dendritic pruning, aging, neurodegenerative diseases
- MeSH terms
- Aging, Animals, Cells, Cultured, Creatine, Dendrites, Energy Metabolism, Hippocampus, Intracellular Membranes, Neurons, Phosphocreatine, Amyloid beta-Peptides, Neuroprotective Agents, Glutamic Acid, Rats
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