Cited by 230Alzheimer's disease research and treatmentsNeuroprotection in Cerebral IschemiaNeuroscience and Neuropharmacology Research

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Protective effect of the energy precursor creatine against toxicity of glutamate and β-amyloid in rat hippocampal neurons

Brewer, Gregory J., Wallimann, Theo W.·2000·Journal of Neurochemistry

DOI 10.1046/j.1471-4159.2000.0741968.x

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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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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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Authors: Brewer, G. J., & Wallimann, T. W.
Affiliations: SIU Medicine (US)
ORCID: Brewer, Gregory J.
Wallimann, Theo W.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2000-05
Volume: 74
Issue: 5
Pages: 1968-1978
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1046/j.1471-4159.2000.0741968.x
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3012 d)
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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Protective effect of the energy precursor creatine against toxicity of glutamate and β-amyloid in rat hippocampal neurons

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