The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Neuroprotective Effects of Creatine and Cyclocreatine in Animal Models of Huntington’s Disease
Open accessAbstract
The gene defect in Huntington’s disease (HD) may result in an impairment of energy metabolism. Malonate and 3-nitropropionic acid (3-NP) are inhibitors of succinate dehydrogenase that produce energy depletion and lesions that closely resemble those of HD. Oral supplementation with creatine or cyclocreatine, which are substrates for the enzyme creatine kinase, may increase phosphocreatine (PCr) or phosphocyclocreatine (PCCr) levels and ATP generation and thereby may exert neuroprotective effects. We found that oral supplementation with either creatine or cyclocreatine produced significant protection against malonate lesions, and that creatine but not cyclocreatine supplementation significantly protected against 3-NP neurotoxicity. Creatine and cyclocreatine increased brain concentrations of PCr and PCCr, respectively, and creatine protected against depletions of PCr and ATP produced by 3-NP. Creatine supplementation protected against 3-NP induced increases in striatal lactate concentrations in vivo as assessed by 1 H magnetic resonance spectroscopy. Creatine and cyclocreatine protected against malonate-induced increases in the conversion of salicylate to 2,3- and 2,5-dihydroxybenzoic acid, biochemical markers of hydroxyl radical generation. Creatine administration protected against 3-NP-induced increases in 3-nitrotyrosine concentrations, a marker of peroxynitrite-mediated oxidative injury. Oral supplementation with creatine or cyclocreatine results in neuroprotective effects in vivo, which may represent a novel therapeutic strategy for HD and other neurodegenerative diseases.
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Cites
Browne, S. E., Bowling, A. C., Macgarvey, U., Baik, M. J., Berger, S. C., Muquit, M. M. K., Bird, E. D., & Beal, M. F. (1997) · Annals of Neurology · doi:10.1002/ana.410410514 · Cited by 885
Self-citationMitochondrial defect in Huntington's disease caudate nucleus
Gu, M., Gash, M. T., Mann, V. M., Javoy‐Agid, F., Cooper, J. M., & Schapira, A. H. V. (1996) · Annals of Neurology · doi:10.1002/ana.410390317 · Cited by 758
Alternative excitotoxic hypotheses
Albin, R. L., & Greenamyre, J. T. (1992) · Neurology · doi:10.1212/wnl.42.4.733 · Cited by 574 · cited 2×
“Key words: creatine; ATP; oxidative injury; 3-nitrotyrosine; 3-nitropropionic acid; Huntington There is substantial evidence that impairment of energy production may play a role in the pathogenesis of neurodegenerative diseases (Albin and Greenamyre, 1992; Beal, 1992).”
BackgroundCreatine deficiency in the brain: A new, treatable inborn error of metabolism
Stöckler, S., Holzbach, U., Hanefeld, F., Marquardt, I., Helms, G., Requart, M., Hänicke, W., & Frahm, J. (1994) · Pediatric Research · doi:10.1203/00006450-199409000-00023 · Cited by 417
Energy metabolism defects in Huntington's disease and effects of coenzyme Q10
Koroshetz, W. J., Jenkins, B. G., Rosen, B. R., & Beal, M. F. (1997) · Annals of Neurology · doi:10.1002/ana.410410206 · Cited by 405
Self-citationCreatine in humans with special reference to creatine supplementation
Balsom, P. D., Söderlund, K., & Ekblom, B. (1994) · Sports Medicine · doi:10.2165/00007256-199418040-00005 · Cited by 404 · cited 1×
“Creatine administration is well tolerated in man and may have benefits in pathological conditions (Balsom et al., 1994; Dawson et al., 1995).”
BackgroundAge-dependent vulnerability of the striatum to the mitochondrial toxin 3-nitropropionic acid
Brouillet, E., Jenkins, B. G., Hyman, B. T., Ferrante, R. J., Kowall, N. W., Srivastava, R., Roy, D. S., Rosen, B. R., & Beal, M. F. (1993) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1993.tb05859.x · Cited by 367
Supplementary creatine as a treatment for gyrate atrophy of the choroid and retina
Sipilä, I., Rapola, J., Simell, O., & Vannas, A. (1981) · New England Journal of Medicine · doi:10.1056/nejm198104093041503 · Cited by 181 · cited 1×
“Long-term administration to patients with gyrate atrophy of the choroid and retina prevented visual field constriction and resulted in improvement of muscle biopsy findings (Sipila et al., 1981).”
Background‘Hot spots’ of creatine kinase localization in brain: cerebellum, hippocampus and choroid plexus
Kaldis, P., Hemmer, W., Zanolla, E., Holtzman, D., & Wallimann, T. (2009) · Developmental Neuroscience · doi:10.1159/000111452 · Cited by 99 · cited 2×
“, molecular layer of the cerebellum, glomerular structures of the granule layer, and the hippocampus (Kaldis et al., 1996).”
Background
Cited by
Ischemic Cell Death in Brain Neurons
Lipton, P. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.4.1431 · Cited by 3,043
Creatine and Creatinine Metabolism
Wyss, M., & Kaddurah-Daouk, R. (2000) · Physiological Reviews · doi:10.1152/physrev.2000.80.3.1107 · Cited by 2,950
Self-citationKreider, R. B., Kalman, D. S., Antonio, J., Ziegenfuss, T. N., Wildman, R., Collins, R., Candow, D. G., Kleiner, S. M., Almada, A. L., & Lopez, H. L. (2017) · Journal of the International Society of Sports Nutrition · doi:10.1186/s12970-017-0173-z · Cited by 1,057
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
Yang, Y., Gehrke, S., Imai, Y., Huang, Z., Ouyang, Y., Wang, J.-W., Yang, L., Beal, M. F., Vogel, H., & Lu, B. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0602493103 · Cited by 798
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Metadata
- Authors
- Matthews, R. T., Yang, L., Jenkins, B. G., Ferrante, R. J., Rosen, B. R., Kaddurah-Daouk, R., & Beal, M. F.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1998-01-01
- Volume
- 18
- Issue
- 1
- Pages
- 156-163
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2125591463
- Cited by
- 430
- References
- 9
- FWCI
- 11.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
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