Effects of creatine treatment on the survival of dopaminergic neurons in cultured fetal ventral mesencephalic tissue

Andres, Robert H.; Huber, Adrian Thomas; Schlattner, Uwe; Pérez-Bouza, Alberto; Krebs, Sandra H.; Seiler, Rolf W.; Wallimann, Theo; Widmer, Hans Rudolf

doi:10.1016/j.neuroscience.2005.03.004

Cited by 75 publications

(56 citation statements)

References 82 publications

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“…24 Data using human fetal striatal and mesencephalic tissue identified creatine as a potent natural survival and neuroprotective factor for γ-aminobutyric acid-ergic neurons in a model for Huntington disease 25 and of dopaminergic neurons in a model for Parkinson disease. 26 Recent interest in routine screening children with ASD for inborn errors of metabolism, and in particular CDS, 27,28 raises the question of how many children with ASD could potentially benefit from such screening. The purpose of the current study is to establish the prevalence of CDS in children with ASD, using a rational approach of biochemical and genetic testing for creatine metabolism.…”

Section: What This Study Addsmentioning

confidence: 99%

Prevalence of Creatine Deficiency Syndromes in Children With Nonsyndromic Autism

et al. 2016

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Section: What This Study Addsmentioning

confidence: 99%

Prevalence of Creatine Deficiency Syndromes in Children With Nonsyndromic Autism

et al. 2016

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“…Promethazine, an antihistamine known to delay the onset of the mPT , prevented the MPP + -induced mitochondrial depolarization, inhibited the Ca 2+ -induced mPT in isolated brain mitochondria and markedly attenuated the loss of nigral neurons (Cleren et al, 2005). Creatine has been shown to protect against MPP + -induced neuronal loss (Matthews et al, 1999;Andres et al, 2005) and against 6-hydroxydopamine neuronal loss (Andres et al, 2005). Similarly, minocycline was found to exert neuroprotective effects against MPTP toxicity both in vivo and in vitro (Du et al, 2001;Wu et al, 2002).…”

Section: Degenerative Diseasesmentioning

confidence: 99%

The mitochondrial permeability transition in neurologic disease

Norenberg

Rao

2007

Neurochemistry International

144

107

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Mitochondria, being the principal source of cellular energy, are vital for cell life. Yet, ironically, they are also major mediators of cell death, either by necrosis or apoptosis. One means by which these adverse effects occur is through the mitochondrial permeability transition (mPT) whereby the inner mitochondrial membrane suddenly becomes excessively permeable to ions and other solutes, resulting in a collapse of the inner membrane potential, ultimately leading to energy failure and cell necrosis. The mPT may also bring about the release of various factors known to cause apoptotic cell death. The principal factors leading to the mPT are elevated levels of intracellular Ca 2+ and oxidative stress. Characteristically, the mPT is inhibited by cyclosporin A. This article will briefly discuss the concept of the mPT, its molecular composition, its inducers and regulators, agents that influence its activity and describe the consequences of its induction. Lastly, we will review its potential contribution to acute neurological disorders, including ischemia, trauma, and toxic-metabolic conditions, as well as its role in chronic neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis.

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“…Several evidences indicate specific protective effects of Cr in various animal models of neurodegenerative diseases or ischemic stroke [7][8][9]. The neuroprotective effects of Cr has been ascribed to the buffering capacity of cellular ATP levels coupled with mitochondrial targeted antioxidant properties in cell and mammalian models [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Attenuation of Rotenone-Induced Mitochondrial Oxidative Damage and Neurotoxicty in Drosophila melanogaster Supplemented with Creatine

2010

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Creatine (Cr), an ergogenic nutritional supplement is demonstrated to possess bioenergetic, antiexcitotoxic and antioxidant properties. This study investigated the neuroprotective effects of Cr against rotenone induced oxidative stress, mortality and neurotoxicty in Drosophila melanogaster. We found significant diminution in the endogenous levels of oxidative markers in whole body homogenates of flies exposed to Cr (2-10 mM). Cr supplementation resulted in reduced mortality in flies exposed to rotenone (500 microM) and better performance in a negative geotaxis assay. Further Cr (10 mM) markedly offset rotenone induced mitochondrial oxidative stress, completely restored the GSH levels, nitric oxide levels, activity of Mn-SOD and dopamine depletion. In an oxidative stress bioassay, flies given Cr prophylaxis exhibited marked resistance to paraquat exposure. These data allow us to hypothesize that the neuroprotective action of Cr in Drosophila may be related to its direct antioxidant activity and ability to abrogate rotenone induced mitochondrial oxidative stress.

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Effects of creatine treatment on the survival of dopaminergic neurons in cultured fetal ventral mesencephalic tissue

Cited by 75 publications

References 82 publications

Prevalence of Creatine Deficiency Syndromes in Children With Nonsyndromic Autism

Prevalence of Creatine Deficiency Syndromes in Children With Nonsyndromic Autism

The mitochondrial permeability transition in neurologic disease

Attenuation of Rotenone-Induced Mitochondrial Oxidative Damage and Neurotoxicty in Drosophila melanogaster Supplemented with Creatine

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