Excitotoxicity, energy metabolism and neurodegeneration
- PMID: 8105145
- DOI: 10.1007/BF00711903
Excitotoxicity, energy metabolism and neurodegeneration
Abstract
There is increasing evidence that the neurotoxic effects of excitatory amino acids and their analogues are part of the pathogenesis of neuronal degeneration in acute and chronic neurological disease. Recent studies indicate that activation of excitatory amino acid receptors is also induced in the mechanism of neuronal damage induced by impairment of cellular energy metabolism. This article briefly summarizes the evidence for the presence of such a mechanism and discusses metabolic diseases in which excitatory amino acids alone or in combination with energy deficiency could play a pathogenetic role. In these and other metabolic diseases, antagonists to excitatory amino acid receptors may offer a therapeutic opportunity; however, there are potential limits that may prevent chronic use.
Similar articles
-
Excitatory aminoacid antagonists provide a therapeutic approach to neurological disorders.Lancet. 1985 Jul 20;2(8447):140-3. doi: 10.1016/s0140-6736(85)90238-7. Lancet. 1985. PMID: 2862329
-
Protection by natural and semisynthetic gangliosides from Ca2(+)-dependent neurotoxicity caused by excitatory amino acid (EAA) neurotransmitters.Adv Exp Med Biol. 1990;268:135-44. doi: 10.1007/978-1-4684-5769-8_16. Adv Exp Med Biol. 1990. PMID: 1981639 Review. No abstract available.
-
Brain neurotransmitters in glycine encephalopathy.Ann Neurol. 1988 Sep;24(3):458-61. doi: 10.1002/ana.410240319. Ann Neurol. 1988. PMID: 2906530
-
[Excitatory amino acids, central nervous system neurotransmitters].Therapie. 1990 May-Jun;45(3):281-5. Therapie. 1990. PMID: 1973004 Review. French.
-
Pathomechanisms of neurodegeneration in glutaryl-CoA dehydrogenase deficiency.Ann Neurol. 2004 Jan;55(1):7-12. doi: 10.1002/ana.10784. Ann Neurol. 2004. PMID: 14705106 Review.
Cited by
-
Additive aluminum as a cause of induced immunoexcitoxicity resulting in neurodevelopmental and neurodegenerative disorders: A biochemical, pathophysiological, and pharmacological analysis.Surg Neurol Int. 2024 May 24;15:171. doi: 10.25259/SNI_296_2024. eCollection 2024. Surg Neurol Int. 2024. PMID: 38840623 Free PMC article.
-
Effects of L-2-hydroxyglutaric acid on various parameters of the glutamatergic system in cerebral cortex of rats.Metab Brain Dis. 2003 Sep;18(3):233-43. doi: 10.1023/a:1025559200816. Metab Brain Dis. 2003. PMID: 14567473
-
The biochemical basis of neurodegenerative disease: The role of immunoexcitoxicity and ways to possibly attenuate it.Surg Neurol Int. 2023 Apr 21;14:141. doi: 10.25259/SNI_250_2023. eCollection 2023. Surg Neurol Int. 2023. PMID: 37151454 Free PMC article. Review.
-
Neurological dysfunction in methylmalonic acidaemia is probably related to the inhibitory effect of methylmalonate on brain energy production.J Inherit Metab Dis. 1997 Nov;20(6):761-8. doi: 10.1023/a:1005359416197. J Inherit Metab Dis. 1997. PMID: 9427143 Review.
-
Apoptotic Inducement of Neuronal Cells by Aluminium Chloride and the Neuroprotective Effect of Eugenol in Wistar Rats.Oxid Med Cell Longev. 2020 Jan 27;2020:8425643. doi: 10.1155/2020/8425643. eCollection 2020. Oxid Med Cell Longev. 2020. PMID: 32089784 Free PMC article.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources