Summary
Fifteen patients with the unequivocal diagnosis of amyotrophic lateral sclerosis (ALS) completed a 1-year randomized double-blind placebo-controlled trial ofl-threonine (2g daily). During the study, patients in the placebo group showed a decline in functional status consistent with the natural history of ALS, which was not statistically different from outcome in the patients in thel-threonine group.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Aprison MH, Davidoff RA, Werman R (1970) Glycine: its metabolic and possible transmitted roles in nervous tissue. In: Lajtha A (ed) Handbook of neurochemistry, vol 3. Plenum Press, New York, pp 381–397
Armitage P (1980) Statistical methods in medical research. Blackwell, Oxford
Barbeau A (1974) A preliminary study of glycine administration in patients with spasticity. Neurology 24:392
Blin O, Serratrice G, Pouget J, Aubrespy G, Guelton C, Crevat A (1989) Essai a court terme en double aveugle contre placebo de lal-threonine dans la sclerose laterale amyotrophique. Presse Med 30:1469–1470
Bonhaus SW, Burge BC, McNamara JO (1987) Biochemical evidence that glycine allosterically regulates a NMDA receptor coupled ion channel. Eur J Pharmacol 142:489–490
Choi DW, Peters S, Viseskul V (1987) Dextrorphan and levorphanol selectively blockN-Methyl-d-Aspartate receptor-mediated neurotoxicity on cortical neurons. J Pharmacol Exp Ther 242:713–720
Davidoff RA, Graham LT, Shank RP, Werman R, Aprison MH (1967) Changes in amino acid concentrations associated with loss of spinal interneurons. J Neurochem 14:1025–1031
Johnson JW, Ascher P (1987) Glycine potentiates the NMDA response in cultured mouse brain neurons. Nature 325:529–531
Lacomblez L, Bouche P, Bensimon G, Meininger V (1989) A double blind placebo-controlled trial of high doses of gangliosides in amyotrophic lateral sclerosis. Neurology 39:1635–1637
Maher TJ, Wurtman RJ (1980)l-Threonine administration increases glycine concentration in the rat central nervous system. Life Sci 26:1283–1286
Mayer ML, Vyklicky L Jr, Clements J (1989) Regulation of NMDA receptor desensitization in mouse hippocampal neurons by glycine. Nature 338:425–427
Olarte MR, Shafter SR (1985) Levamisole is ineffective in the treatment of amyotrophic lateral sclerosis. Neurology 35:1063–1066
Olney JW (1989) Excitotoxicity andN-Methyl-d-Aspartate receptors. Drug Dev Res 17:299–319
Patten BM, Klein LM (1988)l-Threonine and the modification of ALS. Neurology 38 [Suppl 1]:354–355
Patten BM, Harati Y, Acosta L, Jung SS, Felmus MT (1978) Free aminoacids levels in ALS. Ann Neurol 3:305–309
Perry TL, Hansen S, Jones K (1987) Brain glutamate deficiency in amyotrophic lateral sclerosis. Neurology 37:1845–1848
Plaitakis A, Caroscio JT (1987) Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann Neurol 22:575–579
Plaitakis A, Constantakakis E, Smith J (1988) The neuroexcitotoxic amino acids glutamate and aspartate are altered in the spinal cord and brain in amyotrophic lateral sclerosis. Ann Neurol 24:446–449
Plaitakis A, Mandeli J, Smith J, Yahr MD (1988) Pilot trial of branched-chain aminoacids in amyotrophic lateral sclerosis. Lancet I:1015–1018
Stern P, Bokonjic R (1974) Glycine therapy in 7 cases of spasticity. A pilot study. Pharmacology 12:117–119
Testa D, Caraceni T, Fetoni V (1989) Branched-chain amino acids in the treatment of amyotrophic lateral sclerosis. J Neurol 236:445–447
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Blin, O., Pouget, J., Aubrespy, G. et al. A double-blind placebo-controlled trial ofl-threonine in amyotrophic lateral sclerosis. J Neurol 239, 79–81 (1992). https://doi.org/10.1007/BF00862977
Received:
Revised:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF00862977