Is NADH Effective in the Treatment of Parkinson’s Disease?
- 48 Downloads
Most Parkinson’s disease (PD) treatments palliate symptoms by increasing nigrostriatal dopaminergic tone. A unique strategy for accomplishing this pharmacological end-point proposes using reduced nicotinamide adenine dinucleotide (NADH) to boost endogenous dopamine production, since NADH indirectly supplies reducing equivalents to the rate-limiting, tyrosine hydroxylase-catalysed step of dopamine synthesis. Support for using NADH in PD treatment includes claims that NADH stimulates tyrosine hydroxylase and dopamine biosynthesis in tissue culture and humans, as well as case series associating intravenous and oral NADH administration with PD rating scale improvements. Theoretical and practical arguments against NADH include underlying NADH disposal impairment in PD and failure of a placebo-controlled trial to show any clear benefit. While NADH may yet prove to ameliorate parkinsonism, recommendations for its use in PD are premature.
KeywordsNADH Levodopa Adis International Limited Tyrosine Hydroxylase Dopamine Synthesis
Unable to display preview. Download preview PDF.
- 2.Reiderer P, Rausch WD, Birkmayer W, et al. CNS modulation of adrenal tyrosine hydroxylase in Parkinson’s disease and metabolic encephalopathies. J Neural Transm 1978; Suppl. 14: 121–31Google Scholar
- 4.Lewitt PA, Miller LP, Newman RP, et al. Tyrosine hydroxylase cofactor (tetrahydrobiopterin) in parkinsonism. In: Hassler RG, Christ JF, editors. Advances in Neurology 40, New York: Raven Press, 1984: 459–62Google Scholar
- 8.Lhermitte J, Kraus WM, McAlpine B. On the occurrence of abnormal deposit of iron in the brain in parkinsonism with special reference to its localization. J Neural Psychopath 1924; 5: 1810–2Google Scholar
- 15.Birkmayer W, Birkmayer JGD, Vrecko K, et al. The clinical benefit of NADH as stimulator of endogenous L-dopa biosynthesis in Parkinsonian patients. In: Korczyn AD, Melamed E, Youdin MBH, editors. Advances in Neurology 53. New York, Raven Press, 1990: 545–9Google Scholar
- 19.Schapira AHV, Coloper JM, Dexter D, et al. Mitochondrial complex I deficiency in Parkinson’s disease [letter]. Lancet 1989; I: 1289Google Scholar
- 25.Birkmeyer JGD, Vrecko C, Vole D, et al. Nicotinamide adenine dinucleotide (NADH): a new therapeutic approach to Parkinson’s disease. Acta Neurol Scand 1993; 146: 32–5Google Scholar
- 30.Birkmayer W, Birkmayer JGD, Vrecko C, et al. Nicotinamide adenine dinucleotide (NADH) as medication for Parkinson’s disease: experience with 415 patients. New Trends Clin Neuropharm 1990; 4: 7–24Google Scholar