Most Parkinson's disease (PD) treatments palliate symptoms by increasi
ng nigrostriatal dopaminergic tone. A unique strategy for accomplishin
g this pharmacological end-point proposes using reduced nicotinamide a
denine dinucleotide (NADH) to boost endogenous dopamine production, si
nce NADH indirectly supplies reducing equivalents to the rate-limiting
, tyrosine hydroxylase-catalysed step of dopamine synthesis. Support f
or using NADH in PD treatment includes claims that NADH stimulates tyr
osine hydroxylase and dopamine biosynthesis in tissue culture and huma
ns, as well as case series associating intravenous and oral NADH admin
istration 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 benefi
t. While NADH may yet prove to ameliorate parkinsonism, recommendation
s for its use in PD are premature.