The coenzyme nicotinamide adenine dinucleotide (NADH) improves the disability of parkinsonian patients.

The coenzyme nicotinamide adenine dinucleotide (NADH) has been used in an open label trial as novel medication in 34 patients with Parkinson's disease, using an intravenous administration technique. In all patients a beneficial clinical effect was observed. 21 patients (61.7%) showed a very good (better than 30%) improvement of disability, 13 patients (38.3%) a moderate (up to 30%) improvement. Concomitant with the improvement of the disability the urine level of homovanillic acid (HVA) increased significantly in all patients (in some patients by more than a 100%). The daily "on phases" of the patients could be increased from 2 up to 9 hours in the individual patients by NADH administration.

Strategy and tactic of modern Parkinson therapy.

The aim of modern Parkinson therapy is to overcome the dopamine deficit in the brain of parkinsonian patients which is the cause of their motor disability. This can be achieved in two ways: (a) substitution of the lacking dopamine by l-dopa, or (b) stimulation of the endogenous biosynthesis by activating the enzyme tyrosine hydroxylase. The latter approach is possible by the iron compound oxyferriscorbone or by the coenzyme nicotinamide adenine dinucleotide (NADH). In addition to these two major medications the essential therapeutic additives such as the decarboxylase inhibitor benserazide, the monoamineoxidase B inhibitor deprenyl and the dopamine receptor agonist lisuride should be used for the fine adjustment of the individual patient.

Nicotinamidadenindinucleotide (NADH): the new approach in the therapy of Parkinson's disease.

The coenzyme Nicotinamidadenindinucleotide (NADH) has been used as novel medication in 34 Parkinson patients in an open label trial. In all patients, a beneficial clinical effect was observed. Twenty-one patients (61.7 percent) showed a very good (better than 30 percent) improvement of disability and 13 patients (38.3 percent) a moderate (up to 30 percent) improvement. The effect of NADH was dependent on the dosage and the severity of the case. The best therapeutic dose was in the range of 25 to 50 mg per day. The clinical improvement was more pronounced after i.v. and less after i.m. administration. Concomitant with improvement of the disability, the urine level of homovanillinic acid (HVA) increased significantly in all patients (in some patients by more than a 100 percent), indicating a stimulation of the endogenous L-DOPA biosynthesis. The daily "on phases" of the patients could be increased from two up to nine hours in the individual patients by NADH administration.

Stimulation of endogenous L-dopa biosynthesis--a new principle for the therapy of Parkinson's disease. The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotidephosphate (NADPH).

The coenzyme nicotinamide adenine dinucleotide (NADH) has been used as a novel medication in 161 Parkinson patients in an open label trial. In all but 18 patients (11.2%) an improvement in their disability was observed. 115 patients (71.4%) showed a very good (better than 30%) response, and 28 patients (17.4%) a moderate response up to 30%. The best results were obtained with a dose of 25 to 50 mg every second day by i.v. administration. Concomitantly with the improvement in disability, the urine HVA level increased significantly, indicating a stimulation of endogenous L-DOPA biosynthesis. 8 patients have been treated with nicotinamide adenine dinucleotidephosphate (NADPH), 5 of whom exhibited an improvement in their disability from 35 to 55%. The other 3 showed a moderate response of 20 to 25%. In all these patients an increase in the urine level of HVA was detected, reflecting elevated endogenous L-DOPA production.