The compound is a dinucleotide, since it consists of two nucleotides joined through their phosphate groups. One nucleotide contains an adenine base and the other nicotinamide.
The enzymes that make and use NAD+ and NADH are important in both current pharmacology and the research into future treatments for disease.[63]
Drug design and drug development exploits NAD+ in three ways: as a direct target of drugs, by designing enzyme inhibitors or activators based on its structure that change the activity of NAD-dependent enzymes, and by trying to inhibit NAD+ biosynthesis.[64]
The coenzyme NAD+ is not itself currently used as a treatment for any disease. However, it is potentially useful in the therapy of neurodegenerative diseases such as Alzheimer'sand Parkinson disease.[2]
Evidence on the use of NAD+ in neurodegeneration is mixed; studies in mice are promising,[65] whereas a placebo-controlled clinical trial failed to show any effect.[66](from: http://en.wikipedia.org/wiki/NADH)
NADH stands for "nicotinamide adenine dinucleotide (NAD) + hydrogen (H)." This chemical occurs naturally in the body and plays a role in the chemical process that generates energy. People use NADH supplements as medicine.
NADH is used for improving mental clarity, alertness, concentration, and memory; as well as for treating Alzheimer’s disease. Because of its role in energy production, NADH is also used for improving athletic endurance and treating chronic fatigue syndrome (CFS).
Some people use NADH for treating high blood pressure, high cholesterol, jet lag, depression, and Parkinson’s disease; boosting the immune system; opposing alcohol’s effects on the liver and the hormone testosterone; reducing signs of aging; and protecting against the side effects of an AIDS drug called zidovudine (AZT).
Healthcare providers sometimes give NADH by intramuscular (IM) or intravenous (IV) injection for Parkinson's disease and depression.
Safety of NADH: NADH seems safe for most people when used appropriately and short-term, up to 12 weeks. Most people do not experience any side effects when taking the recommended amount each day, which is 10 mg. (from http://www.webmd.com/vitamins-supplements/ingredientmono-1016-NADH.aspx?activeIngredientId=1016&activeIngredientName=NADH)
More on NADH: Neuroprotective effects of the antiparkinson drug Mucuna pruriens
http://onlinelibrary.wiley.com/doi/10.1002/ptr.1514/abstract
Abstract
Mucuna pruriens possesses significantly higher antiparkinson activity compared with levodopa in the 6-hydroxydopamine (6-OHDA) lesioned rat model of Parkinson's disease. The present study evaluated the neurorestorative effect of Mucuna pruriens cotyledon powder on the nigrostriatal tract of 6-OHDA lesioned rats. Mucuna pruriens cotyledon powder significantly increased the brain mitochondrial complex-I activity but did not affect the total monoamine oxidase activity (in vitro). Unlike synthetic levodopa treatment, Mucuna prurienscotyledon powder treatment significantly restored the endogenous levodopa, dopamine, norepinephrine and serotonin content in the substantia nigra. Nicotine adenine dinucleotide (NADH) and coenzyme Q-10, that are shown to have a therapeutic benefit in Parkinson's disease, were present in the Mucuna pruriens cotyledon powder. Earlier studies showed that Mucuna pruriens treatment controls the symptoms of Parkinson's disease. This additional finding of a neurorestorative benefit by Mucuna pruriens cotyledon powder on the degenerating dopaminergic neurons in the substantia nigra may be due to increased complex-I activity and the presence of NADH and coenzyme Q-10.Human Study on Mucuna:
Mucuna pruriens in Parkinson’s disease: a double blind clinical and pharmacological study
http://jnnp.bmj.com/content/75/12/1672.abstract
Abstract
Background: The seed powder of the leguminous plant, Mucuna pruriens has long been used in traditional Ayurvedic Indian medicine for diseases including parkinsonism. We have assessed the clinical effects and levodopa (L-dopa) pharmacokinetics following two different doses of mucuna preparation and compared them with standard L-dopa/carbidopa (LD/CD).Methods: Eight Parkinson’s disease patients with a short duration L-dopa response and on period dyskinesias completed a randomised, controlled, double blind crossover trial. Patients were challenged with single doses of 200/50 mg LD/CD, and 15 and 30 g of mucuna preparation in randomised order at weekly intervals. L-Dopa pharmacokinetics were determined, and Unified Parkinson’s Disease Rating Scale and tapping speed were obtained at baseline and repeatedly during the 4 h following drug ingestion. Dyskinesias were assessed using modified AIMS and Goetz scales.
Results: Compared with standard LD/CD, the 30 g mucuna preparation led to a considerably faster onset of effect (34.6 v 68.5 min; p = 0.021), reflected in shorter latencies to peak L-dopa plasma concentrations. Mean on time was 21.9% (37 min) longer with 30 g mucuna than with LD/CD (p = 0.021); peak L-dopa plasma concentrations were 110% higher and the area under the plasma concentration v time curve (area under curve) was 165.3% larger (p = 0.012). No significant differences in dyskinesias or tolerability occurred.
Conclusions: The rapid onset of action and longer on time without concomitant increase in dyskinesias on mucuna seed powder formulation suggest that this natural source of L-dopa might possess advantages over conventional L-dopa preparations in the long term management of PD. Assessment of long term efficacy and tolerability in a randomised, controlled study is warranted.
Mucuna is neuroprotective:
Anti-parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage
http://onlinelibrary.wiley.com/doi/10.1002/ptr.2219/abstract
Levodopa is considered the ‘gold standard’ for the treatment of Parkinson's disease. However, a serious concern is dyskinesia and motor fluctuation that occurs after several years of use. In vitro experiments have shown that in the presence of divalent copper ions, levodopa may induce intense DNA damage. Mucuna pruriens cotyledon powder (MPCP) has shown anti-parkinson and neuroprotective effects in animal models of Parkinson's disease that is superior to synthetic levodopa. In the present study two different doses of MPCP protected both plasmid DNA and genomic DNA against levodopa and divalent copper-induced DNA strand scission and damage. It exhibited chelation of divalent copper ions in a dose-dependent manner. The copper chelating property may be one of the mechanisms by which MPCP exerts its protective effects on DNA.
