(NADH) Nicotinamide adenine dinucleotide is a coenzyme found in all living cells.

Clinical study confirms NADH has a direct, positive impact on rebuilding brain neurotransmitters, enhances. Production of the neurotransmitter dopamine is increased six-fold when taking NADH supplements.

Summary:
A University of Paris research study shows in brain tissue (neuron cell) cultures, the production of the brain neurotransmitters, such as dopamine, can be increased by adding NADH to the culture medium.

The study's results showed that adding NADH yields a six-fold increase in the production of the neurotransmitter dopamine. It was also found coenzyme NADH stimulates the production of many different brain neurotransmitters, including dopamine, norepinephrine or noradrenaline, and serotonin.

Benefits of dopamine production:

NADH stimulates dopamine production. Clinical research has shown that increased dopamine production has a positive effect on the following brain functions: thinking, cognitive functions, mood, drive, strength, coordination, movement, mobility and much more.

In a double blind placebo controlled study performed at a German university hospital, Parkinsonian patients were treated with NADH or a placebo. The patients receiving NADH showed elevated levels of L-dopa and dopamine in the blood. Medical science has proven that Parkinson's disease occurs when the brain cells that produce dopamine die. All Parkinsonian patients in this German study who were taking NADH improved in their condition. (See the Parkinson's disease section for more information about NADH and Parkinson's disease.)

Dopamine's protection against CNS Fatigue:

In neuron cell cultures, dopamine production can be increased by adding NADH to the culture medium. In a dose dependent manner, NADH yields a six-fold increase production of dopamine. Furthermore, NADH stimulates tyrosine hydroxylase (TH), the key enzyme for the production of dopamine in a dosage dependent manner of up to 70%.

Elevated NADH levels result directly in the elevation of pyridine dinucleotide levels in the brain. The brain has an active uptake mechanism for the accumulation of nicotinamide through the choroid plexus, indicating this is an important functional role for brain metabolism and oxidative defense.

NADH has also shown its ability in creating cellular energy at the muscular level.

Research conducted on competitive athletes indicates NADH enhances energy capacity and reaction times.

17 competitive cyclists and long distance runners were used to reasearch performance quality that determined physical performance and measurements of continuous attention. These tests were taken both before and after the athletes took 5 mg of NADH before breakfast each morning for four weeks.

After four weeks of NADH supplementation, most athletes experienced significantly less scattering of reaction times-it dropped by 10% in five athletes, 10 to 20% in eight athletes, and more than 20% in three athletes. Reaction time overall improved considerably in 16 out of the 17 subjects. Compared to baseline measurements, physical performance also improved. Two subjects improved their maximum work performance by more than 10% with another 7 showing increases of up to 10%.

Similar improvements were made in maximum oxygen uptake. Based on these results, the researchers hypothesized that improved reaction times may have resulted from correcting prior NADH deficiency in some athletes or an increase in dopamine production that led to increased alertness and vigilance. They concluded that stimulation of cellular ATP production by NADH enhanced athletic performance.

References:

NADH oxidation drives respiratory Na(+) transport in mitochondria from Yarrowia lipolytica.

Biochemisches Institut, Universität Zürich, 8057, Zurich, Switzerland.

It is generally assumed that respiratory complexes exclusively use protons to energize the inner mitochondrial membrane. Here we show that oxidation of NADH by submitochondrial particles (SMPs) from the yeast Yarrowia lipolytica is coupled to protonophore-resistant Na(+) uptake, indicating that a redox-driven, primary Na(+) pump is operative in the inner mitochondrial membrane. By purification and reconstitution into proteoliposomes, a respiratory NADH dehydrogenase was identified which coupled NADH-dependent reduction of ubiquinone (1.4 mumol min(-1) mg(-1)) to Na(+) translocation (2.0 mumol min(-1) mg(-1)). NADH-driven Na(+) transport was sensitive towards rotenone, a specific inhibitor of complex I. We conclude that mitochondria from Y. lipolytica contain a NADH-driven Na(+) pump and propose that it represents the complex I of the respiratory chain. Our study indicates that energy conversion by mitochondria does not exclusively rely on the proton motive force but may benefit from the electrochemical Na(+) gradient established by complex I.

BACKGROUND AND PURPOSE: NAD(+) is an essential cofactor for cellular energy production and participates in various signaling pathways that have an impact on cell survival. After cerebral ischemia, oxidative DNA lesions accumulate in neurons because of increased attacks by ROS and diminished DNA repair activity, leading to PARP-1 activation, NAD(+) depletion, and cell death. The objective of this study was to determine the neuroprotective effects of NAD(+) repletion against ischemic injury and the underlying mechanism. METHODS: In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours. NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD. Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion. Knockdown of BER enzymes was achieved in cultures using AAV-mediated transfection of shRNA. RESULTS: Direct NAD(+) repletion in neurons either before or after OGD markedly reduced cell death and OGD-induced accumulation of DNA damage (AP sites, single and double strand breaks) in a concentration- and time-dependent manner. NAD(+) repletion restored nDNA repair activity by inhibiting serine-specific phosphorylation of the essential BER enzymes AP endonuclease and DNA polymerase-beta. Knocking down AP endonuclease expression significantly reduced the prosurvival effect of NAD(+) repletion. CONCLUSIONS: Cellular NAD(+) replenishment is a novel and potent approach to reduce ischemic injury in neuronal cultures. Restoration of DNA repair activity via the BER pathway is a key signaling event mediating the neuroprotective effect of NAD(+) replenishment.