X-Message-Number: 31377 Date: Thu, 5 Feb 2009 10:54:20 -0800 (PST) From: Subject: Should NADH be added to washout fluids? [NADH is not a popular supplement, but judging by its effects on brain function and aging, it should be.] Front Biosci. 2007 Jan 1;12:2728-34. Intranasal administration with NAD+ profoundly decreases brain injury in a rat model of transient focal ischemia. Ying W, Wei G, Wang D, Wang Q, Tang X, Shi J, Zhang P, Lu H. Department of Neurology, University of California at San Francisco and San Francisco Veterans Affairs Medical Center; 4150 Clement Street, San Francisco, CA 94121, USA. Excessive poly(ADP-ribose) polymerase-1 (PARP-1) activation plays a significant role in ischemic brain damage. Increasing evidence has supported the hypothesis that PARP-1 induces cell death by depleting intracellular NAD+. Based on our in vitro finding that NAD+ treatment can abolish PARP-1-mediated cell death, we hypothesized that NAD+ administration may decrease ischemic brain injury. In this study, we used a rat model of transient focal ischemia to test this hypothesis. We observed that intranasal NAD+ delivery significantly increased NAD+ contents in the brains. Intranasal delivery with 10 mg/kg NAD+ at 2 hours after ischemic onset profoundly decreased infarct formation when assessed either at 24 or 72 hours after ischemia. The NAD+ administration also significantly attenuated ischemia-induced neurological deficits. In contrast, intranasal administration with 10 mg/kg nicotinamide did not decrease ischemic brain damage. These results provide the first in vivo evidence that NAD+ metabolism is a new target for treating brain ischemia, and that NAD+ administration may be a novel strategy for decreasing brain damage in cerebral ischemia and possibly other PARP-1-associated neurological diseases. PMID: 17127275 Drugs Exp Clin Res. 2004;30(1):27-33. Treatment of Alzheimer's disease with stabilized oral nicotinamide adenine dinucleotide: a randomized, double-blind study. Demarin V, Podobnik SS, Storga-Tomic D, Kay G. Department of Neurology, Sestre Milosrdnice University Hospital, Zagreb, Croatia. This study was designed to evaluate the effect of stabilized oral reduced nicotinamide adenine dinucleotide (NADH) on cognitive functioning in patients with Alzheimer's disease (AD). NADH is a coenzyme that plays a key role in cellular energy production and stimulates dopamine production. In previous trials NADH has been shown to improve cognitive functioning in patients with Parkinson's disease, depression and AD. The present trial was a randomized, placebo-controlled, matched-pairs, double-blind, 6-month clinical study. Patients with probable AD (n = 26) were randomized to receive either stabilized oral NADH (10 mg/day) or placebo. Twelve pairs of subjects were matched for age and baseline total score on the Mattis Dementia Rating Scale (MDRS) and the Mini Mental State Examination. After 6 months of treatment, subjects treated with NADH showed no evidence of progressive cognitive deterioration and had significantly higher total scores on the MDRS compared with subjects treated with placebo (p < 0.05). Analysis of MDRS subscales revealed significantly better performance by NADH subjects on measures of verbal fluency (p = 0.019), visual-constructional ability (p = 0.038) and a trend (p = 0.08) to better performance on a measure of abstract verbal reasoning. There were no differences between groups in measures of attention, memory, or in clinician ratings of dementia severity (Clinical Dementia Rating). Consistent with earlier studies, the present findings support NADH as a treatment for AD. PMID: 15134388 Clin Exp Dermatol. 2003 Jan;28(1):61-3. Topical application of NADH for the treatment of rosacea and contact dermatitis. Wo niacka A, Sysa-Jedrzejowska A, Adamus J, Gebicki J. Department of Dermatology, Medical University, Lodz, Poland. Among many important physiological functions played by NADH (the reduced form of beta-nicotinamide adenine dinucleotide) its antioxidative properties are remarkable. Acting directly as an antioxidant, NADH can effectively protect the cell and its membrane from destruction by free radicals. NADH can be stabilized as a suspension in hydrophobic ointments prepared in a way that prevents contact with atmosphere containing oxygen and water. We present the first report of NADH as a treatment for some inflammatory dermatoses. It was found that topical application of 1% NADH diluted in Vaseline ointment can be very effective in the treatment of rosacea and contact dermatitis. Since no adverse effects were observed, therapy with NADH can be viewed as a potential alternative to other established treatments. PMID: 12558633 Wien Med Wochenschr. 2002;152(17-18):450-4. [Stabilized NADH (ENADA) improves jet lag-induced cognitive performance deficit][Article in German] Birkmayer GD, Kay GG, Vurre E. Labor Birkmayer & MEDINFO GmbH, Wien. Current remedies for jet lag (phototherapy, melatonin, stimulant, and sedative medications) are limited in efficacy and practicality. The efficacy of a stabilized, sublingual form of reduced nicotinamide adenine dinucleotide (NADH, ENADAlert, Menuco Corp.) as a countermeasure for jet lag was examined. Because NADH increases cellular production of ATP and facilitates dopamine synthesis, it may counteract the effects of jet lag on cognitive functioning and sleepiness. Thirty-five healthy, employed subjects participated in this double-blind, placebo-controlled study. Training and baseline testing were conducted on the West Coast before subjects flew overnight to the East Coast, where they would experience a 3-hour time difference. Upon arrival, individuals were randomly assigned to received either 20 mg of sublingual stabilized NADH (n = 18) or identical placebo tablets (n = 17). All participants completed computer-administered tests (including Cog Screen) to assess changes in cognitive functioning, mood, and sleepiness in the morning and afternoon. Jet lag resulted in increased sleepiness for over half the participants and deterioration of cognitive functioning for approximately one third. The morning following the flight, subjects experienced lapses of attention in addition to disruptions in working memory, divided attention, and visual perceptual speed. Individuals who received NADH performed significantly better on 4 cognitive test measures (P < or = .05) and reported less sleepiness compared with those who received placebo. No adverse effects were observed with NADH treatment. Stabilized NADH significantly reduced jet lag-induced negative cognitive effects and sleepiness, was easily administered, and was found to have no side effects. PMID: 12385067 Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=31377