Standard warning in effect for non-scientists (i.e., skip this post):
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. 
*vida.demarin@zg.tel.hr
  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
___________
Biologist