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

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