X-Message-Number: 29173 Date: Thu, 22 Feb 2007 18:03:30 -0800 (PST) From: Subject: NADH - an underrated supplement [An argument could be made that oral NADH should be part of a standard pretreatment protocol for cryonics, or for that matter, most surgical procedures as well.] 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 [Note that in the above rodent test, a very large dosage was administered during ischemia. Administered before ischemia, a much lower dosage might suffice, as below. As a speculation, routine NADH supplementation might largely eliminate both Alzheimer, and stroke associated mortality in life-extensionists.] 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 Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=29173