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In the Green et al. study, nicotinamide [niacinamide] was found to lower levels of a protein called phosphorylated tau that leads to the development of tangles (see Fig. 1). Of further consequence, the vitamin also strengthened the ``scaffolding'' along which information travels in brain cells. Good scaffolding helps preserve neurons, thereby further preventing symptoms in mice genetically wired to develop Alzheimer's.

In their search for just what was going on, nicotinamide did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer's lesion. Given this lack of effect on beta amyloid levels, the researchers figured the compound must be improving cognition through some other mechanism.

Upon analyzing protein extracts from whole brain samples of treated and control AD mice, they found a 20 percent reduction in levels of tau in the nicotinamide-treated animals. They saw no differences at several tau sites typically phosphorylated in AD mice at the end of eight months, but a whopping 60 percent reduction in Thr231-phospho-tau--a particular species of tau that has been reported to interfere with microtubule polymerization and is a commonly used biomarker for AD--in the nicotinamide group compared with vehicle. ``It's incredibly dramatic,'' Green told the Alzheimer's Research Forum. ``This thing [a biomarker for AD] is just wiped from the brain very specifically.''5

Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer's patients. ``Microtubules are like highways inside cells.

What we're doing with nicotinamide is making a wider, more stable highway,'' Green said. ``In Alzheimer's disease, this highway breaks down. We are preventing that from happening.''

``At the moment we're talking about a disease for which there is no sort of treatment and this is likely to be far safer than any of the upcoming drugs. Nicotinamide is just vitamin B3, it's really cheap, it's safe and easy to get hold of,'' said Green.
http://www.als.net/forum/topic.asp?TOPIC_ID=3799

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Posts: 2966 | From Colorado | Registered: Dec 2005  |  IP: Logged | 

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The hepatotoxic effects of high-dose niacin therapy (e.g. for high blood lipids) first emerged with sustained-release niacin. The sustained-release form was sometimes associated with liver problems at doses as low as 3 grams per day. Even those cases seemed to be presented in the literature as case reports, suggesting it was a somewhat uncommon phenomenon, but certainly worth watching for in all treated patients.

Now, one theory of the increased toxicity of the sustained release formulation is that a greater proportion of it gets shunted down the niacinamide pathway, compared to the conjugation pathway (which causes that yucky flushing feeling). That would seem to implicate niacinamide itself for the toxic reaction, yet I cannot find so much as a case report of a single instance of liver problems related to niacinamede intake.

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[Niacinamide].....Energy Production and Regenerates Glutathione. Niacinamide is the form of niacin that circulates in the bloodstream. Niacinamide is utilized by all body tissues to synthesize nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), the active forms of niacin.

NAD and NADP are essential for over 200 enzymes and function as a hydrogen donor or electron acceptor (important for the synthesis of energy - ATP). NAD is also involved in the activation of folate and regeneration of reduced glutathione. Niacinamide and niacin are the two forms of Vitamin B3. Niacinamide does not cause flushing or skin irritation.

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Posts: 2966 | From Colorado | Registered: Dec 2005  |  IP: Logged |