Niacin, NR, NMN, NAD+,NADH: what is the effect on mitochondria and is it beneficial to PD?

I’m working on understanding the process by which niacin ultimately increases NAD and if supplementing with NMN, a more immediate precursor is more advantageous or perhaps NADH is better?

[Hidden]

NADH

elysiumhealth.com/blogs/sci...

[Gioc]

Perhaps these are relevant and in the correct context:

scienceofparkinsons.com/201...

scienceofparkinsons.com/201...

[Gcf51]

Gioc

I have a problem understanding and compiling all the info in my simple mind.

“N1-methylnicotinamide were as much as 40% reduced in the people with Parkinson’s who were being treated Levodopa”. Quote from scienceofparkinsons.com/201...

I throw out one question: Is this a side-effect of Levodopa or a symptom of PD.

With over 60 yr of data with Levodopa treated PD, the line between side-effect of Levodopa or/and a symptom of PD is blurred.

[Gioc in reply to Gcf51]

Good question!

"Abstract

1. Benserazide and carbidopa, decarboxylase inhibitors used in the treatment of Parkinson's disease, have been shown to inhibit the enzyme kynurenine hydrolase in rat and mouse liver. This results in reduced synthesis of nicotinamide coenzymes from tryptophan, and hence an increased reliance on dietary niacin. 2. Pellagra might be expected as a result of this inhibition of endogenous synthesis of nicotinamide nucleotides, but has not been reported in patients treated with either drug. 3. The urinary excretion of N1-methyl-nicotinamide, a product of nicotinamide nucleotide metabolism, is considerably reduced in patients treated with dopa alone or in combination with an inhibitor of peripheral dopa decarboxylase, to as low as 40% of the control value. This means that many of these patients could be classified as 'at risk' of niacin deficiency, even if not frankly deficient. 4. Patients treated with dopa plus a decarboxylase inhibitor, but not those treated with dopa alone, also show a reduced excretion of xanthurenic acid, and an increased excretion of kynurenine, as would be expected after inhibition of the kynurenine pathway, and possibly indicative of marginal vitamin B6 deficiency."

pubmed.ncbi.nlm.nih.gov/477...

My understanding is that the use Benserazide and carbidopa, decarboxylase inhibitors reduced synthesis of nicotinamide coenzymes from tryptophan, ie niacin, causing a niacin deficiency itself.

ncbi.nlm.nih.gov/labs/pmc/a...

[Hidden in reply to Gioc]

It is my understanding that PWP generally have a niacin deficiency preceding CL then the CL makes it worse. Therefore, supplementing with niacin without being on CL is still beneficial. The deficiency is sub clinical and therefore may appear to be in the “normal range” but that is the normal range for the general population and not taking the unique needs of PWP in to consideration. This is supported by reputable sources. I don’t have time at the moment however to refind them.