LONGECITY

yet science moves on ... and the typical pooh-pooh-ers such as fa guy/girl, sens/sens zealots, etc. face another study ...

"

Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease

Highlights

•NMN improved behavioral measures of cognitive impairments in AD-Tg mice.
•NMN decreased β-amyloid production, amyloid plaque burden, synaptic loss, and inflammatory responses in AD-Tg mice.
•NMN reduced JNK activation in AD-Tg mice.
•NMN regulated the expression of APP cleavage secretase in AD-Tg mice.

Abstract

Amyloid-β (Aβ) oligomers have been accepted as major neurotoxic agents in the therapy of Alzheimer's disease (AD).
It has been shown that the activity of nicotinamide adenine dinucleotide (NAD + ) is related with the decline of Aβ toxicity in AD.
Nicotinamide mononucleotide (NMN), the important precursor of NAD+, is produced during the reaction of nicotinamide phosphoribosyl transferase (Nampt).
This study aimed to figure out the potential therapeutic effects of NMN and its underlying mechanisms in APPswe/PS1dE9 (AD-Tg) mice.
We found that NMN gave rise to a substantial improvement in behavioral measures of cognitive impairments compared to control AD-Tg mice.
In addition, NMN treatment significantly decreased β-amyloid production, amyloid plaque burden, synaptic loss, and inflammatory responses in transgenic animals.
Mechanistically, NMN effectively controlled JNK activation.
Furthermore, NMN potently progressed nonamyloidogenic amyloid precursor protein (APP) and suppressed amyloidogenic APP by mediating
the expression of APP cleavage secretase in AD-Tg mice. Based on our findings, it was suggested that NMN substantially decreases multiple

"


http://www.sciencedi...30439401730246X

Surprised to see no comments on this study.  

Maybe I don't understand the implications well enough.  

It seems to me this demonstrates very powerful possibilities for reversing AD damage.

More so than have been demonstrated previously for NR ?

FULL TEXT:

FULL TEXT:

@ APBT

thanks for posting!

Surprised to see no comments on this study. 

... there are couple individuals here on this forum that have a ton of free time and they spread the idea that "only sens" has a valid approach.

when a study like this one appears, they try to ignore it, or cast doubts on it (look at fightaging guy/girl and michael rae from sens as an example).

but as usual, science moves on, and whatever they do, after a while things come to the light.

Kinda makes sense.  Wonder what the long-term cancer risk is for inhibiting JNK.  

Subcutaneous adiministration of NMN (100 mg/kg, Sigma N3501) in sterile (Phosphate Buffered
Saline) PBS (200 μl) was applied to each mouse of NMN-treated groups every other day for
28 days.

 

 

HED for 70 kg for adult human is 570 mg.  Dosing was SubQ and done every other day for 28 days in 6 mo Tg mouse.  Does this give us any insight into the need for pulsatile exposure vs. continuous availability?  

Is there any reason to think that oral NR wouldn't give you the same result?

And since we have a lot of people taking NR for supposed life/healthspan increases, I too wonder about the long term effects of inhibiting JNK are.

Is there any reason to think that oral NR wouldn't give you the same result?

 

 

And since we have a lot of people taking NR for supposed life/healthspan increases, I too wonder about the long term effects of inhibiting JNK are.

It does seem NR has a similar benefit as found in this recently published study:

https://www.medicaln...cles/320879.php

One thing I did notice in that study:

"Intriguingly, however, their levels of the beta-amyloid protein stayed the same as those of the control mice"

That seems in contrast with the results of the NMN study that is subject of this thread:

"NMN decreased β-amyloid production, amyloid plaque burden, synaptic loss, and inflammatory responses in AD-Tg mice"

Both studies seem positive, but can anyone decipher if this is truly a different effect between the two supplements, and if it is relevant or not?

What do you think about this?  http://www.life-enha...heimers-disease

Sounds quite impressive.  Except that the study that article was based on was in 2008:

https://www.ncbi.nlm...pubmed/18987186

I wonder what happened in the clinical study they mentioned?

In 2011 UC Irvine kept a phase II clinical trial of oral nicotinamide but the data were inconclusive.

https://clinicaltria...inamide&rank=10