Last week we had the suggestion that metforin can act as an anti-aging agent to make oligogendrocyte precursor cells to promote remyelination.
This wasn’t the first time it had been suggested and it clearly was not the last. So this new study claims to be the first study to show metformin-induced AMPK ,could potentially accelerate regeneration . What a difference a week makes, becuase first becomes second, but in realitity its third or more for example. I say just do some reading. I hate “we are the first ” thing in papers.
It should be banned. As soon as I read this, I start searching and it brings out the worse in me, when I find other peoples work is being ignored.
You have to ask “Do you do your lab work, as good as your literature reviews?”. I recently wrote this in a review,, not realising that the review was supposed to be open access. I said I didn’t want to embarrass the author in public but they asked me to re-write the review to be less contensious…I withdrew my review. I couldn’t be bothered to waste my time on the guff being written. Another recent example also made me search and it turned out the authors were guilty of plaguarism….If the editors have any spine to confront this then this is rather bad news for these people.
Anyway now I have that off my chest, I suspect a lot of you have been contemplating taking metformin. This paper will feed into this. What’s is the evidence in the registries about what metformin does to MS? A trial will need to be done, but will it be one or three trials because it seems that every one is having the same idea at the same time. I guess we will have to wait and see.
AMP-Activated Protein Kinase Signaling Protects Oligodendrocytes that Restore Central Nervous System Functions in an Experimental Autoimmune Encephalomyelitis Model https://doi.org/10.1016/j.ajpath.2013.04.030
PURPOSE: Oligodendrocytes (OLGs) damage and myelin distraction is considered as a critical step in many neurological disorders especially multiple sclerosis (MS). Cuprizone (cup) animal model of MS targets OLGs degeneration and frequently used to the mechanistic understanding of de- and remyelination. The aim of this study was exploring the effects of metformin on the OLGs regeneration, myelin repair and profile of neurotrophic factors in the mice brain after cup-induced acute demyelination.
METHODS:Mice (C57BL/6 J) were fed with chow containing 0.2% cup for 5 weeks to induce specific OLGs degeneration and acute demyelination. Next, the cup was withdrawn to allow one-week recovery (spontaneous remyelination). At the end of this period, mature OLGs markers, myelin-associated neurite outgrowth inhibitor protein A (NogoA), premature specific OLGs transcription factor (Olig2), anti-apoptosis marker (survivin), neurotrophic factors, and AMPK activation were monitored in the presence or absence of metformin (50 mg/kg body weight/day) in the corpus callosum (CC).
RESULTS:Our finding indicated that consumption of metformin during the recovery period potentially induced an active form of AMPK (p-AMPK) and promoted repopulation of mature OLGs (MOG+ cells, MBP+ cells) in CC through up-regulation of BDNF, CNTF, and NGF as well as down-regulation of NogoA and recruitment of Olig2+ precursor cells.
CONCLUSIONS:This study for the first time reveals that metformin-induced AMPK, a master regulator of energy homeostasis, activation following toxic demyelination could potentially accelerate regeneration and supports spontaneous demyelination. These findings suggest the development of new therapeutic strategies based on AMPK activation for MS in the near future. Graphical abstract An overview of the possible molecular mechanisms of action of metformin-mediated remyelination.