Great post JTG,

A few old posts and reposts of information here for those (relatively) new to PharmAust. A good post for understanding the use of MPL on MND was done by what may have been a semi-delirious @kpax post COVID(Vaccine) illness here: https://hotcopper.com.au/posts/53516236/single

I can't say enough how much I appreciate the posts by the many here with a great wealth of knowledge and/or ability to research all things MPL, it's all quite fascinating.

@Jockthegreat thank you for that article. The paragraph I quite enjoyed was:


This post has me searching through research articles on why we have a cure for Alzheimers disease as well, and I came across this one (not sure if it has been posted yet) which has more of what @kpax has been "banging on" about for ages regarding TDP-43 (thank you Kpax) and it's possible affects on muscle tissue.

Expanding the TDP-43 Proteinopathy Pathway From Neurons to Muscle: Physiological and Pathophysiological Functions

https://www.frontiersin.org/articles/10.3389/fnins.2022.815765/full

TDP-43 overexpression in myoblasts and muscle tissue of mice is toxic on its own as overexpression reduces cell viability, the size of the myofibers and induces the formation of TDP-43 containing inclusions. These findings point toward an independent muscle-specific pathological mechanism of TDP-43 aggregates in muscle cells.

Maintaining the balance of TDP-43, mitochondria, and autophagy: a promising therapeutic strategy for neurodegenerative diseases
I am pretty sure @Quiltman , @kpax or someone else posted this one not too long ago.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7597011/

Thus, the normal physiological functions of TDP-43 are particularly important for cell survival. Normal TDP-43 is located in various subcellular structures including mitochondria, mitochondrial-associated membrane, RNA particles and stress granules to regulate the endoplasmic reticulum-mitochondrial binding, mitochondrial protein translation, and mRNA transport and translation.

In conclusion, it is evident that TDP-43 protein pathology, mitochondrial disorders, and impaired autophagy are common prominent pathological features of major neurodegenerative diseases including ALS, FTD, and AD. Inhibition of mitochondrial localization of TDP-43 is sufficient to alleviate mitochondrial dynamic abnormalities, neuronal loss, and behavioral defects in transgenic mice with different mutant forms of TDP-43. Due to the close relationship between mitochondrial and autophagy functions and TDP-43, and their contributions to the progression of neurodegenerative diseases, we believe that maintaining the balance among TDP-43, mitochondria, and autophagy is a promising strategy for the treatment of neurodegenerative diseases.

I also had another look at the 70 diseases that Monepantel probably is effective against (https://hotcopper.com.au/posts/44413785/single) and figure there might be a few more as a result of TDP-43 aggregates in muscle cells.

Regards,

Havelots

NLN....