Hi Lastly and all,I noted an unpublished study not peer reviewed...

Hi Lastly and all,


I noted an unpublished study not peer reviewed that came out of the Switzerland MND symposium.

Unsupervised machine learning identifies distinct molecular and phenotypic ALS subtypes in post-mortem motor cortex and blood expression data.
https://www.medrxiv.org/content/10.1101/2023.04.21.23288942v1

It basically states MND ALS is within 3 groups of clusters. So, I cross referenced them with Monepantel the best I could .

The grouping are Biologically homogeneous groups/ Excitotoxicity/ Inflammatory .

Excitotoxicity:Inhibiting Caveolin-1-Related Akt/mTOR Signaling Pathway Protects Against N-methyl-D-Aspartate Receptor Activation-Mediated Dysfunction of Blood-Brain Barrier in vitro. Akt/mTOR might be a key downstream kinase.

Biological homogeneous:The mammalian target of rapamycin (mTOR) pathway has been found to play a critical role in the regulation of **Aergic interneurons and synaptic function. Research suggests that mTOR controls the genesis and autophagy of **Aergic interneurons during brain development, indicating its significance in the maintenance of interneuron number and function.

Additionally, in experimental focal cortical dysplasia, mTOR hyperactivation has been associated with a profound disturbance in **Aergic interneurons and synaptic transmission, which was partially rescued by postnatal mTOR inhibitionFurthermore, mTOR inhibitors have been shown to increase **A (γ-aminobutyric acid) levels, suggesting a potential impact on **Aergic neurotransmission

Inflammatory:The mTORC1 pathway plays a significant role in regulating the miR-125b-5p/STAT3 pathway, which in turn influences cell proliferation and tumor growth. Research has shown that hyperactivated mTORC1 signaling leads to the upregulation of STAT3 and the downregulation of miR-125b-5p, contributing to tumorigenesis. Specifically, mTORC1 upregulates STAT3 through the suppression of miR-125b-5p, and the decreased expression of miR-125b-5p contributes to accelerated cell proliferation and tumor growth driven by aberrantly activated mTORC1. This regulatory relationship suggests that the miR-125b-5p/STAT3 pathway could be a potential target for therapeutic intervention in conditions associated with hyperactivated mTORC1 signaling, such as certain cancers .

The link between autophagy and Monepantel is there. The link between Alzheimer's and Monepantel is less clear but is evident.


mTOR signaling as a molecular target for the alleviation of Alzheimer's disease pathogenesis 2022


https://www.sciencedirect.com/science/article/abs/pii/S0197018622000365

Apologies a technical post for some. I understand this level of science is not easy at times.

Kpax